STRATEGY STUDIO / NONPROFIT PEOPLE SEARCH

BRIGHTFOCUS FOUNDATION: Form 990, tax year 2013

View the entire original 990 at ProPublica ↗

Organization
BRIGHTFOCUS FOUNDATION (EIN 23-7337229)
Tax period
2013-04-01 to 2014-03-31
Filed
2014-08-13
IRS object ID
201422259349301437
Schema version
2013v3.0
Source
Download XML · Original 990 at ProPublica

Every field in the e-filed return. Faint text is the IRS element name, for citing.

Return header ReturnHeader

FieldValueIRS element (for citing)
Return2014-08-13T10:39:21-05:00ReturnTs
Tax Period End2014-03-31TaxPeriodEndDt

Preparer Firm PreparerFirmGrp

FieldValueIRS element (for citing)
Preparer Firm EIN521511275PreparerFirmEIN

Preparer Firm Name PreparerFirmName

FieldValueIRS element (for citing)
Business Name Line1Raffa PCBusinessNameLine1

Preparer US Address PreparerUSAddress

FieldValueIRS element (for citing)
Address Line11899 L Street NW Suite 900AddressLine1
CityWashingtonCity
StateDCState
ZIP Code20036ZIPCode
FieldValueIRS element (for citing)
Return Type990ReturnTypeCd
Tax Period Begin2013-04-01TaxPeriodBeginDt

Filer Filer

FieldValueIRS element (for citing)
EIN237337229EIN

Business Name BusinessName

FieldValueIRS element (for citing)
Business Name Line1BrightFocus FoundationBusinessNameLine1
FieldValueIRS element (for citing)
Business Name ControlBRIGBusinessNameControlTxt
Phone3019483244PhoneNum

US Address USAddress

FieldValueIRS element (for citing)
Address Line122512 Gateway Center DriveAddressLine1
CityClarksburgCity
StateMDState
ZIP Code20871ZIPCode

Business Officer BusinessOfficerGrp

FieldValueIRS element (for citing)
PersonStacy Pagos HallerPersonNm
Person TitlePresident/CEOPersonTitleTxt
Phone3019483244PhoneNum
Signature2014-08-13SignatureDt
Discuss With Paid PreparerYes (1)DiscussWithPaidPreparerInd

Preparer Person PreparerPersonGrp

FieldValueIRS element (for citing)
Preparer PersonFrank H SmithPreparerPersonNm
PTINP00639053PTIN
Phone2028225000PhoneNum
Preparation2014-08-13PreparationDt
FieldValueIRS element (for citing)
Tax2013TaxYr
Build TS2015-11-30 17:44:51ZBuildTS

Form 990 IRS990

FieldValueIRS element (for citing)
Principal OfficerStacy Pagos HallerPrincipalOfficerNm

US Address USAddress

FieldValueIRS element (for citing)
Address Line122512 Gateway Center DriveAddressLine1
CityClarksburgCity
StateMDState
ZIP Code20871ZIPCode
FieldValueIRS element (for citing)
Gross Receipts$32,971,607GrossReceiptsAmt
Group Return For Affiliates0GroupReturnForAffiliatesInd
Organization501c3Yes (X)Organization501c3Ind
Website Addresswww.brightfocus.orgWebsiteAddressTxt
Type Of Organization CorpYes (X)TypeOfOrganizationCorpInd
Formation1973FormationYr
Legal Domicile StateDCLegalDomicileStateCd
Activity Or MissionBrightFocus Foundation seeks to save sight and mind.ActivityOrMissionDesc
Voting Members Governing Body11VotingMembersGoverningBodyCnt
Voting Members Independent11VotingMembersIndependentCnt
Total Employee51TotalEmployeeCnt
Total Volunteers96TotalVolunteersCnt
Total Gross UBI$0TotalGrossUBIAmt
Net Unrelated Bus Txbl Incm$0NetUnrelatedBusTxblIncmAmt
PY Contributions Grants$23,534,029PYContributionsGrantsAmt
CY Contributions Grants$25,126,233CYContributionsGrantsAmt
PY Program Service Revenue$0PYProgramServiceRevenueAmt
CY Program Service Revenue$0CYProgramServiceRevenueAmt
PY Investment Income$614,981PYInvestmentIncomeAmt
CY Investment Income$766,939CYInvestmentIncomeAmt
PY Other Revenue$734,020PYOtherRevenueAmt
CY Other Revenue$830,470CYOtherRevenueAmt
PY Total Revenue$24,883,030PYTotalRevenueAmt
CY Total Revenue$26,723,642CYTotalRevenueAmt
PY Grants And Similar Paid$7,527,500PYGrantsAndSimilarPaidAmt
CY Grants And Similar Paid$8,755,315CYGrantsAndSimilarPaidAmt
PY Benefits Paid To Members$0PYBenefitsPaidToMembersAmt
CY Benefits Paid To Members$0CYBenefitsPaidToMembersAmt
PY Salaries Comp Emp Bnft Paid$3,758,245PYSalariesCompEmpBnftPaidAmt
CY Salaries Comp Emp Bnft Paid$4,031,826CYSalariesCompEmpBnftPaidAmt
PY Total Prof Fndrsng Expns$512,040PYTotalProfFndrsngExpnsAmt
CY Total Prof Fndrsng Expns$407,033CYTotalProfFndrsngExpnsAmt
CY Total Fundraising Expense$4,854,132CYTotalFundraisingExpenseAmt
PY Other Expenses$11,776,521PYOtherExpensesAmt
CY Other Expenses$11,933,206CYOtherExpensesAmt
PY Total Expenses$23,574,306PYTotalExpensesAmt
CY Total Expenses$25,127,380CYTotalExpensesAmt
PY Revenues Less Expenses$1,308,724PYRevenuesLessExpensesAmt
CY Revenues Less Expenses$1,596,262CYRevenuesLessExpensesAmt
Total Assets BOY$42,238,889TotalAssetsBOYAmt
Total Assets EOY$48,181,675TotalAssetsEOYAmt
Total Liabilities BOY$14,204,661TotalLiabilitiesBOYAmt
Total Liabilities EOY$16,829,153TotalLiabilitiesEOYAmt
Net Assets Or Fund Balances BOY$28,034,228NetAssetsOrFundBalancesBOYAmt
Net Assets Or Fund Balances EOY$31,352,522NetAssetsOrFundBalancesEOYAmt
Info In Schedule O Part IIIYes (X)InfoInScheduleOPartIIIInd
MissionBrightFocus Foundation seeks to save mind and sight by funding innovative research worldwide and by promoting better health through education. Please refer to Schedule O for a complete overview of our mission.MissionDesc
Significant New Program Srvc0SignificantNewProgramSrvcInd
Significant Change0SignificantChangeInd
Expense$11,186,265ExpenseAmt
Grant$5,211,638GrantAmt
DescAlzheimer's Disease Research (ADR) -- BrightFocus's ADR program funds research focused on understanding Alzheimer's disease's causes, its early detection, and treatments to help slow or stop its progression, and ultimately to prevent the disease altogether. ADR annually awards peer-reviewed grants to scientists from institutions worldwide who are conducting biomedical and clinical research on Alzheimer's disease.BrightFocus is honored to have supported the early research of two eventual Nobel Prize winners: Dr. Stanley Prusiner and Dr. Paul Greengard, whose work has been instrumental to our current understanding of Alzheimer's disease. Further illustrating BrightFocus's impact, a third-party roster of papers that considered milestones in Alzheimer's disease lists 19 BrightFocus-supported papers, six percent of the total recognized.During the fiscal year ended March 31, 2014, ADR grants included funding for 25 new projects, totaling $5,071,638, and awarded $136,000 for four special projects, including big data approaches to Alzheimer's disease and research into the basis of gender differences in risk of Alzheimer's. Additional information about specific projects are included in Schedules F & I.BrightFocus continues to develop its partnership with the academic journal "Molecular Neurodegeneration" as the official journal of the BrightFocus Foundation. The journal publishes technical papers primarily on topics related to the ADR program. As an "open access" journal, there is no fee for readers, and all content is freely available through its website. This ensures maximal exposure of journal contents to scientists and care providers world-wide.ADR-supported research made the news in this fiscal year, including high visibility reports relating diabetes drugs to severity of Alzheimer's disease, and pointing to reasons why current drugs fail to address the underlying causes of Alzheimer's. Both areas of research are the subject of ongoing BrightFocus funded clinical trials. More details are available in the news updates section of the BrightFocus.org website.In addition to supporting cutting-edge research, Alzheimer's Disease Research provides excellent resources on detecting, treating, and living with the disease. Alzheimer's disease ranks as at least the sixth leading cause of death in the United States, yet it is the only cause of death among the top 10 in America without a way to prevent, cure, or even slow its progression. It is an irreversible degeneration of the brain that causes disruptions in memory, cognition, personality, and other functions and inevitably leads to death. More than 5 million Americans aged 65 and older are thought to have Alzheimer's disease today, and that number is expected to triple in the next 40 years. Every 67 seconds, someone in America develops Alzheimer's. By mid-century, someone in America will develop the disease every 33 seconds.Desc

Prog Srvc Accom Acty2 ProgSrvcAccomActy2Grp

FieldValueIRS element (for citing)
Expense$4,176,400ExpenseAmt
Grant$1,945,400GrantAmt
DescMacular Degeneration Research (MDR), a program of BrightFocus, has awarded nearly $14 million to scientists studying the disease. The latest research is focused on novel treatments for the disease, understanding its causes and progression, drug therapies, and new screening techniques.During the fiscal year ending March 31, 2014, MDR grants included $1,920,000 in peer-reviewed grant awards to 16 new research projects that range from studies to simultaneously photograph and test the function of AMD affected retinas to those aimed at designing new cell-based therapies to target and eliminate the molecular changes that lead to macular degeneration. Additional details about specific projects are included in Schedule I.MDR-funded projects were featured in media articles, including progress in the development of a molecular switch to replace dying photoreceptors, as well as progress in treating the currently untreatable dry form of macular degeneration. More details on this and other successful outcomes achieved through MDR funding are available in the news updates section of the BrightFocus.org website.In addition to supporting cutting-edge research, Macular Degeneration Research provides excellent resources on detecting, treating, and living with this disease. Age-related macular degeneration is a leading cause of vision loss in the United States. It destroys the macula, the part of the eye that provides sharp, central vision needed for seeing objects clearly. The most common eye condition in people age 60 and older, it can lead to vision loss in one or both eyes, making it difficult to recognize faces, drive a car, or read.Desc

Prog Srvc Accom Acty3 ProgSrvcAccomActy3Grp

FieldValueIRS element (for citing)
Expense$2,133,187ExpenseAmt
Grant$1,598,277GrantAmt
DescBrightFocus's National Glaucoma Research (NGR) program has awarded more than $22.6 million worldwide for the study of glaucoma. NGR-supported research has been focused on the eye-brain connection, the mechanisms for pressure buildup in the eye, preventing damage to the optic nerve, and understanding the role genes play in order to develop early glaucoma screening and targeted treatments.NGR grants are available to glaucoma researchers worldwide. NGR places special emphasis on encouraging applications from young scientists and those with cutting-edge ideas. Annual grant applications are peer-reviewed, and recipient selections are based on scientific merit. During the fiscal year ending March 31, 2014, NGR awarded $1,398,277 for 14 new projects that range from calculating individual risk for glaucoma to real-time monitoring and control of pressure in the eye, a significant risk factor for glaucoma. In addition, the NGR program launched a $200,000 investigation into the suitability of two already existing drugs for potential ability to repair or enhance vision in glaucoma patients. Additional details about specific projects are included in Schedules F & I.NGR-funded research was recognized by the media this year, including an NGR supported strategy to block the accumulation of toxic proteins that can lead to early onset glaucoma. More details are available in the news updates section of the BrightFocus.org website.In addition to supporting cutting-edge research, National Glaucoma Research provides excellent resources on detecting, treating, and living with the disease. Glaucoma is a group of diseases that damage the eye's optic nerve and can result in vision loss and permanent blindness. More than 3 million Americans age 40 and older have glaucoma. More than 60 million people in the world have the disease, and that number is expected to increase by as much as 20 million by 2020. With early detection and treatment, glaucoma often can be managed to protect eyes from more serious vision loss, but it is estimated that only half of the people living with glaucoma are aware that they have the disease.Desc
FieldValueIRS element (for citing)
Total Program Service Expenses$17,495,852TotalProgramServiceExpensesAmt
Described In Section501c3Yes (1)DescribedInSection501c3Ind
Schedule B RequiredYes (1)ScheduleBRequiredInd
Political Campaign Acty0PoliticalCampaignActyInd
Lobbying ActivitiesYes (1)LobbyingActivitiesInd
Subject To Proxy Tax0SubjectToProxyTaxInd
Donor Advised Fund0DonorAdvisedFundInd
Conservation Easements0ConservationEasementsInd
Collections Of Art0CollectionsOfArtInd
Credit Counseling0CreditCounselingInd
Temp Or Permanent EndowmentsYes (1)TempOrPermanentEndowmentsInd
Report Land Building EquipmentYes (1)ReportLandBuildingEquipmentInd
Report Investments Other SecYes (1)ReportInvestmentsOtherSecInd
Report Program Related Invst0ReportProgramRelatedInvstInd
Report Other Assets0ReportOtherAssetsInd
Report Other LiabilitiesYes (1)ReportOtherLiabilitiesInd
Include FIN48 FootnoteYes (1)IncludeFIN48FootnoteInd
Independent Audit Fincl Stmt0IndependentAuditFinclStmtInd
Consolidated Audit Fincl StmtYes (1)ConsolidatedAuditFinclStmtInd
School Operating0SchoolOperatingInd
Foreign Office0ForeignOfficeInd
Foreign ActivitiesYes (1)ForeignActivitiesInd
More Than5000 K To OrgYes (1)MoreThan5000KToOrgInd
More Than5000 K To Individuals0MoreThan5000KToIndividualsInd
Professional FundraisingYes (1)ProfessionalFundraisingInd
Fundraising Activities0FundraisingActivitiesInd
Gaming Activities0GamingActivitiesInd
Operate Hospital0OperateHospitalInd
Grants To OrganizationsYes (1)GrantsToOrganizationsInd
Grants To Individuals0GrantsToIndividualsInd
Schedule J RequiredYes (1)ScheduleJRequiredInd
Tax Exempt Bonds0TaxExemptBondsInd
Engaged In Excess Benefit Trans0EngagedInExcessBenefitTransInd
PY Excess Benefit Trans0PYExcessBenefitTransInd
Loan Outstanding0LoanOutstandingInd
Grant To Related Person0GrantToRelatedPersonInd
Business Rln With Org Mem0BusinessRlnWithOrgMemInd
Business Rln With Fam Mem0BusinessRlnWithFamMemInd
Business Rln With Officer Ent0BusinessRlnWithOfficerEntInd
Deductible Non Cash ContriYes (1)DeductibleNonCashContriInd
Deductible Art Contribution0DeductibleArtContributionInd
Terminate Operations0TerminateOperationsInd
Partial Liquidation0PartialLiquidationInd
Disregarded EntityYes (1)DisregardedEntityInd
Related Entity0RelatedEntityInd
Related Organization Ctrl Ent0RelatedOrganizationCtrlEntInd
Trnsfr Exmpt Non Chrtbl Rltd Org0TrnsfrExmptNonChrtblRltdOrgInd
Activities Conducted Prtshp0ActivitiesConductedPrtshpInd
Schedule O RequiredYes (1)ScheduleORequiredInd
IRP Document212IRPDocumentCnt
IRP Document W2 G0IRPDocumentW2GCnt
Backup Wthld ComplianceYes (1)BackupWthldComplianceInd
Employee51EmployeeCnt
Employment Tax Returns FiledYes (1)EmploymentTaxReturnsFiledInd
Unrelated Bus Incm Over Limit0UnrelatedBusIncmOverLimitInd
Foreign Financial Account0ForeignFinancialAccountInd
Prohibited Tax Shelter Trans0ProhibitedTaxShelterTransInd
Taxable Party Notification0TaxablePartyNotificationInd
Nondeductible Contributions0NondeductibleContributionsInd
Quid Pro Quo Contributions0QuidProQuoContributionsInd
Form8282 Property Disposed Of0Form8282PropertyDisposedOfInd
Rcv Fnds To Pay Prsnl Bnft Cntrct0RcvFndsToPayPrsnlBnftCntrctInd
Pay Premiums Prsnl Bnft Cntrct0PayPremiumsPrsnlBnftCntrctInd
Indoor Tanning Services0IndoorTanningServicesInd
Info In Schedule O Part VIYes (X)InfoInScheduleOPartVIInd
Governing Body Voting Members11GoverningBodyVotingMembersCnt
Independent Voting Member11IndependentVotingMemberCnt
Family Or Business Rln0FamilyOrBusinessRlnInd
Delegation Of Mgmt Duties0DelegationOfMgmtDutiesInd
Change To Org Documents0ChangeToOrgDocumentsInd
Material Diversion Or Misuse0MaterialDiversionOrMisuseInd
Members Or Stockholders0MembersOrStockholdersInd
Election Of Board Members0ElectionOfBoardMembersInd
Decisions Subject To Approva0DecisionsSubjectToApprovaInd
Minutes Of Governing BodyYes (1)MinutesOfGoverningBodyInd
Minutes Of CommitteesYes (1)MinutesOfCommitteesInd
Officer Mailing Address0OfficerMailingAddressInd
Local Chapters0LocalChaptersInd
Form990 Provided To Gvrn BodyYes (1)Form990ProvidedToGvrnBodyInd
Conflict Of Interest PolicyYes (1)ConflictOfInterestPolicyInd
Annual Disclosure Covered PrsnYes (1)AnnualDisclosureCoveredPrsnInd
Regular Monitoring EnfrcYes (1)RegularMonitoringEnfrcInd
Whistleblower PolicyYes (1)WhistleblowerPolicyInd
Document Retention PolicyYes (1)DocumentRetentionPolicyInd
Compensation Process CEOYes (1)CompensationProcessCEOInd
Compensation Process Other0CompensationProcessOtherInd
Investment In Joint Venture0InvestmentInJointVentureInd
States Where Copy Of Return Is FldAKStatesWhereCopyOfReturnIsFldCd
States Where Copy Of Return Is FldALStatesWhereCopyOfReturnIsFldCd
States Where Copy Of Return Is FldARStatesWhereCopyOfReturnIsFldCd
States Where Copy Of Return Is FldAZStatesWhereCopyOfReturnIsFldCd
States Where Copy Of Return Is FldCAStatesWhereCopyOfReturnIsFldCd
States Where Copy Of Return Is FldCTStatesWhereCopyOfReturnIsFldCd
States Where Copy Of Return Is FldFLStatesWhereCopyOfReturnIsFldCd
States Where Copy Of Return Is FldGAStatesWhereCopyOfReturnIsFldCd
States Where Copy Of Return Is FldHIStatesWhereCopyOfReturnIsFldCd
States Where Copy Of Return Is FldILStatesWhereCopyOfReturnIsFldCd
States Where Copy Of Return Is FldKSStatesWhereCopyOfReturnIsFldCd
States Where Copy Of Return Is FldKYStatesWhereCopyOfReturnIsFldCd
States Where Copy Of Return Is FldMEStatesWhereCopyOfReturnIsFldCd
States Where Copy Of Return Is FldMDStatesWhereCopyOfReturnIsFldCd
States Where Copy Of Return Is FldMAStatesWhereCopyOfReturnIsFldCd
States Where Copy Of Return Is FldMIStatesWhereCopyOfReturnIsFldCd
States Where Copy Of Return Is FldMNStatesWhereCopyOfReturnIsFldCd
States Where Copy Of Return Is FldMSStatesWhereCopyOfReturnIsFldCd
States Where Copy Of Return Is FldNHStatesWhereCopyOfReturnIsFldCd
States Where Copy Of Return Is FldNJStatesWhereCopyOfReturnIsFldCd
States Where Copy Of Return Is FldNMStatesWhereCopyOfReturnIsFldCd
States Where Copy Of Return Is FldNYStatesWhereCopyOfReturnIsFldCd
States Where Copy Of Return Is FldNCStatesWhereCopyOfReturnIsFldCd
States Where Copy Of Return Is FldNDStatesWhereCopyOfReturnIsFldCd
States Where Copy Of Return Is FldOHStatesWhereCopyOfReturnIsFldCd
States Where Copy Of Return Is FldOKStatesWhereCopyOfReturnIsFldCd
States Where Copy Of Return Is FldORStatesWhereCopyOfReturnIsFldCd
States Where Copy Of Return Is FldPAStatesWhereCopyOfReturnIsFldCd
States Where Copy Of Return Is FldRIStatesWhereCopyOfReturnIsFldCd
States Where Copy Of Return Is FldSCStatesWhereCopyOfReturnIsFldCd
States Where Copy Of Return Is FldTNStatesWhereCopyOfReturnIsFldCd
States Where Copy Of Return Is FldUTStatesWhereCopyOfReturnIsFldCd
States Where Copy Of Return Is FldVAStatesWhereCopyOfReturnIsFldCd
States Where Copy Of Return Is FldWAStatesWhereCopyOfReturnIsFldCd
States Where Copy Of Return Is FldWVStatesWhereCopyOfReturnIsFldCd
States Where Copy Of Return Is FldWIStatesWhereCopyOfReturnIsFldCd
Own WebsiteYes (X)OwnWebsiteInd
Other WebsiteYes (X)OtherWebsiteInd
Upon RequestYes (X)UponRequestInd

