Attach to Form 990 or Form 990-EZ.
Go to
www.irs.gov/Form990 for instructions and the latest information.
| (i) Name of supported organization | (ii) EIN | (iii) Type of organization (described on lines 1- 10 above (see instructions)) | (iv) Is the organization listed in your governing document? | (v) Amount of monetary support (see instructions) | (vi) Amount of other support (see instructions) | |
|---|---|---|---|---|---|---|
| Yes | No | |||||
|
Total |
||||||
Calendar year
(or fiscal year beginning in)
![]() |
(a) 2018 | (b) 2019 | (c) 2020 | (d) 2021 | (e) 2022 | (f) Total | |
|---|---|---|---|---|---|---|---|
| 1 | Gifts, grants, contributions, and membership fees received. (Do not include any "unusual grant.") .. | 39,635,190 | 35,740,875 | 48,502,473 | 46,522,410 | 43,451,535 | 213,852,483 |
| 2 | Tax revenues levied for the organization's benefit and either paid to or expended on its behalf.... | ||||||
| 3 | The value of services or facilities furnished by a governmental unit to the organization without charge.. | ||||||
| 4 | Total. Add lines 1 through 3 | 39,635,190 | 35,740,875 | 48,502,473 | 46,522,410 | 43,451,535 | 213,852,483 |
| 5 | The portion of total contributions by each person (other than a governmental unit or publicly supported organization) included on line 1 that exceeds 2% of the amount shown on line 11, column (f) .. | 483,485 | |||||
| 6 | Public support. Subtract line 5 from line 4. | 213,368,998 | |||||
Calendar year
(or fiscal year beginning in)
![]() |
(a) 2018 | (b) 2019 | (c) 2020 | (d) 2021 | (e) 2022 | (f) Total | |
|---|---|---|---|---|---|---|---|
| 7 | Amounts from line 4.. | 39,635,190 | 35,740,875 | 48,502,473 | 46,522,410 | 43,451,535 | 213,852,483 |
| 8 | Gross income from interest, dividends, payments received on securities loans, rents, royalties and income from similar sources... | 1,925,519 | 2,176,998 | 1,887,633 | 2,074,361 | 1,972,869 | 10,037,380 |
| 9 | Net income from unrelated business activities, whether or not the business is regularly carried on.. | ||||||
| 10 | Other income. Do not include gain or loss from the sale of capital assets (Explain in Part VI.).. | 7,500 | 7,500 | ||||
| 11 | Total support. Add lines 7 through 10 | 223,897,363 | |||||
Calendar year (or fiscal year beginning in) ![]() |
(a) 2018 | (b) 2019 | (c) 2020 | (d) 2021 | (e) 2022 | (f) Total | |
|---|---|---|---|---|---|---|---|
| 1 | Gifts, grants, contributions, and membership fees received. (Do not include any "unusual grants.") . | ||||||
| 2 | Gross receipts from admissions, merchandise sold or services performed, or facilities furnished in any activity that is related to the organization's tax-exempt purpose | ||||||
| 3 | Gross receipts from activities that are not an unrelated trade or business under section 513 ..... | ||||||
| 4 | Tax revenues levied for the organization's benefit and either paid to or expended on its behalf... | ||||||
| 5 | The value of services or facilities furnished by a governmental unit to the organization without charge | ||||||
| 6 | Total. Add lines 1 through 5 | ||||||
| 7a | Amounts included on lines 1, 2, and 3 received from disqualified persons | ||||||
| b | Amounts included on lines 2 and 3 received from other than disqualified persons that exceed the greater of $5,000 or 1% of the amount on line 13 for the year. | ||||||
| c | Add lines 7a and 7b.. | ||||||
| 8 | Public support. (Subtract line 7c from line 6.) | ||||||
Calendar year (or fiscal year beginning in) ![]() |
(a) 2018 | (b) 2019 | (c) 2020 | (d) 2021 | (e) 2022 | (f) Total | |
|---|---|---|---|---|---|---|---|
| 9 | Amounts from line 6... | ||||||
| 10a | Gross income from interest, dividends, payments received on securities loans, rents, royalties and income from similar sources.. | ||||||
| b | Unrelated business taxable income (less section 511 taxes) from businesses acquired after June 30, 1975. | ||||||
| c | Add lines 10a and 10b. | ||||||
| 11 | Net income from unrelated business activities not included on line 10b, whether or not the business is regularly carried on. | ||||||
| 12 | Other income. Do not include gain or loss from the sale of capital assets (Explain in Part VI.) .. | ||||||