Books In Care Of Detail BooksInCareOfDetail

Business Name BusinessName

FieldValueIRS element (for citing)
Business Name Line1David F Marks CPA CMABusinessNameLine1
FieldValueIRS element (for citing)
Phone3019483244PhoneNum

US Address USAddress

FieldValueIRS element (for citing)
Address Line122512 Gateway Center DriveAddressLine1
CityClarksburgCity
StateMDState
ZIP Code20871ZIPCode

Form990 Part VII Section A Form990PartVIISectionAGrp (16 entries)

TitleTitleTxtAverage Hours Per WeekAverageHoursPerWeekRtIndividual Trustee Or DirectorIndividualTrusteeOrDirectorIndOfficerOfficerIndReportable Comp From OrgReportableCompFromOrgAmtReportable Comp From Rltd OrgReportableCompFromRltdOrgAmtOther CompensationOtherCompensationAmtKey EmployeeKeyEmployeeIndHighest Compensated EmployeeHighestCompensatedEmployeeInd
Grace Frisone
Chair16.00Yes (X)Yes (X)$0$0$0
Michael H Barnett Esq
Vice Chair7.00Yes (X)Yes (X)$0$0$0
Nicholas W Raymond
Treasurer12.00Yes (X)Yes (X)$0$0$0
Scott Rodgville CPA
Secretary4.00Yes (X)Yes (X)$0$0$0
June Kinoshita
Director3.00Yes (X)$0$0$0
Judith Lee
Director5.00Yes (X)$0$0$0
Diane Marcello
Director3.00Yes (X)$0$0$0
Henry Pownall PhD
Director2.00Yes (X)$0$0$0
Brian K Regan PhD
Director4.00Yes (X)$0$0$0
Jonathan Rice Esq
Director3.00Yes (X)$0$0$0
Eltjo R Ed Schoonveld
Director3.00Yes (X)$0$0$0
Stacy Pagos Haller
President/CEO55.00Yes (X)$352,415$0$71,690
Donna Callison
VP, Development45.00$181,739$0$41,308Yes (X)
David F Marks CPA CMA
VP, Finance & Administration45.00$154,253$0$46,283Yes (X)
Guy Eakin Ph D
VP, Scientific Affairs45.00$151,149$0$48,531Yes (X)
Bridget Hart Shea
Sr. Dir. Major & Planned Gifts40.00$123,037$0$23,964Yes (X)
FieldValueIRS element (for citing)
Total Reportable Comp From Org$962,593TotalReportableCompFromOrgAmt
Tot Reportable Comp Rltd Org$0TotReportableCompRltdOrgAmt
Total Other Compensation$231,776TotalOtherCompensationAmt
Indiv Rcvd Greater Than100 K5IndivRcvdGreaterThan100KCnt
Former Ofcr Employees Listed0FormerOfcrEmployeesListedInd
Total Comp Greater Than150 KYes (1)TotalCompGreaterThan150KInd
Compensation From Other Srcs0CompensationFromOtherSrcsInd

Contractor Compensation ContractorCompensationGrp (5 entries)

Address Line1ContractorAddress/USAddress/AddressLine1CityContractorAddress/USAddress/CityStateContractorAddress/USAddress/StateZIP CodeContractorAddress/USAddress/ZIPCodeServicesServicesDescCompensationCompensationAmt
WildeLW Robbins Associates Inc
201 Summer StreetHollistonMA01746Public awareness consul. & materials$5,382,488
Data Management Inc
160 Stone StreetStonevilleNC27048Database management$216,131
Global Technology Solutions Inc
2977 Stewart Loop Unit BFort MeadeMD20755Building & office services$181,131
Blackbaud Inc
2000 Daniel Island DriveCharlestonSC29492Database management$171,126
EU Services Inc
649 Horners LaneRockvilleMD20850Printing$156,776
FieldValueIRS element (for citing)
Cntrct Rcvd Greater Than100 K6CntrctRcvdGreaterThan100KCnt
Federated Campaigns$208,600FederatedCampaignsAmt
All Other Contributions$24,917,633AllOtherContributionsAmt
Noncash Contributions$28,644NoncashContributionsAmt
Total Contributions$25,126,233TotalContributionsAmt

Investment Income InvestmentIncomeGrp

FieldValueIRS element (for citing)
Total Revenue Column$665,408TotalRevenueColumnAmt
Exclusion$665,408ExclusionAmt

Royalties Revenue RoyaltiesRevenueGrp

FieldValueIRS element (for citing)
Total Revenue Column$307,970TotalRevenueColumnAmt
Exclusion$307,970ExclusionAmt

Gross Rents GrossRentsGrp

FieldValueIRS element (for citing)
Real$566,205RealAmt

Less Rental Expenses LessRentalExpensesGrp

FieldValueIRS element (for citing)
Real$43,705RealAmt

Rental Income Or Loss RentalIncomeOrLossGrp

FieldValueIRS element (for citing)
Real$522,500RealAmt

Net Rental Income Or Loss NetRentalIncomeOrLossGrp

FieldValueIRS element (for citing)
Total Revenue Column$522,500TotalRevenueColumnAmt
Exclusion$522,500ExclusionAmt

Gross Amount Sales Assets GrossAmountSalesAssetsGrp

FieldValueIRS element (for citing)
Securities$6,305,791SecuritiesAmt

Less Cost Oth Basis Sales Expnss LessCostOthBasisSalesExpnssGrp

FieldValueIRS element (for citing)
Securities$6,204,260SecuritiesAmt

Gain Or Loss GainOrLossGrp

FieldValueIRS element (for citing)
Securities$101,531SecuritiesAmt

Net Gain Or Loss Investments NetGainOrLossInvestmentsGrp

FieldValueIRS element (for citing)
Total Revenue Column$101,531TotalRevenueColumnAmt
Exclusion$101,531ExclusionAmt

Total Revenue TotalRevenueGrp

FieldValueIRS element (for citing)
Total Revenue Column$26,723,642TotalRevenueColumnAmt
Related Or Exempt Func Income$0RelatedOrExemptFuncIncomeAmt
Unrelated Business Revenue$0UnrelatedBusinessRevenueAmt
Exclusion$1,597,409ExclusionAmt

Grants To Domestic Orgs GrantsToDomesticOrgsGrp

FieldValueIRS element (for citing)
Total$7,862,765TotalAmt
Program Services$7,862,765ProgramServicesAmt

Grants To Domestic Individuals GrantsToDomesticIndividualsGrp

FieldValueIRS element (for citing)
Total$4,000TotalAmt
Program Services$4,000ProgramServicesAmt

Foreign Grants ForeignGrantsGrp

FieldValueIRS element (for citing)
Total$888,550TotalAmt
Program Services$888,550ProgramServicesAmt

Comp Current Ofcr Directors CompCurrentOfcrDirectorsGrp

FieldValueIRS element (for citing)
Total$1,028,650TotalAmt
Program Services$590,597ProgramServicesAmt
Management And General$255,262ManagementAndGeneralAmt
Fundraising$182,791FundraisingAmt

Other Salaries And Wages OtherSalariesAndWagesGrp

FieldValueIRS element (for citing)
Total$2,139,360TotalAmt
Program Services$1,050,137ProgramServicesAmt
Management And General$698,083ManagementAndGeneralAmt
Fundraising$391,140FundraisingAmt

Pension Plan Contributions PensionPlanContributionsGrp

FieldValueIRS element (for citing)
Total$225,963TotalAmt
Program Services$111,685ProgramServicesAmt
Management And General$73,804ManagementAndGeneralAmt
Fundraising$40,474FundraisingAmt

Other Employee Benefits OtherEmployeeBenefitsGrp

FieldValueIRS element (for citing)
Total$437,381TotalAmt
Program Services$216,334ProgramServicesAmt
Management And General$142,648ManagementAndGeneralAmt
Fundraising$78,399FundraisingAmt

Payroll Taxes PayrollTaxesGrp

FieldValueIRS element (for citing)
Total$200,472TotalAmt
Program Services$99,132ProgramServicesAmt
Management And General$65,415ManagementAndGeneralAmt
Fundraising$35,925FundraisingAmt

Fees For Services Legal FeesForServicesLegalGrp

FieldValueIRS element (for citing)
Total$83,044TotalAmt
Program Services$25,332ProgramServicesAmt
Management And General$57,712ManagementAndGeneralAmt

Fees For Services Accounting FeesForServicesAccountingGrp

FieldValueIRS element (for citing)
Total$15,258TotalAmt
Program Services$10,145ProgramServicesAmt
Management And General$2,487ManagementAndGeneralAmt
Fundraising$2,626FundraisingAmt

Fees For Services Prof Fundraising FeesForServicesProfFundraising

FieldValueIRS element (for citing)
Total$407,033TotalAmt
Fundraising$407,033FundraisingAmt

Fees For Srvc Invst Mgmnt Fees FeesForSrvcInvstMgmntFeesGrp

FieldValueIRS element (for citing)
Total$151,982TotalAmt
Management And General$151,982ManagementAndGeneralAmt

Fees For Services Other FeesForServicesOtherGrp

FieldValueIRS element (for citing)
Total$1,035,589TotalAmt
Program Services$924,251ProgramServicesAmt
Management And General$84,545ManagementAndGeneralAmt
Fundraising$26,793FundraisingAmt

Office Expenses OfficeExpensesGrp

FieldValueIRS element (for citing)
Total$1,363,124TotalAmt
Program Services$1,034,191ProgramServicesAmt
Management And General$223,051ManagementAndGeneralAmt
Fundraising$105,882FundraisingAmt

Information Technology InformationTechnologyGrp

FieldValueIRS element (for citing)
Total$547,203TotalAmt
Program Services$324,781ProgramServicesAmt
Management And General$146,179ManagementAndGeneralAmt
Fundraising$76,243FundraisingAmt

Occupancy OccupancyGrp

FieldValueIRS element (for citing)
Total$334,789TotalAmt
Program Services$182,397ProgramServicesAmt
Management And General$108,618ManagementAndGeneralAmt
Fundraising$43,774FundraisingAmt

Travel TravelGrp

FieldValueIRS element (for citing)
Total$232,126TotalAmt
Program Services$119,655ProgramServicesAmt
Management And General$90,105ManagementAndGeneralAmt
Fundraising$22,366FundraisingAmt

Conferences Meetings ConferencesMeetingsGrp

FieldValueIRS element (for citing)
Total$133,637TotalAmt
Program Services$125,350ProgramServicesAmt
Management And General$6,639ManagementAndGeneralAmt
Fundraising$1,648FundraisingAmt

Depreciation Depletion DepreciationDepletionGrp

FieldValueIRS element (for citing)
Total$273,699TotalAmt
Program Services$147,854ProgramServicesAmt
Management And General$85,894ManagementAndGeneralAmt
Fundraising$39,951FundraisingAmt

Insurance InsuranceGrp

FieldValueIRS element (for citing)
Total$82,850TotalAmt
Program Services$38,789ProgramServicesAmt
Management And General$29,795ManagementAndGeneralAmt
Fundraising$14,266FundraisingAmt

Other Expenses OtherExpensesGrp (4 entries)

DescDescTotalTotalAmtProgram ServicesProgramServicesAmtManagement And GeneralManagementAndGeneralAmtFundraisingFundraisingAmt
Pub. awareness postage$4,098,157$2,155,178$279,132$1,663,847
Pub. awareness printing$1,931,997$707,024$170,392$1,054,581
Pub. awareness comp.$932,337$501,479$59,628$371,230
List rental$717,414$376,226$46,025$295,163

Total Functional Expenses TotalFunctionalExpensesGrp

FieldValueIRS element (for citing)
Total$25,127,380TotalAmt
Program Services$17,495,852ProgramServicesAmt
Management And General$2,777,396ManagementAndGeneralAmt
Fundraising$4,854,132FundraisingAmt
FieldValueIRS element (for citing)
Joint CostsYes (X)JointCostsInd

Total Joint Costs TotalJointCostsGrp

FieldValueIRS element (for citing)
Total$8,593,054TotalAmt
Program Services$4,227,648ProgramServicesAmt
Management And General$613,423ManagementAndGeneralAmt
Fundraising$3,751,983FundraisingAmt

Cash Non Interest Bearing CashNonInterestBearingGrp

FieldValueIRS element (for citing)
BOY$3,920,291BOYAmt
EOY$6,219,243EOYAmt

Savings And Temp Cash Invst SavingsAndTempCashInvstGrp

FieldValueIRS element (for citing)
BOY$1,418,430BOYAmt
EOY$395,903EOYAmt

Pledges And Grants Receivable PledgesAndGrantsReceivableGrp

FieldValueIRS element (for citing)
BOY$5,336,038BOYAmt
EOY$4,184,603EOYAmt

Oth Notes Loans Receivable Net OthNotesLoansReceivableNetGrp

FieldValueIRS element (for citing)
BOY$176,008BOYAmt

Inventories For Sale Or Use InventoriesForSaleOrUseGrp

FieldValueIRS element (for citing)
BOY$19,646BOYAmt
EOY$16,291EOYAmt

Prepaid Expenses Defrd Charges PrepaidExpensesDefrdChargesGrp

FieldValueIRS element (for citing)
BOY$104,897BOYAmt
EOY$46,374EOYAmt
FieldValueIRS element (for citing)
Land Bldg Equip Cost Or Other Bss$11,166,311LandBldgEquipCostOrOtherBssAmt
Land Bldg Equip Accum Deprec$2,781,227LandBldgEquipAccumDeprecAmt

Land Bldg Equip Basis Net LandBldgEquipBasisNetGrp

FieldValueIRS element (for citing)
BOY$8,602,822BOYAmt
EOY$8,385,084EOYAmt

Investments Pub Traded Sec InvestmentsPubTradedSecGrp

FieldValueIRS element (for citing)
BOY$19,464,859BOYAmt
EOY$24,677,383EOYAmt

Investments Other Securities InvestmentsOtherSecuritiesGrp

FieldValueIRS element (for citing)
BOY$2,364,446BOYAmt
EOY$3,425,000EOYAmt

Other Assets Total OtherAssetsTotalGrp

FieldValueIRS element (for citing)
BOY$831,452BOYAmt
EOY$831,794EOYAmt

Total Assets TotalAssetsGrp

FieldValueIRS element (for citing)
BOY$42,238,889BOYAmt
EOY$48,181,675EOYAmt

Accounts Payable Accr Expnss AccountsPayableAccrExpnssGrp

FieldValueIRS element (for citing)
BOY$584,225BOYAmt
EOY$689,531EOYAmt

Grants Payable GrantsPayableGrp

FieldValueIRS element (for citing)
BOY$11,924,959BOYAmt
EOY$14,604,652EOYAmt

Other Liabilities OtherLiabilitiesGrp

FieldValueIRS element (for citing)
BOY$1,695,477BOYAmt
EOY$1,534,970EOYAmt

Total Liabilities TotalLiabilitiesGrp

FieldValueIRS element (for citing)
BOY$14,204,661BOYAmt
EOY$16,829,153EOYAmt
FieldValueIRS element (for citing)
Organization Follows SFAS117Yes (X)OrganizationFollowsSFAS117Ind

Unrestricted Net Assets UnrestrictedNetAssetsGrp

FieldValueIRS element (for citing)
BOY$15,916,258BOYAmt
EOY$18,308,429EOYAmt

Temporarily Rstr Net Assets TemporarilyRstrNetAssetsGrp

FieldValueIRS element (for citing)
BOY$12,027,970BOYAmt
EOY$12,954,093EOYAmt

Permanently Rstr Net Assets PermanentlyRstrNetAssetsGrp

FieldValueIRS element (for citing)
BOY$90,000BOYAmt
EOY$90,000EOYAmt

Total Net Assets Fund Balance TotalNetAssetsFundBalanceGrp

FieldValueIRS element (for citing)
BOY$28,034,228BOYAmt
EOY$31,352,522EOYAmt

Tot Liab Net Assets Fund Balance TotLiabNetAssetsFundBalanceGrp

FieldValueIRS element (for citing)
BOY$42,238,889BOYAmt
EOY$48,181,675EOYAmt
FieldValueIRS element (for citing)
Info In Schedule O Part XIYes (X)InfoInScheduleOPartXIInd
Reconcilation Revenue Expnss$1,596,262ReconcilationRevenueExpnssAmt
Net Unrlzd Gains Losses Invst$1,580,201NetUnrlzdGainsLossesInvstAmt
Other Changes In Net Assets$141,831OtherChangesInNetAssetsAmt
Method Of Accounting AccrualYes (X)MethodOfAccountingAccrualInd
Accountant Compile Or Review0AccountantCompileOrReviewInd
FS AuditedYes (1)FSAuditedInd

FS Audited Basis FSAuditedBasisGrp

FieldValueIRS element (for citing)
Consolidated Basis Fincl StmtYes (X)ConsolidatedBasisFinclStmtInd
FieldValueIRS element (for citing)
Audit CommitteeYes (1)AuditCommitteeInd
Federal Grant Audit Required0FederalGrantAuditRequiredInd

Schedule A IRS990ScheduleA

FieldValueIRS element (for citing)
Public Organization170Yes (X)PublicOrganization170Ind

Gifts Grants Contri Rcvd170 GiftsGrantsContriRcvd170Grp

FieldValueIRS element (for citing)
Current Tax Year Minus4 Years$21,879,337CurrentTaxYearMinus4YearsAmt
Current Tax Year Minus3 Years$18,261,062CurrentTaxYearMinus3YearsAmt
Current Tax Year Minus2 Years$22,601,859CurrentTaxYearMinus2YearsAmt
Current Tax Year Minus1 Year$23,534,029CurrentTaxYearMinus1YearAmt
Current Tax Year$25,126,233CurrentTaxYearAmt
Total$111,402,520TotalAmt

Total Calendar Year170 TotalCalendarYear170Grp

FieldValueIRS element (for citing)
Current Tax Year Minus4 Years$21,879,337CurrentTaxYearMinus4YearsAmt
Current Tax Year Minus3 Years$18,261,062CurrentTaxYearMinus3YearsAmt
Current Tax Year Minus2 Years$22,601,859CurrentTaxYearMinus2YearsAmt
Current Tax Year Minus1 Year$23,534,029CurrentTaxYearMinus1YearAmt
Current Tax Year$25,126,233CurrentTaxYearAmt
Total$111,402,520TotalAmt
FieldValueIRS element (for citing)
Public Support Total170$111,402,520PublicSupportTotal170Amt

Gross Investment Income170 GrossInvestmentIncome170Grp

FieldValueIRS element (for citing)
Current Tax Year Minus4 Years$1,572,008CurrentTaxYearMinus4YearsAmt
Current Tax Year Minus3 Years$1,443,239CurrentTaxYearMinus3YearsAmt
Current Tax Year Minus2 Years$1,345,423CurrentTaxYearMinus2YearsAmt
Current Tax Year Minus1 Year$1,323,906CurrentTaxYearMinus1YearAmt
Current Tax Year$1,539,583CurrentTaxYearAmt
Total$7,224,159TotalAmt

Other Income170 OtherIncome170Grp

FieldValueIRS element (for citing)
Current Tax Year Minus4 Years$1,132CurrentTaxYearMinus4YearsAmt
Current Tax Year Minus3 Years$14CurrentTaxYearMinus3YearsAmt
Current Tax Year Minus2 Years$16CurrentTaxYearMinus2YearsAmt
Total$1,162TotalAmt
FieldValueIRS element (for citing)
Total Support$118,627,841TotalSupportAmt
Gross Receipts Rltd Activities$37,705GrossReceiptsRltdActivitiesAmt
Public Support CY1700.93910PublicSupportCY170Pct
Public Support PY1700.93650PublicSupportPY170Pct
Thirty Thr Pct Suprt Tests CY170Yes (X)ThirtyThrPctSuprtTestsCY170Ind

Form990 Schedule A Part IV Form990ScheduleAPartIVGrp

FieldValueIRS element (for citing)
Form And Line ReferenceSchedule A, Part II, Line 10, Explanation of Other Income:FormAndLineReferenceDesc
ExplanationOther revenue - 2009 Amount: $ 1,132. 2010 Amount: $ 14. 2011 Amount: $ 16.ExplanationTxt

Schedule B IRS990ScheduleB

Contributor Information ContributorInformationGrp

FieldValueIRS element (for citing)
ContributorRESTRICTEDContributorNum

Contributor Business Name ContributorBusinessName

FieldValueIRS element (for citing)
Business Name Line1RESTRICTEDBusinessNameLine1

Contributor US Address ContributorUSAddress

FieldValueIRS element (for citing)
Address Line1RESTRICTEDAddressLine1
Address Line2RESTRICTEDAddressLine2
CityRESTRICTEDCity
StateRESTRICTEDState
ZIP CodeRESTRICTEDZIPCode
FieldValueIRS element (for citing)
Total ContributionsRESTRICTEDTotalContributionsAmt

Schedule C IRS990ScheduleC

Other Exempt Purpose Expend OtherExemptPurposeExpendGrp

FieldValueIRS element (for citing)
Filing Organizations Total$24,720,347FilingOrganizationsTotalAmt

Total Exempt Purpose Expend TotalExemptPurposeExpendGrp

FieldValueIRS element (for citing)
Filing Organizations Total$24,720,347FilingOrganizationsTotalAmt

Lobbying Nontaxable Amount LobbyingNontaxableAmountGrp

FieldValueIRS element (for citing)
Filing Organizations Total$1,000,000FilingOrganizationsTotalAmt

Grassroots Nontaxable GrassrootsNontaxableGrp

FieldValueIRS element (for citing)
Filing Organizations Total$250,000FilingOrganizationsTotalAmt

Tot Lbbyng Grassroot Mns Non Tx TotLbbyngGrassrootMnsNonTxGrp

FieldValueIRS element (for citing)
Filing Organizations Total$0FilingOrganizationsTotalAmt

Tot Lbby Expend Mns Lbbyng Non Tx TotLbbyExpendMnsLbbyngNonTxGrp

FieldValueIRS element (for citing)
Filing Organizations Total$0FilingOrganizationsTotalAmt

Avg Lobbying Nontaxable Amount AvgLobbyingNontaxableAmountGrp

FieldValueIRS element (for citing)
Current Year Minus3$1,000,000CurrentYearMinus3Amt
Current Year Minus2$1,000,000CurrentYearMinus2Amt
Current Year Minus1$1,000,000CurrentYearMinus1Amt
Current Year$1,000,000CurrentYearAmt
Total$4,000,000TotalAmt
FieldValueIRS element (for citing)
Lobbying Ceiling$6,000,000LobbyingCeilingAmt

Avg Grassroots Nontaxable AvgGrassrootsNontaxableGrp

FieldValueIRS element (for citing)
Current Year Minus3$250,000CurrentYearMinus3Amt
Current Year Minus2$250,000CurrentYearMinus2Amt
Current Year Minus1$250,000CurrentYearMinus1Amt
Current Year$250,000CurrentYearAmt
Total$1,000,000TotalAmt
FieldValueIRS element (for citing)
Grassroots Ceiling$1,500,000GrassrootsCeilingAmt

Schedule D IRS990ScheduleD

CY Endwmt Fund CYEndwmtFundGrp

FieldValueIRS element (for citing)
Beginning Year Balance$90,000BeginningYearBalanceAmt
Contributions$3,933ContributionsAmt
Other Expenditures$3,933OtherExpendituresAmt
End Year Balance$90,000EndYearBalanceAmt

CY Minus1 Yr Endwmt Fund CYMinus1YrEndwmtFundGrp

FieldValueIRS element (for citing)
Beginning Year Balance$90,000BeginningYearBalanceAmt
Contributions$2,316ContributionsAmt
Other Expenditures$2,316OtherExpendituresAmt
End Year Balance$90,000EndYearBalanceAmt

CY Minus2 Yr Endwmt Fund CYMinus2YrEndwmtFundGrp

FieldValueIRS element (for citing)
Beginning Year Balance$90,000BeginningYearBalanceAmt
Contributions$1,312ContributionsAmt
Other Expenditures$1,312OtherExpendituresAmt
End Year Balance$90,000EndYearBalanceAmt

CY Minus3 Yr Endwmt Fund CYMinus3YrEndwmtFundGrp

FieldValueIRS element (for citing)
Beginning Year Balance$90,000BeginningYearBalanceAmt
Contributions$3,792ContributionsAmt
Other Expenditures$3,792OtherExpendituresAmt
End Year Balance$90,000EndYearBalanceAmt

CY Minus4 Yr Endwmt Fund CYMinus4YrEndwmtFundGrp

FieldValueIRS element (for citing)
Beginning Year Balance$90,000BeginningYearBalanceAmt
Contributions$3,715ContributionsAmt
Other Expenditures$3,715OtherExpendituresAmt
End Year Balance$90,000EndYearBalanceAmt
FieldValueIRS element (for citing)
Board Designated Balance EOY0.00000BoardDesignatedBalanceEOYPct
Prmnnt Endowment Balance EOY1.00000PrmnntEndowmentBalanceEOYPct
Term Endowment Balance EOY0.00000TermEndowmentBalanceEOYPct
Endowments Held Unrelated OrgYes (1)EndowmentsHeldUnrelatedOrgInd
Endowments Held Related Org0EndowmentsHeldRelatedOrgInd

Land LandGrp

FieldValueIRS element (for citing)
Investment Cost Or Other Basis$2,800,000InvestmentCostOrOtherBasisAmt
Other Cost Or Other Basis$1,147,363OtherCostOrOtherBasisAmt
Book Value$3,947,363BookValueAmt

Buildings BuildingsGrp

FieldValueIRS element (for citing)
Investment Cost Or Other Basis$1,629,400InvestmentCostOrOtherBasisAmt
Other Cost Or Other Basis$4,651,844OtherCostOrOtherBasisAmt
Depreciation$2,046,923DepreciationAmt
Book Value$4,234,321BookValueAmt

Equipment EquipmentGrp

FieldValueIRS element (for citing)
Other Cost Or Other Basis$750,379OtherCostOrOtherBasisAmt
Depreciation$560,597DepreciationAmt
Book Value$189,782BookValueAmt

Other Land Buildings OtherLandBuildingsGrp

FieldValueIRS element (for citing)
Other Cost Or Other Basis$187,325OtherCostOrOtherBasisAmt
Depreciation$173,707DepreciationAmt
Book Value$13,618BookValueAmt
FieldValueIRS element (for citing)
Total Book Value Land Buildings$8,385,084TotalBookValueLandBuildingsAmt

Other Securities OtherSecuritiesGrp

FieldValueIRS element (for citing)
DescAlternative investments - hedge fundDesc
Book Value$3,425,000BookValueAmt
Method ValuationFMethodValuationCd
FieldValueIRS element (for citing)
Total Book Value Securities$3,425,000TotalBookValueSecuritiesAmt

Other Liabilities Org OtherLiabilitiesOrgGrp (3 entries)

DescDescAmtAmt
Charitable gift annuities$1,346,011
Rental deposits$80,000
Capital lease obligations$108,959
FieldValueIRS element (for citing)
Total Liability$1,534,970TotalLiabilityAmt
Footnote TextYes (X)FootnoteTextInd
Total Rev Etc Audited Fincl Stmt$45,927,920TotalRevEtcAuditedFinclStmtAmt
Net Unrealized Gains Invst$1,580,201NetUnrealizedGainsInvstAmt
Donated Services And Use Fclts$17,597,705DonatedServicesAndUseFcltsAmt
Recoveries Prior Year Grants$136,575RecoveriesPriorYearGrantsAmt
Revenue Not Reported$19,314,481RevenueNotReportedAmt
Revenue Subtotal$26,613,439RevenueSubtotalAmt
Investment Expenses Not Incld$151,982InvestmentExpensesNotIncldAmt
Other Revenues Not Included-$41,779OtherRevenuesNotIncludedAmt
Revenue Not Reported Fincl Stmt$110,203RevenueNotReportedFinclStmtAmt
Total Revenue Per Form990$26,723,642TotalRevenuePerForm990Amt
Tot Expns Etc Audited Fincl Stmt$42,609,626TotExpnsEtcAuditedFinclStmtAmt
Donated Services Use Fclts$17,597,705DonatedServicesUseFcltsAmt
Expenses Not Reported$17,597,705ExpensesNotReportedAmt
Expenses Subtotal$25,011,921ExpensesSubtotalAmt
Investment Expenses Not Incld2$151,982InvestmentExpensesNotIncld2Amt
Other Expenses Not Included-$36,523OtherExpensesNotIncludedAmt
Expenses Not Rpt Fincl Stmt$115,459ExpensesNotRptFinclStmtAmt
Total Expenses Per Form990$25,127,380TotalExpensesPerForm990Amt

Supplemental Information Detail SupplementalInformationDetail (4 entries)

Form And Line ReferenceFormAndLineReferenceDescExplanationExplanationTxt
Part V, Line 4:The earnings on this endowment are available for the Alzheimer's Disease Research program and are recorded as temporarily restricted investment income, and are released as spent.
Part X, Line 2:BrightFocus performed an evaluation of uncertain tax positions for the year ended March 31, 2014, and determined that there were no matters that would require recognition in the consolidated financial statements or that may have any effect on its tax-exempt status.
Part XI, Line 4b - Other Adjustments:Depreciation on rental property -41,779.
Part XII, Line 4b - Other Adjustments:Depreciation on rental property -41,779. Change in present value of grants 5,256.

Schedule F IRS990ScheduleF

FieldValueIRS element (for citing)
Grant Records MaintainedYes (1)GrantRecordsMaintainedInd

Account Activities Outside US AccountActivitiesOutsideUSGrp (3 entries)

RegionRegionTxtOfficesOfficesCntEmployeeEmployeeCntType Of Activities ConductedTypeOfActivitiesConductedTxtRegion Total ExpendituresRegionTotalExpendituresAmt
East Asia and the Pacific - Australia, Brunei, Burma, Cambodia,00Grantmaking$99,550
Europe (Including Iceland & Greenland) - Albania, Andorra, Austria, Belgium00Grantmaking$539,000
Middle East and North Africa - Algeria, Bahrain, Djibouti, Egypt,00Grantmaking$250,000
FieldValueIRS element (for citing)
Subtotal Offices0SubtotalOfficesCnt
Subtotal Employees0SubtotalEmployeesCnt
Continutation Total Office0ContinutationTotalOfficeCnt
Continutation Total Employee0ContinutationTotalEmployeeCnt
Total Office0TotalOfficeCnt
Total Employee0TotalEmployeeCnt
Subtotal Spent$888,550SubtotalSpentAmt
Continuation Spent$0ContinuationSpentAmt
Total Spent$888,550TotalSpentAmt

Grants To Org Outside US GrantsToOrgOutsideUSGrp (6 entries)

RegionRegionTxtPurpose Of GrantPurposeOfGrantTxtCash GrantCashGrantAmtManner Of Cash DisbursementMannerOfCashDisbursementTxt
East Asia and the PacificNational Glaucoma Research by David Mackey, MD Entitled: (G2014032)$99,550Wire
Middle East and North AfricaAlzheimer's Disease Research by Michal Schnaider Beeri, PhD Entitled: (A2014268S)$250,000Wire
Europe (Including Iceland & Greenland)Alzheimer's Disease Research by Elena Marcello, PhD Entitled: (A2014314F)$120,000Wire
Europe (Including Iceland & Greenland)Alzheimer's Disease Research by Enrico Glaab, PhD Entitled:$50,000Wire
Europe (Including Iceland & Greenland)Alzheimer's Disease Research by Rik Ossenkoppele, PhD Entitled: (A2014083F)$120,000Wire
Europe (Including Iceland & Greenland)Alzheimer's Disease Research by Carlos Saura, PhD Entitled: (A2014417S)$249,000Wire
FieldValueIRS element (for citing)
Total501c3 Org6Total501c3OrgCnt
Total Other Org0TotalOtherOrgCnt
Transfer To Foreign CorpYes (1)TransferToForeignCorpInd
Interest In Foreign Trust0InterestInForeignTrustInd
Foreign Corp OwnershipYes (1)ForeignCorpOwnershipInd
Passive Foreign Investmest Co0PassiveForeignInvestmestCoInd
Foreign Partnership0ForeignPartnershipInd
Boycott Countries0BoycottCountriesInd

Supplemental Information Detail SupplementalInformationDetail

FieldValueIRS element (for citing)
Form And Line ReferencePart I, Line 2:FormAndLineReferenceDesc
ExplanationBrightFocus interacts with all grantees at least quarterly by e-mail or at scientific meetings. In addition to these interactions, each grant recipient is required to submit separate detailed annual Scientific Progress and Financial Reports to BrightFocus. These are received by the BrightFocus Scientific Affairs department, and reviewed by scientific staff with broad expertise in molecular biology, cell biology, biochemistry, imaging and genetics. Senior staff reviews each Progress Report and evaluates the project for sufficient progress towards the specific aims proposed in the original application or any budgetary concerns. This effort is supported by additional scientific counsel from members of the BrightFocus Scientific Review Committees, when required. In addition to statements of experimental progress, all grantees are asked to report any technical publications, media reports, or patent applications in which BrightFocus-sponsored research is described. If significant concerns related to progress on the awards are discovered, and not resolved after interaction with the award grantee, the BrightFocus staff recommends appropriate actions to the Chair of the Board of Directors Grants Committee. The Scientific Affairs senior staff is empowered to authorize the withholding of funding, or discontinuation of awards, for any grantees that fail to achieve sufficient progress or fail to submit required reports. At the conclusion of the grant award period, each grantee must complete and submit a Final Report that is also reviewed by the BrightFocus senior scientific staff. Evaluation of the work of each grantee is qualitatively and quantitatively assessed through various metrics related to the impact of the grant on its targeted disease field. Such impact metrics have revealed that 95% of BrightFocus-supported research results in research publications that advance the fields served by BrightFocus. This impact is further supported by annual citation analysis that compares BrightFocus-supported works to a statistical sample of works supported by either the US Federal Government or that of other funding agencies. BrightFocus-supported publications are consistently cited at nearly twice the frequency of any other comparison group. A final example of impact assessment revealed that the successes of BrightFocus grantees continue long after the grant expires. On average, each grantee receives 2.2 additional grants for projects spawned by the BrightFocus grant. These come at values nearly 10 times the level of the initial BrightFocus investment. BrightFocus solicits feedback from its grantees, and provides an anonymous forum for collecting such information. Through the BrightFocus Foundation website and within In the Final Scientific Progress Report, there are designated sections where awardees are asked to provide feedback to the foundation. Through this mechanism, they are given the ability to anonymously provide feedback or communicate their concerns to Program Staff or the BrightFocus' Compliance Office. Any suggestions, concerns, complaints, or positive experiences can be outlined and brought to the attention of BrightFocus in this manner, so that BrightFocus can address any areas needing improvement, reaffirm praise-worthy policies, or otherwise assess needs for programmatic change. The senior Scientific Staff present and summarize the status and progress on grants to the BrightFocus Board of Directors at each of their quarterly Board Meetings.ExplanationTxt

Schedule G IRS990ScheduleG

FieldValueIRS element (for citing)
Mail SolicitationsYes (X)MailSolicitationsInd
Email SolicitationsYes (X)EmailSolicitationsInd
In Person SolicitationsYes (X)InPersonSolicitationsInd
Solicitation Of Non Govt GrantsYes (X)SolicitationOfNonGovtGrantsInd
Agrmt Prof Fundraising ActyYes (1)AgrmtProfFundraisingActyInd

Fundraiser Activity Info FundraiserActivityInfoGrp

Organization Business Name OrganizationBusinessName

FieldValueIRS element (for citing)
Business Name Line1WildeLW Robbins Associates IncBusinessNameLine1

US Address USAddress

FieldValueIRS element (for citing)
Address Line1201 Summer StreetAddressLine1
CityHollistonCity
StateMAState
ZIP Code07146ZIPCode
FieldValueIRS element (for citing)
ActivityFundraising and communications consultantActivityTxt
Fundraiser Control Of Funds0FundraiserControlOfFundsInd
Gross Receipts$16,091,182GrossReceiptsAmt
Retained By Contractor$407,033RetainedByContractorAmt
Net To Organization$15,684,149NetToOrganizationAmt
FieldValueIRS element (for citing)
Total Gross Receipts$16,091,182TotalGrossReceiptsAmt
Total Retained By Contractors$407,033TotalRetainedByContractorsAmt
Total Net To Organization$15,684,149TotalNetToOrganizationAmt
Licensed StatesALLicensedStatesCd
Licensed StatesAKLicensedStatesCd
Licensed StatesAZLicensedStatesCd
Licensed StatesARLicensedStatesCd
Licensed StatesCALicensedStatesCd
Licensed StatesCOLicensedStatesCd
Licensed StatesCTLicensedStatesCd
Licensed StatesDCLicensedStatesCd
Licensed StatesFLLicensedStatesCd
Licensed StatesGALicensedStatesCd
Licensed StatesHILicensedStatesCd
Licensed StatesILLicensedStatesCd
Licensed StatesKSLicensedStatesCd
Licensed StatesKYLicensedStatesCd
Licensed StatesLALicensedStatesCd
Licensed StatesMELicensedStatesCd
Licensed StatesMDLicensedStatesCd
Licensed StatesMALicensedStatesCd
Licensed StatesMILicensedStatesCd
Licensed StatesMNLicensedStatesCd
Licensed StatesMSLicensedStatesCd
Licensed StatesMOLicensedStatesCd
Licensed StatesNHLicensedStatesCd
Licensed StatesNJLicensedStatesCd
Licensed StatesNMLicensedStatesCd
Licensed StatesNYLicensedStatesCd
Licensed StatesNCLicensedStatesCd
Licensed StatesNDLicensedStatesCd
Licensed StatesOHLicensedStatesCd
Licensed StatesOKLicensedStatesCd
Licensed StatesORLicensedStatesCd
Licensed StatesPALicensedStatesCd
Licensed StatesRILicensedStatesCd
Licensed StatesSCLicensedStatesCd
Licensed StatesTNLicensedStatesCd
Licensed StatesUTLicensedStatesCd
Licensed StatesVALicensedStatesCd
Licensed StatesWALicensedStatesCd
Licensed StatesWVLicensedStatesCd
Licensed StatesWILicensedStatesCd

Supplemental Information Detail SupplementalInformationDetail

FieldValueIRS element (for citing)
Form And Line ReferenceSchedule G, Part I, Line 2b, Column (v)FormAndLineReferenceDesc
ExplanationIn the contract with Wilde/LW Robbins Associates, Inc., the management fees are fixed amounts per month for in-scope services that totals $951,319 per year of which $544,286 has been allocated under Part XI, line 11(g) to program and management and are not considered to be the professional fundraising consultant fee. Work performed out of the scope of fundraising counsel services are approved by BrightFocus before they are performed and paid. During the year ended, $4,100,338 was paid to Wilde/WL Robbins Associates, Inc. for production and mailing of public awareness materials, and is included in Part XI, 13, 24 (b), (c) & (d).ExplanationTxt

Schedule I IRS990ScheduleI

FieldValueIRS element (for citing)
Grant Records MaintainedYes (1)GrantRecordsMaintainedInd

Recipient Table RecipientTable (55 entries)

Address Line1USAddress/AddressLine1CityUSAddress/CityStateUSAddress/StateZIP CodeUSAddress/ZIPCodeRecipient EINRecipientEINIRC SectionIRCSectionDescCash GrantCashGrantAmtPurpose Of GrantPurposeOfGrantTxt
Boston University
72 East Concord StreetBostonMA02118042103547501(c)(3)$16,000Alzheimer's Disease Research by Benjamin Wolozin, MD, PhD Entitled: (A2012054)
University of Pennsylvania School of Medicine
3451 Walnut StreetPhiladelphiaPA19104231352685501(c)(3)$120,000Alzheimer's Disease Research by Jing Guo, PhD Entitled: (A2014005F)
University of Rochester Medical Center
601 Elmwood AveRochesterNY14642160743209501(c)(3)$250,000Alzheimer's Disease Research by Gail Johnson, PhD Entitled: (A2014018S)
University of Kentucky
109 Kinkead HallLexingtonKY40506616033693501(c)(3)$244,926Alzheimer's Disease Research by Harry LeVine, III, PhD Entitled: (A2014044S)
University of Florida
1600 SW Archer RoadGainesvilleFL32611596002052501(c)(3)$248,009Alzheimer's Disease Research by Yona Levites, PhD Entitled: (A2014105S)
University of Florida
1600 SW Archer RoadGainesvilleFL32611596002052501(c)(3)$249,703Alzheimer's Disease Research by Guilian Xu, PhD Entitled: (A2014108S)
Mayo Clinic Jacksonville
4500 San Pablo Road SouthJacksonvilleFL32224593337028501(c)(3)$120,000Alzheimer's Disease Research by Mitsuru Shinohara, PhD Entitled: (A2014137F)
Washington University
660 South Euclid AveSt LouisMO63110916001537501(c)(3)$120,000Alzheimer's Disease Research by Kristen Funk, PhD Entitled: (A2014164F)
Columbia University Medical Center
630 West 168th StreetNew YorkNY10032135598093501(c)(3)$120,000Alzheimer's Disease Research by Tal Nuriel, PhD Entitled: (A2014200F)
University of Kentucky
109 Kinkead HallLexingtonKY40506616033693501(c)(3)$250,000Alzheimer's Disease Research by Steven Estus, PhD Entitled: (A2014210S)
University of Washington School of Medicine
4333 Brooklyn Ave NESeattleWA98195916001534501(c)(3)$250,000Alzheimer's Disease Research by Richard Morrison, PhD Entitled: (A2014237S)
Washington University
660 South Euclid AveSt LouisMO63110916001537501(c)(3)$250,000Alzheimer's Disease Research by David Brody, MD, PhD Entitled: (A2014270S)
University of Kentucky
109 Kinkead HallLexingtonKY40506616033693501(c)(3)$250,000Alzheimer's Disease Reasearch by M. Paul Murphy, MA, PhD Entitled: (A2014280S)
Washington University
660 South Euclid AveSt LouisMO63110916001537501(c)(3)$250,000Alzheimer's Disease Research by Richard Perrin, MD, PhD Entitled: (A2014296S)
The Ohio State University
1960 Kenny RoadColumbusOH43210316401599501(c)(3)$250,000Alzheimer's Disease Research by Chien-liang Lin, PhD Entitled: (A2014315S)
University of Chicago
5801 South Ellis AveChicagoIL60637362177139501(c)(3)$120,000Alzheimer's Disease Research by Virginie Buggia-Prevot, PhD Entitled: (A2014316F)
Northwestern University
633 Clark StreetEvanstonIL60208362167817501(c)(3)$120,000Alzheimer's Disease Research by Jian Li, PhD Entitled: (A2014349F)
Washington University
660 South Euclid AveSt LouisMO63110916001537501(c)(3)$250,000Alzheimer's Disease Research by Randall Bateman, MD Entitled: (A2014384S)
University of South Dakota
414 E Clark StreetVermillionSD57069466003541501(c)(3)$250,000Alzheimer's Disease Research by Hongmin Wang, PhD Entitled: (A2014420S)
Stanford University
300 Pasteur DriveStanfordCA94305941156365501(c)(3)$250,000Alzheimer's Disease Research by Katrin Andreasson, MD Entitled: (A2014423S)
Columbia University Medical Center
630 West 168th StreetNew YorkNY10032135598093501(c)(3)$120,000Alzheimer's Disease Research by Alice Lepelley, PhD Entitled: (A2014425F)
Seattle Institute for Biomedical and Clinical Research
1660 S Columbian Way 151 FSeattleWA98108911452438501(c)(3)$250,000Alzheimer's Disease Research by Brian Kraemer, PhD Entitled: (A2014438S)
Alzheimer's Drug Discovery Foundation
57 West 57th Street Suite 904New YorkNY10019201082179501(c)(3)$20,000Access Platform seeks to pair academic researchers with contract research organizations
Sage Bionetworks
1100 Fairview Ave NSeattleWA98109264489946501(c)(3)$50,000Support for DREAM 8.5 Alzheimer's Disease Big Data Challenge #1.
University of California San Diego
9500 Gilman DriveLa JollaCA92093956006144501(c)(3)$200,000National Glaucoma Research by Jeffrey L Goldberg, MD, PhD Entitled: (C2015200)
University of California San Francisco
3333 California Street Suite 315San FranciscoCA94143946036493501(c)(3)$100,000National Glaucoma Research by Douglas Gould, PhD Entitled: (G2014007)
Washington University
660 South Euclid AveSt LouisMO63110916001537501(c)(3)$100,000National Glaucoma Research by Jeff Gidday, PhD Entitled: (G2014012)
University of Wisconsin
21 N Park Street Suite 6401MadisonWI53715396006492501(c)(3)$100,000National Glaucoma Research by Donna Peters, PhD Entitled: (G2014051)
Oregon Health and Science University
3181 SW Terwilliger BlvdPortlandOR97239931176109501(c)(3)$100,000National Glaucoma Research by Janice Vranka, PhD Entitled: (G2014058)
Legacy Health System
1225 NE 2nd AvePortlandOR97232930386823501(c)(3)$100,000National Glaucoma Research by Lin Wang, MD, PhD Entitled: (G2014059)
University of North Texas Health Science Center
3500 Camp Bowie BlvdFort WorthTX76107756064033501(c)(3)$100,000National Glaucoma Research by Colleen McDowell, PhD Entitled: (G2014063)
University of Nebraska Medical Center
987835 Nebraska Medical CenterOmahaNE68198470049123501(c)(3)$98,727National Glaucoma Research by Dhirendra Singh, PhD Entitled: (G2014067)
Duke University Eye Center
106 Science Center DriveDurhamNC27705560532129501(c)(3)$100,000National Glaucoma Research by Stuart McKinnon, MD, PhD Entitled: (G2014076)
University of Pittsburgh
4200 Fifth AvenuePittsburghPA15260250965591501(c)(3)$100,000National Glaucoma Research by Yiqin Du, MD, PhD Entitled: (G2014086)
Indiana University School of Medicine
1160 West Michigan StreetIndianapolisIN46202356001673501(c)(3)$100,000National Glaucoma Research by Lyne Racette, PhD Entitled: (G2014096)
University of South Florida
4202 E Fowler AvenueTampaFL33620593102112501(c)(3)$100,000National Glaucoma Research by Chris Passaglia, PhD Entitled: (G2014105)
Massachusetts Eye and Ear Infirmary
243 Charles StreetBostonMA02114042103591501(c)(3)$100,000National Glaucoma Research by Baojian Fan, MD, PhD Entitled: (G2014107)
Johns Hopkins University
720 Rutland Avenue Ross 558BaltimoreMD21205520595110501(c)(3)$100,000National Glaucoma Research by Derek Welsbie, PhD Entitled: (G2014119)
University of Colorado Eye Center
1675 Aurora CourtAuroraCO80045846000555501(c)(3)$120,000Macular Degeneration Research by Omid Masihzadeh, PhD Entitled: (M2014014)
The Schepens Eye Research Institute
20 Staniford StreetBostonMA02114256638196501(c)(3)$120,000Macular Degeneration Research by Andrius Kazlauskas, PhD Entitled: (M2014025)
Georgetown University
37th and O Streets NWWashingtonDC20057530196603501(c)(3)$120,000Macular Degeneration Research by Nady Golestaneh, MS, PhD Entitled: (M2014039)
Children's Hospital Boston Harvard Medical School
300 Longwood AveBostonMA02115042103580501(c)(3)$120,000Macular Degeneration Research by Michael Do, PhD Entitled: (M2014055)
Tufts University
55 Kneeland StreetBostonMA02111042103634501(c)(3)$120,000Macular Degeneration Research by Behzad Gerami-Naini, PhD Entitled: (M2014059)
University of California San Francisco
3333 California Street Suite 315San FranciscoCA94143946036493501(c)(3)$120,000Macular Degeneration Research by Sara Venters, PhD Entitled: (M2014060)
Regents of the University of Michigan
3003 South State StreetAnn ArborMI48109386006309501(c)(3)$120,000Macular Degeneration Research by Debra Thompson, PhD Entitled: (M2014073)
The Schepens Eye Research Institute
20 Staniford StBostonMA02114256638196501(c)(3)$120,000Macular Degeneration Research by Neena Haider, PhD Entitled: (M2014084)
University of Maryland Baltimore
620 W Lexington St 4 th FloorBaltimoreMD21201526002033501(c)(3)$120,000Macular Degeneration Research by Richard Thompson, PhD Entitled: (M2014085)
University of Illinois at Chicago
1855 W Taylor St MB 502 M/C 551ChicagoIL60612376000511501(c)(3)$120,000Macular Degeneration Research by David Pepperberg, PhD Entitled: (M2014091)
Duke University Eye Center
106 Science Center DriveDurhamNC27705560532129501(c)(3)$120,000Macular Degeneration Research by Priyatham Mettu, MD Entitled: (M2014099)
Johns Hopkins University
720 Rutland Avenue Ross 558BaltimoreMD21205520595110501(c)(3)$120,000Macular Degeneration Research by Debasish Sinha, PhD Entitled: (M2014109)
Massachusetts General Hospital
55 Fruit StreetBostonMA02114041564655501(c)(3)$120,000Macular Degeneration Research by Alexander Marneros, MD, PhD Entitled: (M2014120)
Wilmer Eye Institute
400 N BroadwayBaltimoreMD21287721483530501(c)(3)$120,000Macular Degeneration Research by Hu Huang, PhD Entitled: (M2014124)
Wilmer Eye Institute
400 N BroadwayBaltimoreMD21287721483530501(c)(3)$120,000Macular Degeneration Research by Imran Bhutto, MD, PhD Entitled: (M2014128)
Stanford University
300 Pasteur DriveStanfordCA94305941156365501(c)(3)$120,000Macular Degeneration Research by Douglas Vollrath, MD, PhD Entitled: (M2014137)
Oklahoma University Health Sciences Center
941 Stanton L Young BlvdOklahoma CityOK73104736017987501(c)(3)$25,400Retinal Degeneration Meeting Grant
FieldValueIRS element (for citing)
Total501c3 Org55Total501c3OrgCnt
Total Other Org0TotalOtherOrgCnt

Supplemental Information Detail SupplementalInformationDetail

FieldValueIRS element (for citing)
Form And Line ReferencePart I, Line 2:FormAndLineReferenceDesc
ExplanationBrightFocus interacts with all grantees at least quarterly by e-mail or at scientific meetings. In addition to these interactions, each grant recipient is required to submit separate detailed annual Scientific Progress and Financial Reports to BrightFocus. These are received by the BrightFocus Scientific Affairs department, and reviewed by scientific staff with broad expertise in molecular biology, cell biology, biochemistry, imaging and genetics. Senior staff reviews each Progress Report and evaluates the project for sufficient progress towards the specific aims proposed in the original application or any budgetary concerns. This effort is supported by additional scientific counsel from members of the BrightFocus Scientific Review Committees, when required. In addition to statements of experimental progress, all grantees are asked to report any technical publications, media reports, or patent applications in which BrightFocus-sponsored research is described. If significant concerns related to progress on the awards are discovered, and not resolved after interaction with the award grantee, the BrightFocus staff recommends appropriate actions to the Chair of the Board of Directors Grants Committee. The Scientific Affairs senior staff is empowered to authorize the withholding of funding, or discontinuation of awards, for any grantees that fail to achieve sufficient progress or fail to submit required reports. At the conclusion of the grant award period, each grantee must complete and submit a Final Report that is also reviewed by the BrightFocus senior scientific staff. Evaluation of the work of each grantee is qualitatively and quantitatively assessed through various metrics related to the impact of the grant on its targeted disease field. Such impact metrics have revealed that 95% of BrightFocus-supported research results in research publications that advance the fields served by BrightFocus. This impact is further supported by annual citation analysis that compares BrightFocus-supported works to a statistical sample of works supported by either the US Federal Government or that of other funding agencies. BrightFocus-supported publications are consistently cited at nearly twice the frequency of any other comparison group. A final example of impact assessment revealed that the successes of BrightFocus grantees continue long after the grant expires. On average, each grantee receives 2.2 additional grants for projects spawned by the BrightFocus grant. These come at values nearly 10 times the level of the initial BrightFocus investment. BrightFocus solicits feedback from its grantees, and provides an anonymous forum for collecting such information. Through the BrightFocus Foundation website and within In the Final Scientific Progress Report, there are designated sections where awardees are asked to provide feedback to the foundation. Through this mechanism, they are given the ability to anonymously provide feedback or communicate their concerns to Program Staff or the BrightFocus' Compliance Officer. Any suggestions, concerns, complaints, or positive experiences can be outlined and brought to the attention of BrightFocus in this manner, so that BrightFocus can address any areas needing improvement, reaffirm praise-worthy policies, or otherwise assess needs for programmatic change. The senior Scientific Staff present and summarize the status and progress on grants to the BrightFocus Board of Directors at each of their quarterly Board Meetings.ExplanationTxt

Schedule J IRS990ScheduleJ

FieldValueIRS element (for citing)
Compensation CommitteeYes (X)CompensationCommitteeInd
Independent ConsultantYes (X)IndependentConsultantInd
Form990 Of Other OrganizationsYes (X)Form990OfOtherOrganizationsInd
Compensation SurveyYes (X)CompensationSurveyInd
Board Or Committee ApprovalYes (X)BoardOrCommitteeApprovalInd
Severance Payment0SeverancePaymentInd
Supplemental Nonqual Rtr Plan0SupplementalNonqualRtrPlanInd
Equity Based Comp Arrngm0EquityBasedCompArrngmInd
Comp Based On Revenue Of Flng Org0CompBasedOnRevenueOfFlngOrgInd
Comp Bsd On Rev Related Orgs0CompBsdOnRevRelatedOrgsInd
Comp Bsd Net Earns Flng Org0CompBsdNetEarnsFlngOrgInd
Comp Bsd Net Earns Rltd Orgs0CompBsdNetEarnsRltdOrgsInd
Any Non Fixed PaymentsYes (1)AnyNonFixedPaymentsInd
Initial Contract Exception0InitialContractExceptionInd

Rltd Org Officer Trst Key Empl RltdOrgOfficerTrstKeyEmplGrp (4 entries)

TitleTitleTxtBase Compensation Filing OrgBaseCompensationFilingOrgAmtCompensation Based On Rltd OrgsCompensationBasedOnRltdOrgsAmtBonus Filing OrganizationBonusFilingOrganizationAmountBonus Related OrganizationsBonusRelatedOrganizationsAmtOther Compensation Filing OrgOtherCompensationFilingOrgAmtOther Compensation Rltd OrgsOtherCompensationRltdOrgsAmtDeferred Compensation Flng OrgDeferredCompensationFlngOrgAmtDeferred Comp Rltd OrgsDeferredCompRltdOrgsAmtNontaxable Benefits Filing OrgNontaxableBenefitsFilingOrgAmtNontaxable Benefits Rltd OrgsNontaxableBenefitsRltdOrgsAmtTotal Compensation Filing OrgTotalCompensationFilingOrgAmtTotal Compensation Rltd OrgsTotalCompensationRltdOrgsAmtComp Report Prior990 Filing OrgCompReportPrior990FilingOrgAmtComp Report Prior990 Rltd OrgsCompReportPrior990RltdOrgsAmt
Stacy Pagos Haller
President/CEO$300,480$0$50,000$0$1,935$0$38,250$0$33,440$0$424,105$0$0$0
Donna Callison
VP, Development$170,155$0$10,000$0$1,584$0$25,601$0$15,707$0$223,047$0$0$0
David F Marks CPA CMA
VP, Finance & Administration$148,701$0$5,000$0$552$0$23,913$0$22,370$0$200,536$0$0$0
Guy Eakin Ph D
VP, Scientific Affairs$140,933$0$10,000$0$216$0$23,447$0$25,084$0$199,680$0$0$0

Supplemental Information Detail SupplementalInformationDetail (2 entries)

Form And Line ReferenceFormAndLineReferenceDescExplanationExplanationTxt
Part I, Line 3Before approving the compensation of the President/CEO, the Board determines the total compensation to be provided by BrightFocus to the President/CEO is reasonable in light of the position, responsibility and qualification of the position held including the result of an evaluation of prior performance for BrightFocus, if applicable. The President/CEO is evaluated annually by the Board of Directors through the use of an in-depth goal attainment structure, (developed with advice from Board Source) that includes a self assessment and a Board of Directors assessment and evaluation against set goals, outcomes and deliverables. The Board of Directors obtains and considers appropriate data, including a salary survey, which includes information compiled from the federal Form 990 of other organizations, concerning compensation paid to President/CEOs in like circumstances. In making the determination, the Board of Directors shall consider total compensation to include the salary and value of all benefits provided by BrightFocus to the individual in payment for services. At the time of the BrightFocus Board discussion and decision concerning the President/CEO's compensation, the President/CEO is not present in the meeting.
Part I, Line 7As the President/CEO's bonus was not a fixed payment specified in her employment contract, this item has been answered 'yes' in accordance with the Internal Revenue Service instructions. However, it should be noted that her bonus was a non-fixed payment based on BrightFocus' internal procedures. The Board of Directors considers the award of a discretionary bonus each year. The determination of the bonus compensation is capped as specified in her employment contract, and if not warranted will not be awarded at all. The determination is made by the full Board upon recommendation of its Executive Committee that is responsible for the review of CEO compensation. The Committee considers a set of goals for the CEO's performance developed at the beginning of the year in consultation with the President/CEO. Each goal is evaluated at the end of the fiscal year to determine whether the goal has been met or exceeded. The Bonus is awarded based on a detailed review by the Board of whether each goal has been met or exceeded.

Schedule M IRS990ScheduleM

Securities Publicly Traded SecuritiesPubliclyTradedGrp

FieldValueIRS element (for citing)
Non Cash CheckboxYes (X)NonCashCheckboxInd
Contribution11ContributionCnt
Noncash Contributions Rpt F990$28,644NoncashContributionsRptF990Amt
Method Of Determining RevenuesFMVMethodOfDeterminingRevenuesTxt
FieldValueIRS element (for citing)
Any Property That Must Be Held0AnyPropertyThatMustBeHeldInd
Review Process Unusual NC GiftsYes (1)ReviewProcessUnusualNCGiftsInd
Third Parties UsedYes (1)ThirdPartiesUsedInd

Supplemental Information Detail SupplementalInformationDetail

FieldValueIRS element (for citing)
Form And Line ReferencePart I, Line 32b:FormAndLineReferenceDesc
ExplanationAs directed by the BrightFocus investment policy, BrightFccus' investment advisor sells all donated securities at fair market value when received.ExplanationTxt

Schedule O IRS990ScheduleO

Supplemental Information Detail SupplementalInformationDetail (25 entries)

Form And Line ReferenceFormAndLineReferenceDescExplanationExplanationTxt
Form 990, Part III, Line 1, Description of Organization Mission:BrightFocus Foundation seeks to save mind and sight by funding innovative research worldwide and by promoting better health through education. We focus our efforts on three incurable diseases affecting mind and sight: Alzheimer's disease, macular degeneration, and glaucoma. Collectively, one in 16 people over the age of 40 in the U.S. alone has one of these diseases. BrightFocus has a proven track record of supporting the most innovative, early-stage research seeking better understanding, treatments, or, ultimately, a cure for these diseases. Since 1973, BrightFocus has awarded more than $140 million in research grants to thousands of scientists around the world. Our research funding has led to major contributions to the understanding of these diseases and to the awarding of two Nobel prizes. BrightFocus-supported findings are consistently cited by other scientists at twice the frequency as other research findings. Our funding acts as a catalyst in early-stage research. The BrightFocus research programs are designed to provide initial funding for highly innovative experimental ideas. Due to the structured grant review and approval process, most recipients of BrightFocus funding go on to receive future grants from other sources that are 10 times larger than the original BrightFocus award. This one thousand percent return on BrightFocus investment speaks to our ability to identify promising research and spawn future scientific discoveries. It is our firm belief that having the courage to invest in innovative ideas will lead to revolutionary approaches and life-saving breakthroughs. Indisputably, the world-class research identified and supported by BrightFocus is more than promising: it is making a real contribution to revolutionary science in the fight to save mind and sight. Along with funding cutting-edge research to find cures to some of society's costliest diseases, BrightFocus also provides free educational materials and support to hundreds of thousands of patients and families affected by these diseases nationwide. BrightFocus increases public awareness of Alzheimer's, macular degeneration, and glaucoma, and communicates with elected officials about the importance of scientific research in these areas. BrightFocus' award-winning Public Service Announcements (PSA) have appeared on television, radio, and in print throughout the nation. Both Now is the Moment to Stop Alzheimer's Disease and See a Better Tomorrow powerfully seek to raise awareness and early detection, and similar messages have been delivered through donated print PSA space in airports and train stations, as well as at pharmacies and supermarkets. In Fiscal Year 2014, these PSA messages generated $17,597,705 in donated media services and garnered 1.5 billion impressions. We held three community forums on brain and eye diseases, and recently launched BrightFocus Chats, a free, interactive monthly telephone forum that brings together patients and caregivers to learn from, and ask questions of, leading researchers and specialists. We have launched the series through discussions related to macular degeneration, and hope to expand the program into other disease areas. The Chats are archived on our web site, with audio and print transcripts available in a number of accessible formats. We continue to increase our print publications, many in Spanish, that provide helpful information to patients and caregivers, and regularly unveil new video and audio resources in conjunction with allies in the medical and scientific communities. We have expanded our written content of key research findings, promoting and sharing this information through our web site and social media platforms. Capitalizing on emerging use of data visualization, our BrightFocus "Snapshot" series graphically communicates information on detection and treatment of macular degeneration and glaucoma. Through our social media and web resources, we conduct contests and promotions to increase awareness of these diseases and further share BrightFocus publications and events. For example, our Healthy Recipe Contest drew attention to the importance of preventive lifestyle choices, and through over 6,000 on-line votes in the Geoffrey Beene research challenge, we increased public exposure of the need for increased scientific research on gender differences in Alzheimer's. More specifically, each of these program areas mail awareness-raising materials to hundreds of thousands of households, with messages focusing on: -Symptom recognition and steps the public should take, such as making an appointment with the doctor if symptoms exist. -Lifestyle choices that promote good health, encouraging readers to take action to reduce the likelihood of the onset of the disease. -Research results and treatments available to address the disease. BrightFocus regularly interacts with members of the media, as well as elected officials and federal agency staff. We communicated to policymakers the results of our survey of leading researchers, showing the dire consequences of cutbacks in federal research budgets. Through media interviews and placements, as well as participation in advocacy coalitions, we help advance the cause of pioneering science and better expose BrightFocus as a resource for those struggling with, and searching for cures for, these terrible diseases.
Form 990, Part VI, Section B, line 11A draft of the federal Form 990 shall be distributed to the Audit Committee for review prior to being submitted to the Internal Revenue Service. The draft federal Form 990 shall be distributed early enough to provide each Committee member with a reasonable amount of time for review and submission of questions or comments prior to the filing deadline. The final federal Form 990 shall be distributed to each Board member prior to being filed with the Internal Revenue Service. The draft and final Form 990 may be distributed in person, by regular mail, e-mail, or fax.
Form 990, Part VI, Section B, line 12cBrightFocus has all employees, officers, and directors agree to the code of conduct that includes adherence to the Conflict of Interest and Implementation Policy. Each board director, officer, and employee is required annually to complete a conflict of interest disclosure statement. Employees meet annually with the BrightFocus Chief Compliance Officer to review their conflict of interest statements, and gives an annual conflict of interest compliance report to the Board Chair and Vice Chair. If a conflict is reported, it is then referred to the CEO and/or BrightFocus legal counsel and, if appropriate and necessary, then to the Board of Directors or its appointed Committee for further action. The director's and officer's statements are reviewed by the BrightFocus legal counsel. If a conflict is reported, it is then referred to the Board of Directors or its appointed Committee for further action. At the time of the BrightFocus discussion and decision concerning a conflict of interest, the conflicted party is not present in the meeting.
Form 990, Part VI, Section B, line 15aThe BrightFocus Foundation (BrightFocus) Board of Directors has overall authority and responsibility for approving the annual budget which includes compensation for all employees at every level including non-director officers. All pay adjustments are made on a yearly basis effective April 1st, the beginning of the BrightFocus fiscal year. Before approving the compensation of the CEO, the Board determines the total compensation to be provided by BrightFocus to the CEO is reasonable in light of the position, responsibility and qualification of the position held including the result of an evaluation of prior performance for BrightFocus, if applicable. The CEO is evaluated annually by the Board of Directors through the use of an in-depth goal attainment structure, (developed with advice from Board Source) that includes a self assessment and a Board of Directors assessment and evaluation against set goals, outcomes and deliverables. In addition, the Board of Directors periodically engages an outside consultant to obtain and consider appropriate data, including a salary survey, which includes information compiled from the federal Form 990 of other organizations, concerning compensation paid to CEOs in like circumstances. In making the determination, the Board of Directors shall consider total compensation to include the salary and value of all benefits provided by BrightFocus to the individual in payment for services. At the time of the BrightFocus Board discussion and decision concerning the CEO's compensation, the CEO is not present in the meeting. The Board shall set forth the basis for its decisions with respect to compensation in the minutes of the meeting at which the decisions are made, including the conclusions of the evaluation and the basis for determining that the individual's compensation was reasonable in light of the evaluation and comparability data.
Form 990, Part VI, Section C, line 19BrightFocus makes its governing documents including its articles of incorporation and bylaws, conflict of interest policy, audited financial statements and federal Form 990 available to the public upon request. In addition, the public also has access to the annual report, the federal Form 1023, audited financial statements, the 501(c)(3) letter of determination from the Internal Revenue Service, and federal Form 990 on the BrightFocus website.
Form 990, Part XI, line 9:Recoveries of prior year grants 136,575. Change in present value of grants 5,256.
Schedule F, Part II, Line 1, Column D:Region: East Asia and the Pacific (D) Purpose of Grant: National Glaucoma Research by David Mackey, MD Entitled: (G2014032) Optic Nerve Structure Gene/environment Association. Investigators Summary: What genes affect the optic nerve and put it at risk of glaucoma? Knowing which gene changes increase the risk of glaucoma will enable us to diagnose people early and allow treatment to prevent blindness. We have previously measured photos of the optic nerve of 1400 20-year olds and identified genes associated with the size of the nerves. We now propose to analyze high resolution scans of the same nerves to search for new genes. Grant Awarded: $99,550. Lions Eye Institute, Nedlands, Australia. Region: Middle East and North Africa (D) Purpose of Grant: Alzheimer's Disease Reasearch by Michal Schnaider Beeri, PhD Entitled: (A2014268S) Vascular Function and Cognition in Type 2 Diabetes. Investigators Summary: The risk for cognitive impairment and Alzheimer's disease is increased in patients with Type 2 Diabetes (T2D), potentially due to impairments in the structure and function of blood vessels in the brain. Previous studies have shown that the problems of the functioning of blood vessels, which can be treated and reversed, is impaired before the structure of blood vessels becomes impaired, and that treatment of impaired blood vessel functioning may prevent impairment in its structure, which is irreversible. In this application we propose to study the role of blood vessel functioning in cognitive impairment in T2D patients and how different factors within T2D (for example glucose levels in the blood) affect this relationship. The results of this study may help develop treatments for the prevention of cognitive impairment in T2D and may help better understand factors that affect deleteriously cognition in all elderly. Grant Awarded: $250,000. Sheba Medical Center, Tel Hashomer, Israel. Region: Europe (D) Purpose of Grant: Alzheimer's Disease Reasearch by Elena Marcello, PhD Entitled: (A2014314F) Validating ADAM10 as Therapeutic Target for Dementia. Investigators Summary: Alzheimer's disease affects a number of elderly people, who lose their memory and their ability to take care of themselves. Such disease is caused by a substance that kills neurons. Our work is intended to develop a drug able to promote a pathway in the cell that limits the formation of this substance. We hope that our results will contribute to help people suffering of Alzheimer's disease to recover their memory. Grant Awarded: $120,000. University of Milan, Italy
Schedule F, Part II, Line 1, Column D:Region: Europe (D) Purpose of Grant: Alzheimer's Disease Research by Enrico Glaab, PhD Entitled: Age-Related Gender Differences in brain expression Levels of Tau-Interacting Ubiquitin-specific Peptidase 9 and possible implications for Alzheimer's Disease. Grant Awarded: $50,000. University of Luxemburg, Luxemburg. Region: Europe (D) Purpose of Grant: Alzheimer's Disease Research by Rik Ossenkoppele, PhD Entitled: (A2014083F) Tau, AB and Network Degeneration in Alzheimer's Disease. Investigators Summary: Alzheimer's disease is characterized by the protein amyloid-beta that emerges 15 years before symptom onset, but its working mechanisms are not clear. Animal and post-mortem studies suggest that tau proteins may be the missing link between amyloid-beta and clinical symptoms, and since very recently, this protein can be visualized in the living human brain using positron emission tomography (PET) scans. We propose to study the role of tau in Alzheimer's disease patients by investigating its relationships with amyloid-beta, shrinkage of the brain and communication between brain cells. This study will lead to better understanding of the disease and could stimulate development of novel therapeutic agents to prevent or slow-down the devastating effects of Alzheimer's disease. Grant Awarded: $120,000. Alzheimer Center of the VU University Medical Center, Amsterdam, Netherlands. Region: Europe (D) Purpose of Grant: Alzheimer's Disease Research by Carlos Saura, PhD Entitled: (A2014417S) Transcriptional Mechanisms of Memory Loss in Alzheimer's Disease. Investigators Summary: Memory impairment is one of the earliest clinical features of AD, but the cellular events that cause brain dysfunction and memory loss are largely unclear. Memory processing depends on activation of gene expression programs in specific memory neuronal circuits. In this project, we will study the transcriptional mechanisms of gene regulation underlying memory processing in normal and AD pathology conditions. This information will be valuable to understand the causes of memory circuit dysfunction and develop novel and innovative therapies for the treatment of memory loss in AD. Grant Awarded: $249,000. Universitat Autonoma de Barcelona, Bellaterra, Spain.
Schedule I, Part II, Line 1, Column (H):Name of organization or government: Boston University (H) Purpose of Grant or Assistance: Alzheimer's Disease Reasearch by Benjamin Wolozin, MD, PhD Entitled: (A2012054) RNA Binding Proteins in Alzheimer's Disease. Name of organization or government: University of Pennsylvania School of Medicine (H) Purpose of Grant or Assistance: Alzheimer's Disease Reasearch by Jing Guo, PhD Entitled: (A2014005F) Mouse Model for Sporadic Tauopathies. Investigator's Summary: Accumulation of misfolded tau protein in neurons is a hallmark lesion of Alzheimer's disease and many other neurodegenerative diseases. Recent studies have demonstrated that misfolded tau can spread from one cell to another and corrupt the folding of normal tau in healthy cells. We will utilize this mechanism to create a mouse model mimicking sporadically-occurring neurodegenerative diseases with tau aggregation. We will also explore the existence of distinct forms of pathological tau in different diseases. Name of organization or government: University of Rochester Medical Center (H) Purpose of Grant or Assistance: Alzheimer's Disease Reasearch by Gail Johnson, PhD Entitled: (A2014018S) Nrf2 Regulates Tau Clearance: an AD Treatment Strategy. Investigator's Summary: This focus of this study is to determine how brain cells get rid of excess tau protein. This is important because in Alzheimer disease there is a buildup of tau protein and this contributes to the ill health and eventual death of the nerve cell. We are focused on a particular system that identifies proteins that are no longer needed and engulfs and digests them. This system is called "autophagy" and in Alzheimer disease brain it is does not work efficiently. Therefore finding ways to make it work better and to selectively target tau for clearance could be beneficial to people who have Alzheimer disease. We have found that one way to improve the removal of tau from the neuron by autophagy is to upregulate proteins that make the process work better and directly deliver tau to the autophagy machinery. We have found that chemicals in foods like broccoli and green tea can cause increases in autophagy and decreases in the levels of tau. In this project we will determining how these types of chemicals improve the ability of nerve cells to get rid of excess or damaged tau protein. We will be doing this, using studies both in nerve cells that we grow in dishes and in mice. These studies will help us understand how a nerve cell normally gets rid of unwanted tau protein, what might be going wrong with this "disposal system" in Alzheimer disease and what we can do to make it work better.
Schedule I, Part II, Line 1, Column (H):Name of organization or government: University of Kentucky (H) Purpose of Grant or Assistance: Alzheimer's Disease Reasearch by Harry LeVine, III, PhD Entitled: (A2014044S) AD Brain Neuronal Types Accumulating PIB-Binding Abeta. Investigator's Summary: Binding of a fluorescent form of the human-specific amyloid imaging ligand PIB will use flow cytometry to isolate synaptosomes from Alzheimer's disease brain to identify the type of nerve cell carrying the PIB binding amyloid pathology. The biochemical components of the synaptosomes will be determined by high sensitivity high resolution mass spectrometry. Comparison with synaptosomes isolated from a mouse model of Alzheimer's pathology with similar identifying neuronal markers will be used to identify candidates that could account for the lack of significant PIB binding in animal models and their failure to progress beyond very early AD stages to neuronal cell death and dementia. Future studies will investigate the manipulation of the candidates to increase PIB binding to better model the human AD phenotype. Name of organization or government: University of Florida (H) Purpose of Grant or Assistance: Alzheimer's Disease Reasearch by Yona Levites, PhD Entitled: (A2014105S) Targeting Intra vs Extracellular Tau by Recombinant Antibodies. Investigator's Summary: In our search for potential modifiers of Alzheimer's disease (AD) pathology in mouse models, we have developed a "somatic brain transgenics" paradigm, established by delivery of genes packaged into adeno-associated viral vectors and injected into the brains of newborn mice. Tau protein is known to go through abnormal phosphorylation and accumulation in AD for yet unclear reasons. Anti-tau immunotherapy has recently emerged as a promising approach to target tau, but many questions regarding the optimal form of anti-tau immunotherapy remain open. We propose to compare the ability of recombinant intracellular and extracellular antibodies to attenuate tau pathology in two mouse models. These studies will provide critical insights into i) whether targeting tau in the extracellular vs. intracellular compartment is more efficacious and ii) whether full length antibody and not just its binding fragment antibody effector functions are required. Name of organization or government: University of Florida (H) Purpose of Grant or Assistance: Alzheimer's Disease Research by Guilian Xu, PhD Entitled: (A2014108S) Protein Homeostasis in Mouse Models of Alzheimer Pathology. Investigator's Summary: In this proposal, we investigate fundamental changes that occur in way nerve cells manage the production of new proteins and the disposal of old proteins. This process is essential to the normal functioning of the brain. In work prior to this proposal, we have identified a new pathology associated with Alzheimer's disease that we call secondary misfolding pathology, which describes changes in the ability of nerve cells to produce functional enzymes and proteins. In this proposal we will be working to better understand how this new pathology we have discovered may be affecting the ability of brain to function.
Schedule I, Part II, Line 1, Column (H):Name of organization or government: Mayo Clinic Jacksonville (H) Purpose of Grant or Assistance: Alzheimer's Disease Research by Mitsuru Shinohara, PhD Entitled: (A2014137F) Synaptic Regulation of AB Metabolism and Secreted Markers. Investigator's Summary: To understand why your friends or relatives develop Alzheimer's disease (so-called etiology), we need to develop bio-markers that can evaluate the disease progression as well as the underlying disease processes, especially those related to toxic AB accumulation in brains. Recent studies, including our study, demonstrate that synapses (neuronal connections in brain) play important roles in toxic AB accumulation. By elucidating how these synapses regulate the metabolism of toxic AB in brains at a molecular level and what proteins or molecules in body fluids are associated with these phenomena; this proposed research will be able to identify appropriate biomarkers that indicate disturbances in synaptic AB metabolism in brains, before the development of Alzheimer's disease. Such bio-markers would be very useful in order to identify and clarify the etiology underlying the progression of AB accumulation in individual persons, and may ultimately lead to effective treatments for Alzheimer's disease. Name of organization or government: Washington University (H) Purpose of Grant or Assistance: Alzheimer's Disease Research by Kristen Funk, PhD Entitled: (A2014164F) Differential Uptake of Tau Fibrils into Neurons and Glia. Investigator's Summary: Alzheimer's disease is defined, in part, by deposits of aggregated tau protein within neurons of affected brain. Recent data have suggested that progression of AD may be due to the release of tau aggregates from afflicted neurons, followed by the uptake of tau fibrils into naive neurons, resulting in the propagation of tau pathology. To date, the role of glia in this model has remained unexplored; however, we hypothesize that promoting uptake into glia may clear tau aggregates without contributing to disease progression. Studies proposed here will establish the mechanisms of tau uptake that differ between neurons and glia with the goal to identify potential therapeutic targets that block uptake into neurons while promoting uptake into glia. Name of organization or government: Columbia University Medical Center (H) Purpose of Grant or Assistance: Alzheimer's Disease Research by Tal Nuriel, PhD Entitled: (A2014200F) Metabolomic/Lipidomic Analysis of ApoE Isoform Effects. Investigator's Summary: Carriers of the APOE e4 gene are at significantly increased risk for developing Alzheimer's disease. In order to understand the cause of this increased Alzheimer's risk, we will utilize emerging technology to measure the levels of lipids and small-molecules in mouse and human brain tissues possessing differing forms of APOE. We anticipate that the results of this study will shed new light on why carriers of the APOE e4 gene are more susceptible to Alzheimer's disease and how Alzheimer's disease can be prevented in these individuals.
Schedule I, Part II, Line 1, Column (H):Name of organization or government: University of Kentucky (H) Purpose of Grant or Assistance: Alzheimer's Disease Research by Steven Estus, PhD Entitled: (A2014210S) Genomic Editing to Elucidate CD33 Function. Investigator's Summary: About 70% of Alzheimer's disease risk is due to differences in DNA sequences between people. Here, we have identified how one of these DNA sequence variations changes gene expression to reduce Alzheimer's risk. The action of the DNA sequence difference is a modest 15% decrease in functional gene expression. Remarkably, an inhibitor of this gene has already been in clinical trials for leukemia, and will be tested here for its ability to act similarly to the DNA sequence variation. Name of organization or government: University of Washington School of Medicine (H) Purpose of Grant or Assistance: Alzheimer's Disease Research by Richard Morrison, PhD Entitled: (A2014237S) Bif-1 Therapy for Cognitive Impairment and Neuropathology in AD. Investigator's Summary: We have identified a protein with a unique protective function in nerve cells and this protein is lost in the brains of patients with Alzheimer's disease. The loss of this protein may make the disease worse based on studies we've done where we eliminate the protein in mice that also express symptoms of Alzheimer's disease. We would like to determine if we can improve cognitive function in patients with Alzheimer's disease by restoring the expression of this protein. We will test this possibility by developing a method to restore this protein in the nerve cells of mice that also express symptoms of Alzheimer's disease and we will determine if their cognitive abilities improve. Name of organization or government: Washington University (H) Purpose of Grant or Assistance: Alzheimer's Disease Research by David Brody, MD, PhD Entitled: (A2014270S) Purification and Characterization of Amyloid-beta Oligomers from Human Brain. Investigator's Summary: Alzheimer's disease is the most common cause of problems with memory, thinking, and behavior in older people; it is most likely caused by accumulation of a small protein called amyloid-beta. There is no cure or effective treatment for Alzheimer's disease despite decades of work, in part because our attempts so far have not focused on the most toxic forms of amyloid-beta. We have developed methods to accurately measure these toxic forms of amyloid-beta in the brains of Alzheimer's disease patients, and we now propose to purify them so that we can study them in detail. This project is vital because understanding the toxic forms of amyloid-beta will help us efficiently design effective treatments to prevent them from forming, block their toxicity, or destroy them.
Schedule I, Part II, Line 1, Column (H):Name of organization or government: University of Kentucky (H) Purpose of Grant or Assistance: Alzheimer's Disease Research by M. Paul Murphy, MA, PhD Entitled: (A2014280S) A Novel Therapy for the Treatment of Dementia. Investigator's Summary: We are going to use a unique mouse model that we have developed (the db/AD mouse) to test a potential treatment for Alzheimer's disease (AD). Many cases of AD are also accompanied by large amounts of vascular pathology in the brain. The mouse we have developed has cognitive deficits reflective of the deficits seen in AD, and the db/AD mice also experience aneurysms and strokes which indicate the presence of vascular disturbances in the brain. In the hopes of improving the vascular pathology, we are going to treat these mice with a drug that is already approved for human use, and we will perform MRI imaging at regular time points to monitor any effect the drug treatment has on the vascular pathology in the brain. Name of organization or government: Washington University (H) Purpose of Grant or Assistance: Alzheimer's Disease Research by Richard Perrin, MD, PhD Entitled: (A2014296S) Novel CSF Biomarkers in Familial Alzheimer Disease. Investigator's Summary: The goal of this study is to discover a timeline of protein changes within the cerebrospinal fluid (the fluid that bathes the brain) that can be used to diagnose and monitor Alzheimer's disease (AD), even years before symptoms of the disease appear. To accomplish this goal, we will apply a powerful new technique (quantitative label-free proteomics) to measure hundreds of proteins in cerebrospinal fluid samples from people enrolled in the Dominantly Inherited Alzheimer Network (DIAN) study. Familial AD is uniquely suited to this mapping study of very early changes because the age at which symptoms begin can be reliably predicted from affected family members, and diagnosis can be definitively established by genetic testing even decades before symptoms are predicted. Such a timeline will improve the accuracy of early diagnosis, maximize the efficiency of clinical trials, and move effective treatments more quickly and cheaply from the laboratory to the pharmacy. Name of organization or government: The Ohio State University (H) Purpose of Grant or Assistance: Alzheimer's Disease Research by Chien-liang Lin, PhD Entitled: (A2014315S) Regulating Glutamate Levels as a Therapeutic Strategy for Alzheimer's Disease. Investigator's Summary: The glial glutamate transporter EAAT2 is responsible for maintaining low extracellular glutamate concentrations in our brains. Loss of EAAT2 protein and function is commonly found in patients with Alzheimer's disease. We discovered that restoration of EAAT2 function can reverse Alzheimer phenotypes in an animal model of Alzheimer's disease. The goal of this research is to develop restoration of EAAT2 function as a therapeutic strategy for Alzheimer's disease.
Schedule I, Part II, Line 1, Column (H):Name of organization or government: University of Chicago (H) Purpose of Grant or Assistance: Alzheimer's Disease Research by Virginie Buggia-Prevot, PhD Entitled: (A2014316F) Role of EHD Proteins in Alzheimer's Disease Pathogenesis. Investigator's Summary: The goal of my research is to better understand the causes of Alzheimer's disease by studying the mechanisms that contribute to the disease apparition, in order to identify potential therapeutic targets. In the brain of individuals with Alzheimer's disease, a toxic peptide called amyloid is overproduced and leads to dysfunction of memory functions and ultimately the death of the nerve cells. I recently found two proteins called EHD, which are involved in amyloid peptide production in cultured neurons. The proposed investigation would determine if there is an alteration of EHD in human brains that could facilitate amyloid overproduction, and to test if amyloid overproduction could be blocked by abolishing the expression of EHD in mice that are engineered to develop Alzheimer's Disease pathology. Thus, the proposal investigates neuronal mechanisms that are intimately associated with Alzheimer's disease with the goal of establishing EHD proteins as one of the molecular players in disease pathogenesis. Name of organization or government: Northwestern University (H) Purpose of Grant or Assistance: Alzheimer's Disease Research by Jian Li, PhD Entitled: (A2014349F) Stress Response Networks in Organismal Proteostasis. Investigator's Summary: Alzheimer's disease patients are featured with aggregation of abnormally folded beta amyloid proteins in the brain that interfere with the cellular functions and eventually lead to degeneration of neurons. Stress response factors have been suggested to protect the protein toxicity associated with Alzheimer's disease. This protection could occur both in the beta amyloid expressed tissue and the neighboring tissues. Here we set out to characterize the protective mechanisms mediated by stress response pathways especially how neurons sense the toxic aggregation and how they communicate with neighboring tissues to end up an organismal protection. Name of organization or government: Washington University (H) Purpose of Grant or Assistance: Alzheimer's Disease Research by Randall Bateman, MD Entitled: (A2014384S) Stable Isotope Labeling Kinetics of Human TAU In Alzheimer's Disease. Investigator's Summary: In Alzheimer's disease Tau is increased in the brain and fluid that surrounds the brain. It is unclear why it is increased. Is this due to increased production or impaired clearance? How much is production or clearance altered? Can drugs be developed that can correct abnormal tau production or clearance? These questions can now be answered and give drugs which target tau a better chance of working in Alzheimer's disease.
Schedule I, Part II, Line 1, Column (H):Name of organization or government: University of South Dakota (H) Purpose of Grant or Assistance: Alzheimer's Disease Research by Hongmin Wang, PhD Entitled: (A2014420S) Using Mouse Models to Study the Role of Ubiquilin-1 in Alzheimer's Disease. Investigator's Summary: A protein named ubiquilin-1, has long been considered to play a role in Alzheimer's disease. However, the exact role of the protein in Alzheimer's disease remains unclear. This research project is to investigate whether increase or depletion of ubiquilin-1 protein in genetically modified mice changes the signs and conditions of Alzheimer's disease. Name of organization or government: Stanford University (H) Purpose of Grant or Assistance: Alzheimer's Disease Research by Katrin Andreasson, MD Entitled: (A2014423S) Inhibiting Tryptophan Metabolism in Alzheimer's Disease. Investigator's Summary: The proposed work will determine whether degradation of the amino acid tryptophan by the enzymes TDO2 and IDO1 functions in development of Alzheimer's disease. We will use genetic and pharmacologic approaches in a mouse model of AD to identify mechanisms of action of these enzymes in early and late stages of AD development. Successful completion of these studies may lead to a novel preventive and therapeutic strategies to delay onset of AD in at-risk aging populations. Name of organization or government: Columbia University Medical Center (H) Purpose of Grant or Assistance: Alzheimer's Disease Research by Alice Lepelley, PhD Entitled: (A2014425F) Implication of a Mitochondrial Protein, ECSIT, in the Oxidative Stress Leading to Alzheimer's Disease. Investigator's Summary: Alzheimer's Disease is the world's most common cause of dementia and oxidative stress has emerged as a key feature and possible cause of the disease. It appears early and can accelerate progression of the disease. However, only a few treatments trying to prevent oxidative stress have provided positive results. With this project we will study a promising novel mechanism causing oxidative stress in hope to provide ideas for more efficient therapeutics.
Schedule I, Part II, Line 1, Column (H):Name of organization or government: Seattle Institute for Biomedical and Clinical Research (H) Purpose of Grant or Assistance: Alzheimer's Disease Research by Brian Kraemer, PhD Entitled: (A2014438S) Dopamine Signaling Controls Pathological Tau. Investigator's Summary: A number of neurodegenerative disorders have tau deposits including Alzheimer's disease. Abnormal tau protein can cause age dependent neurodegeneration in Alzheimer's disease and related disorders. We have identified a class of drugs that prevent abnormal tau formation in animal models of disease. The goal of this project is to understand how these drugs prevent abnormal tau so we can develop these drugs further ultimately setting the stage for clinical trials in Alzheimer's patients. Name of organization or government: University of California, San Francisco (H) Purpose of Grant or Assistance: National Glaucoma Research by Jeffrey L Goldberg, MD, PhD Entitled: (C2015200) Early Phase Testing of Regenerative Therapies in Glaucoma. Name of organization or government: University of California, San Francisco (H) Purpose of Grant or Assistance: National Glaucoma Research by Douglas Gould, PhD Entitled: (G2014007) Identification and in Vivo Balidation of Novel Genes for Developmental Glaucoma. Investigator's Summary: Anterior segment dysgenesis (ASD) describes problems affecting the front part of the eye. One of the major consequences of ASD is glaucoma which can lead to irreversible blindness at a young age. Our goal is to understand how these problems come about with the end goal of establishing treatments.
Schedule I, Part II, Line 1, Column (H):Name of organization or government: Washington University (H) Purpose of Grant or Assistance: National Glaucoma Research by Jeff Gidday, PhD Entitled: (G2014012) Hypoxic Conditioning for Protection in DBA/2J Glaucoma. Investigator's Summary: A fundamental principle of biology (and evolution) is that organisms, and cells, adapt to a stress imposed on them so that they can better handle that stress if encountered again in the future. The studies in this research project are designed to leverage this concept as a way of protecting the eye from glaucoma. In particular, we will test whether intermittently exposing mice to a hypoxic or low-oxygen stress, that by itself is not harmful; will trigger adaptive responses in the eye that make it more resistant to the damaging effects of glaucoma. If successful, these studies will confirm the presence of innate protective responses in the eye that someday could be activated in humans with glaucoma, thereby reducing the vision loss and blindness that characterizes this devastating disease. Name of organization or government: University of Wisconsin (H) Purpose of Grant or Assistance: National Glaucoma Research by Donna Peters, PhD Entitled: (G2014051) Use of Small Molecules to Control ECM Homeostasis. Investigator's Summary: A major risk factor for glaucoma is an elevation of intraocular pressure caused by the reduced movement of fluid out of the eye. This movement is restricted because the passageways that allow fluid to exit the eye are clogged with too much protein. The goals of this research are to understand how these proteins are deposited in these passageways and to identify ways to prevent the proteins from being deposited. Name of organization or government: Oregon Health and Science University (H) Purpose of Grant or Assistance: National Glaucoma Research by Janice Vranka, PhD Entitled: (G2014058) Altered Versican Fibrillar Interactions in the Outflow Pathway. Investigator's Summary: Our research focuses on the trabecular meshwork, a discrete tissue located in the eye around the base of the cornea, near the ciliary body, which is responsible for draining the aqueous humor from the eye via the anterior chamber and is believed to be the tissue that regulates intraocular pressure, a critical factor in the development of glaucoma. Our laboratory is investigating the hypothesis that a specific subset of complex molecules that reside in the trabecular meshwork, and that interact with each other, are important in the regulation of aqueous humor outflow resistance. When these processes are disrupted there will be changes in the tissue that lead to alterations in outflow facility. Thus our primary objective is aimed at improving the overall understanding of how aqueous humor outflow resistance is regulated and what are the triggers in the development of glaucoma in order to facilitate the development of novel therapies aimed at helping glaucoma patients.
Schedule I, Part II, Line 1, Column (H):Name of organization or government: Legacy Health System (H) Purpose of Grant or Assistance: National Glaucoma Research by Lin Wang, MD, PhD Entitled: (G2014059) Glia-mediated Blood Flow Autoregulation in Glaucoma. Investigator's Summary: Glaucoma is the second most common cause of blindness worldwide. Studies over the past few years have shown that blood flow and the way it changes in the diseased eye play a role. This project will look at what causes the blood flow change and this could lead to an original treatment for this disease. Name of organization or government: University of North Texas Health Science Center (H) Purpose of Grant or Assistance: National Glaucoma Research by Colleen McDowell, PhD Entitled: (G2014063) Crosstalk of TGF-beta and TLR4 pathways in the trabecular meshwork. Investigator's Summary: One of the major risk factors for the development of glaucoma is an increased pressure inside the eye. An increase of pressure occurs in the eye when fluid is not drained properly through the drainage structures in the front of the eye. Our project aims to understand what regulates the arrangement and construction of the drainage structures and how changes in this makeup prevent proper drainage in the eye. Name of organization or government: University of Nebraska Medical Center (H) Purpose of Grant or Assistance: National Glaucoma Research by Dhirendra Singh, PhD Entitled: (G2014067) Oxidative Stress and Sumoylation in Pathobiology of Trabecular Meshwork. Investigator's Summary: Glaucoma is related to overstimulation of certain genes/proteins in the trabecular meshwork (TM), a condition caused by reduced expression of antioxidants which results from aging or oxidative stress. We propose to examine further the underlying causes and mechanisms by which pathobiology of the TM develops, and explore novel targets for glaucoma therapy, including antioxidant therapy based on the protective protein Prdx6.
Schedule I, Part II, Line 1, Column (H):Name of organization or government: Duke University Eye Center (H) Purpose of Grant or Assistance: National Glaucoma Research by Stuart McKinnon, MD, PhD Entitled: (G2014076) Neuroinflammation: the Role of Lymphocytes in Glaucoma. Investigator's Summary: In glaucoma, permanent vision loss and blindness occur when retinal ganglion cells (RGCs) that make up the optic nerve are lost. Increasing evidence points to a central role of the immune system in the death of RGCs in glaucoma. We have recently shown the surprising finding that in an experimental mouse model of glaucoma, a severely immunodeficient transgenic mouse that lacks T- and B-lymphocytes (Rag1 knockout) is robustly protected against optic nerve damage due to chronic exposure to elevated intraocular pressure (IOP). These transgenic mice lack expression of Rag1, a protein essential to the generation of mature T- and B-lymphocytes, and are thus immunodeficient. This finding generates the novel hypothesis that immune system events involving lymphocytes are necessary for RGC cell death and optic nerve axon loss in glaucoma. This project will determine whether specific populations of lymphocytes are required for RGC death in glaucoma, and to determine if blocking lymphocyte extravasation into ocular tissues (diapedesis) rescues RGCs in a mouse glaucoma model. We will isolate T- or B-cells using standard immunology techniques and transfer these cells to Rag1 knockout mice to reconstitute this portion of the mouse immune system. We will then utilize our well-established mouse glaucoma model to determine if either T- or B-cells are necessary for RGC axon loss. Lymphocytes migrate from the bloodstream to tissues by the process of diapedesis, which requires the expression of a4 integrin protein on vascular endothelium. We will induce glaucoma in transgenic mice that carry a point mutation in a4 integrin to determine if blocking lymphocyte diapedesis is neuroprotective in our mouse glaucoma model. We will also test whether pharmacological blockage of a4 integrin-mediated diapedesis with a murine version of natalizumab (Tysabri, Biogen, Inc.) is neuroprotective in our mouse glaucoma model. If T- or B-cells are necessary for glaucoma damage, further research will be designed to determine whether specific lymphocyte subpopulations (e.g. CD4+, CD8+, etc.) can be identified as crucial to RGC axon loss in glaucoma. Given the existing literature, data supporting or refuting the roles of lymphocytes in glaucomatous RGC death would represent a significant advance for the field and therapies can be designed to modulate the immune system and prevent vision loss and blindness in our human glaucoma patients. Name of organization or government: University of Pittsburgh (H) Purpose of Grant or Assistance: National Glaucoma Research by Yiqin Du, MD, PhD Entitled: (G2014086) A Mouse Glaucoma Model and Stem Cell-Based Therapy for Glaucoma. Investigator's Summary: Glaucoma is a leading cause of irreversible blindness; elevated intraocular pressure is a major risk factor and it is controllable. The trabecular meshwork acts as a drainage system to the eye, and blockage of this drainage, such as by irregularities in the cells and matrix of the meshwork, can lead to a build-up of aqueous fluid in the eye and subsequent elevation of intraocular pressure. We have isolated and characterized immature stem cells from the trabecular meshwork with the ability to seek out and repair the damage in this tissue. This project will identify a drug enabling us to model elevated pressure by damaging trabecular meshwork in a mouse, then to apply trabecular meshwork stem cells with the purpose of restoring a functioning meshwork and reducing the intraocular pressure. Name of organization or government: Indiana University School of Medicine (H) Purpose of Grant or Assistance: National Glaucoma Research by Lyne Racette, PhD Entitled: (G2014096) An Individualized Model to Monitor Laucoma Progression. Investigator's Summary: Glaucoma is an eye disease that can lead to blindness. We propose a new model to detect glaucoma changes over time. This model will be tailored for each patient and tested in a different group of patients. We will use this model to predict which patients are likely to change over time.
Schedule I, Part II, Line 1, Column (H):Name of organization or government: University of South Florida (H) Purpose of Grant or Assistance: National Glaucoma Research by Chris Passaglia, PhD Entitled: (G2014105) An Implantable System for Intraocular Pressure Measurement and Control. Investigator's Summary: To understand the causes and effects of glaucoma, researchers often rely on animal models in which eye pressure is elevated by experimental means. Traditional methods of elevating pressure can reproduce key features of the disease, but they are limited by finite success rates, sporadic pressure information, and variable exposure histories. These limitations hamper research progress and may prevent major breakthroughs. The overarching goal of this project to develop a smart pump that would for the first time gives glaucoma researchers and clinicians unprecedented control over eye pressure. Name of organization or government: Massachusetts Eye and Ear Infirmary (H) Purpose of Grant or Assistance: National Glaucoma Research by Baojian Fan, MD, PhD Entitled: (G2014107) Discovery of PDS/PG Genes by Exome Sequencing. Investigator's Summary: Pigment dispersion syndrome (PDS) causes pigmentary glaucoma which is a common form of open-angle glaucoma that usually affects young adults and can be inherited. No genes responsible for this condition have been identified so far in humans. In this proposal, we will use whole exome sequencing, a new and powerful technology to find genes that can cause this common form of glaucoma. The results from this project can be used to develop new methods of diagnosis and treatment for PDS and pigmentary glaucoma. Name of organization or government: Johns Hopkins University (H) Purpose of Grant or Assistance: National Glaucoma Research by Derek Welsbie, PhD Entitled: (G2014119) Developing Dual Leucine Zipper Kinase Inhibitors for Glaucoma. Investigator's Summary: Nerve cells called retinal ganglion cells from the connection between the eye and the brain. In glaucoma, these nerve cells die and vision is permanently lost. We have previously shown that a protein called dual leucine zipper kinase (DLK) is critical for the death of these cells. Thus, this proposal seeks to identify a drug that might block interfere with DLK and prevent retinal ganglion cell death.
Schedule I, Part II, Line 1, Column (H):Name of organization or government: University of Colorado Eye Center (H) Purpose of Grant or Assistance: Macular Degeneration Research by Omid Masihzadeh, PhD Entitled: (M2014014) Simultaneous, Structural And Functional Imaging Of The Retinal Pigment Epithelium. Investigator's Summary: Progression of age-related macular degeneration (AMD) coincides with structural changes to the eye. Currently, clinicians and researches use visible light and histological sectioning to study these changes, but are limited to detections of only fairly large structures and lack necessary information associated with the disease. We propose a new paradigm in light microscopy to detect both structures changes and functional abnormalities associated with AMD. Currently, this detection method is unknown and unavailable to researchers and clinicians. We propose to investigate the viability of this technique for studying AMD. Name of organization or government: The Schepens Eye Research Institute (H) Purpose of Grant or Assistance: Macular Degeneration Research by Andrius Kazlauskas, PhD Entitled: (M2014025) HtrA1 is required for RPE Survival During ER Stress. Investigator's Summary: In aging patients with central vision loss, a group of cells in the back of the eye, retinal pigment epithelia (RPE) is specifically injured. The aim of this study is to examine whether RPE injury arises from sustained, irreparable damage to the cell's protein factories. We predict that patients with changes to a protein called HtrA1 are particularly prone to such damages. We propose that rectifying RPE injury with "chemical chaperones" can benefit these patients, and that this class of drugs can be used as a strategy to manage central vision loss. Name of organization or government: Georgetown University (H) Purpose of Grant or Assistance: Macular Degeneration Research by Nady Golestaneh, MS, PhD Entitled: (M2014039) Autophagy, a Critical Pathway in the Pathophysiology of Age-related Macular Degeneration. Investigator's Summary: Age-related macular degeneration (AMD) is the leading cause of vision loss in the elderly. More than 11 million Americans are affected by AMD with no effective treatments available. Autophagy is a self-eating process in the cells that involves degradation of unwanted cellular components to supply the cell with energy when needed. Failure in autophagy is related to diseases. We propose to study the role of autophagy and its possible dysfunction in AMD.
Schedule I, Part II, Line 1, Column (H):Name of organization or government: Children's Hospital Boston, Harvard Medical School (H) Purpose of Grant or Assistance: Macular Degeneration Research by Michael Do, PhD Entitled: (M2014055) Mechanisms of Signaling in the Fovea. Investigator's Summary: Few organisms have a more detailed visual experience than humans. The reason is that we possess a specialization of our retina, called the fovea, that constitutes an extraordinarily "high definition" pixel array. Macular degeneration is a leading cause of blindness that devastates vision by attacking the fovea. By investigating how the fovea works, we will help the diagnosis, prevention, and treatment of macular degeneration, while also gaining insight into how our power of sight outstrips that of most other creatures. Name of organization or government: Tufts University (H) Purpose of Grant or Assistance: Macular Degeneration Research by Behzad Gerami-Naini, PhD Entitled: (M2014059) Tissue Engineering Dental Pulp Stem Cell Derived-RPE on a Bio-mimetic Silk Membrane. Investigator's Summary: Age-related macular degeneration (AMD) is a devastating eye disease that affects a large percentage of the American population. Although we don't have a cure or a good way to restore vision in individuals affected by the disease, there are ways to prevent further vision loss for patients that are suffering from AMD. Our approach is to extract the stem cells from a patient's tooth and turn them into an important eye cell that we can then transplant back into the patient's eye. In order to transplant these eye cells, we need the cells to remain intact and will be using silk as a natural product that the body won't reject to deliver these eye cells. Name of organization or government: University of California, San Francisco (H) Purpose of Grant or Assistance: Macular Degeneration Research by Sara Venters, PhD Entitled: (M2014060) Establishing the Foveal Retina During Embryonic Development. Investigator's Summary: The central retina is the small portion of the eye used for our clearest and sharpest vision. Anatomically, it is different from the rest of the eye, and we do not understand exactly why. The central retina is specifically affected in several eye diseases, and trying to understand how exactly it differs can help with treatment and future therapies for re-growing this portion. In this proposal we will first follow the development of the precursors to the central retina, and next we will determine which, if any, of the environments that they pass through during development is important for making them specifically central retina.
Schedule I, Part II, Line 1, Column (H):Name of organization or government: Regents of the University of Michigan (H) Purpose of Grant or Assistance: Macular Degeneration Research by Debra Thompson, PhD Entitled: (M2014073) Control of Innate Inflammatory Responses in the Retina. Investigator's Summary: One aspect of the damage to the retina that occurs in age-related macular degeneration (AMD), a disease responsible for visual handicap in millions of elderly people, is caused by the presence of low grade inflammation over long periods of time. Specialized cells in the retina express a class of cell-surface proteins that are known to play a role in opposing inflammatory responses in other tissues of the body. The purpose of the proposed studies is to determine the role of these proteins in decreasing inflammatory responses in the retina. The outcome of these studies will lead to increased understanding of the control inflammation in the retina, and the possibilities for developing novel therapies aimed at regulating this mechanism. Name of organization or government: The Schepens Eye Research Institute (H) Purpose of Grant or Assistance: Macular Degeneration Research by Neena Haider, PhD Entitled: (M2014084) Novel Genetic Model of Choroidal Neovascular Age-related Macular Degeneration. Investigator's Summary: Age related macular degeneration (AMD) is easily becoming the number one cause of blindness in the world today. A major problem in finding a cure is not knowing what causes the disease and having a good model system to test a therapy. In this study, we utilize a novel genetic model that recapitulates the blood vessel defect seen in AMD patients and thus have a powerful tool to identify a factor that can cause this disease outcome, understand the disease process, and a model to test therapies. Name of organization or government: University of Maryland, Baltimore (H) Purpose of Grant or Assistance: Macular Degeneration Research by Richard Thompson, PhD Entitled: (M2014085) Role of Zn and HAP in Inducing Sub-RPE Deposits and Age-related Macular Degeneration. Investigator's Summary: We have discovered what appears to be an early step in the process of developing deposits (drusen) in the aging retina, which can lead to macular degeneration (AMD). We believe that zinc and inflammation are involved, and have developed a method for visualizing when the step has occurred in the intact eye. The thrust of our project is to see how zinc and inflammation are involved in this step and how early and broadly the step may occur in ordinary eyes: does the step happen at 40 years of age, at 60 years of age, and does it occur in everybody? We anticipate our visualization method may be usable as a screening test for AMD (patent pending), and our improved understanding of how AMD develops may lead to new, early treatments.
Schedule I, Part II, Line 1, Column (H):Name of organization or government: University of Illinois at Chicago (H) Purpose of Grant or Assistance: Macular Degeneration Research by David Pepperberg, PhD Entitled: (M2014091) Exogenous Peptidase for Amyloid-beta Degradation. Investigator's Summary: Current knowledge suggests that the development of age-related macular degeneration (AMD), a blinding disease that affects many older individuals, may involve the abnormally high build-up of a protein known as "amyloid-beta" in the eye. If abnormally high amyloid-beta indeed promotes AMD, removing this excessive amyloid-beta could be a therapy for AMD. It is known that a type of enzyme termed "peptidase" can break down amyloid-beta. Accordingly, using mice with AMD-like disease as our experimental system, we propose to study whether artificially increasing the amount of peptidase in the eye can slow or block the progress of the disease. Name of organization or government: Duke University Eye Center (H) Purpose of Grant or Assistance: Macular Degeneration Research by Priyatham Mettu, MD Entitled: (M2014099) Macrophages Drive Neovascular Remodeling in NV Age-related Macular Degeneration. Investigator's Summary: Our research is trying to understand what causes the severe form of wet macular degeneration, a common disease of the back of the eye (retina) and one of the leading causes of blindness in the United States. Macrophages are cells in the body that fight off infection, but in some cases, can cause damage to tissues in the body. We are trying to determine how macrophages make wet macular degeneration worse and harder to treat with available medicines. If we can understand how macrophages make this disease worse, we hope that we can develop new medicines to treat patients with the disease who continue to lose vision. Name of organization or government: Johns Hopkins University (H) Purpose of Grant or Assistance: Macular Degeneration Research by Debasish Sinha, PhD Entitled: (M2014109) Understanding How Dysregulation of Autophagy/phagocytosis activates the Immune System in RPE Cells, Leading to Age-related Macular Degeneration-like Pathology. Investigator's Summary: The Retinal Pigmented Epithelium (RPE) is a single layer of pigmented cells situated between the neurosensory retina and the choroid, the vascular layer at the back of the eye. The RPE is involved in the phagocytosis of photoreceptor outer segments (OS), a role essential for the maintenance and survival of the photoreceptors (light sensitive cells) as well as autophagy (self digestion by a cell), and may be of particular importance because of the very high metabolic activity of RPE. We have generated a RPE-specific Cryba1 gene knockout mouse, which will serve as a genetic tool to better understand the processes of phagocytosis and autophagy in RPE. Our studies may lead to development of therapeutic targets in the future for some manifestations of AMD that result from defective phagocytosis and/or autophagy in RPE.
Schedule I, Part II, Line 1, Column (H):Name of organization or government: Massachusetts General Hospital (H) Purpose of Grant or Assistance: Macular Degeneration Research by Alexander Marneros, MD, PhD Entitled: (M2014120) Inflammasome regulation in age-related Macular Degeneration. Investigator's Summary: Age-related macular degeneration (AMD) is the most common cause of irreversible blindness in the elderly and is caused by a local inflammatory response affecting the function of the retinal pigment epithelium and the photoreceptors. In a mouse model of AMD we could show that inhibiting a molecular complex that is important for propagating this inflammatory response, the inflammasome, reduces pathologies of AMD in this model. Thus, we propose that mechanisms that inhibit the inflammasome are likely to reduce AMD progression in patients as well. Here, we will test mechanisms that control inflammasome activation in a mouse model of AMD to identify potential novel treatment approaches for AMD. Name of organization or government: Wilmer Eye Institute (H) Purpose of Grant or Assistance: Macular Degeneration Research by Hu Huang, PhD Entitled: (M2014124) Mechanisms by Cxcr5 Regulates Pathogenesis of Macular Degeneration. Investigator's Summary: I have recently found that a new gene is potentially involved in the disease of age-related macular degeneration (AMD). Without this gene, the aged mice develop a number of anomalies that resemble AMD pathologies. So this proposed research is to determine if this gene is involved in AMD progression. Name of organization or government: Wilmer Eye Institute (H) Purpose of Grant or Assistance: Macular Degeneration Research by Imran Bhutto, MD, PhD Entitled: (M2014128) The Inflammatory Cells of Choroid in Age-related Macular Degeneration. Investigator's Summary: Macular degeneration is a progressive eye condition affecting as many as 15 million Americans. The disease attacks the macula of the eye, where our sharpest central vision occurs, affecting reading, driving, identifying faces, watching television, safely navigating stairs and performing other daily tasks. The retinal pigment epithelium and choriocapillaris, the blood vessels that provide nutrition to the outer retina, die in age-related macular degeneration (AMD). This study will document the inflammatory cells under retina that may contribute to this death if activated. Drugs already exist to control their activation so this study could suggest new therapies for AMD. Name of organization or government: Stanford University (H) Purpose of Grant or Assistance: Macular Degeneration Research by Douglas Vollrath, MD, PhD Entitled: (M2014137) Genetics of RPE Metabolism: Implications for Age-related Macular Degeneration. Investigator's Summary: The nerves that sense light in the eye and the cells of the retinal pigment epithelium (RPE) form a critical partnership necessary for vision. We seek to understand how the capability of RPE cells to get energy from food molecules varies among human individuals due to differences in their genes and how RPE cells control this process. Success of this project may help us to better understand why macular degeneration affects some people more than others, eventually leading to improved treatment for this disease.

Schedule R IRS990ScheduleR

Id Disregarded Entities IdDisregardedEntitiesGrp (2 entries)

Address Line1USAddress/AddressLine1CityUSAddress/CityStateUSAddress/StateZIP CodeUSAddress/ZIPCodeEINEINPrimary ActivitiesPrimaryActivitiesTxtLegal Domicile StateLegalDomicileStateCdTotal IncomeTotalIncomeAmtEnd Of Year AssetsEndOfYearAssetsAmtDirect Controlling NADirectControllingNACd
National Development LLC
22512 Gateway Center DriveClarksburgMD20871237337229Property rental and managementMD$566,205$4,792,949N/A
American Health Assistance LLC
22512 Gateway Center DriveClarksburgMD20871237337229Owner of BrightFocus headquartersMD$0$4,162,074N/A