| 13 | Total support. (Add lines 9, 10c, 11, and 12.).. | ||||||
| Section A - Adjusted Net Income | (A) Prior Year |
(B) Current Year (optional) |
||||
| 1 | Net short-term capital gain | 1 | ||||
| 2 | Recoveries of prior-year distributions | 2 | ||||
| 3 | Other gross income (see instructions) | 3 | ||||
| 4 | Add lines 1 through 3 | 4 | ||||
| 5 | Depreciation and depletion | 5 | ||||
| 6 | Portion of operating expenses paid or incurred for production or collection of gross income or for management, conservation, or maintenance of property held for production of income (see instructions) | 6 | ||||
| 7 | Other expenses (see instructions) | 7 | ||||
| 8 | Adjusted Net Income (subtract lines 5, 6 and 7 from line 4) | 8 | ||||
| Section B - Minimum Asset Amount | (A) Prior Year |
(B) Current Year (optional) |
||||
| 1 | Aggregate fair market value of all non-exempt-use assets (see instructions for short tax year or assets held for part of year): | 1 | ||||
| a | Average monthly value of securities | 1a | ||||
| b | Average monthly cash balances | 1b | ||||
| c | Fair market value of other non-exempt-use assets | 1c | ||||
| d | Total (add lines 1a, 1b, and 1c) | 1d | ||||
| e |
Discount claimed for blockage or other factors (explain in detail in Part VI): |
|||||
| 2 | Acquisition indebtedness applicable to non-exempt use assets | 2 | ||||
| 3 | Subtract line 2 from line 1d | 3 | ||||
| 4 | Cash deemed held for exempt use. Enter 0.015 of line 3 (for greater amount, see instructions). | 4 | ||||
| 5 | Net value of non-exempt-use assets (subtract line 4 from line 3) | 5 | ||||
| 6 | Multiply line 5 by 0.035 | 6 | ||||
| 7 | Recoveries of prior-year distributions | 7 | ||||
| 8 | Minimum Asset Amount (add line 7 to line 6) | 8 | ||||
| Section C - Distributable Amount | Current Year | |||||
| 1 | Adjusted net income for prior year (from Section A, line 8, Column A) | 1 | ||||
| 2 | Enter 85% of line 1 | 2 | ||||
| 3 | Minimum asset amount for prior year (from Section B, line 8, Column A) | 3 | ||||
| 4 | Enter greater of line 2 or line 3 | 4 | ||||
| 5 | Income tax imposed in prior year | 5 | ||||
| 6 | Distributable Amount. Subtract line 5 from line 4, unless subject to emergency temporary reduction (see instructions) | 6 | ||||
| Section D - Distributions | Current Year | |
|---|---|---|
| 1 Amounts paid to supported organizations to accomplish exempt purposes | 1 | |
|
2
Amounts paid to perform activity that directly furthers exempt purposes of supported organizations, in excess of income from activity |
2 | |
| 3 Administrative expenses paid to accomplish exempt purposes of supported organizations | 3 | |
| 4 Amounts paid to acquire exempt-use assets | 4 | |
| 5 Qualified set-aside amounts (prior IRS approval required - provide details in Part VI) | 5 | |
| 6 Other distributions (describe in Part VI). See instructions | 6 | |
| 7Total annual distributions. Add lines 1 through 6. | 7 | |
|
8
Distributions to attentive supported organizations to which the organization is responsive (provide details in Part VI). See instructions |
8 | |
| 9 Distributable amount for 2022 from Section C, line 6 | 9 | |
| 10 Line 8 amount divided by Line 9 amount | 10 | |
| Section E - Distribution Allocations (see instructions) |
(i) Excess Distributions |
(ii) Underdistributions Pre-2022 |
(iii) Distributable Amount for 2022 |
|
|---|---|---|---|---|
| 1 Distributable amount for 2022 from Section C, line 6 | ||||
|
2
Underdistributions, if any, for years prior to 2022 (reasonable cause required-- explain in Part VI).
See instructions. |
||||
| 3 Excess distributions carryover, if any, to 2022: | ||||
| a From 2017....... | ||||
| b From 2018....... | ||||
| c From 2019....... | ||||
| d From 2020....... | ||||
| e From 2021....... | ||||
| fTotal of lines 3a through e | ||||
| g Applied to underdistributions of prior years | ||||
| h Applied to 2022 distributable amount | ||||
|
i
Carryover from 2017 not applied (see instructions) |
||||
| j Remainder. Subtract lines 3g, 3h, and 3i from line 3f. | ||||
| 4Distributions for 2022 from Section D, line 7: | ||||
| $ | ||||
| a Applied to underdistributions of prior years | ||||
| b Applied to 2022 distributable amount | ||||
| c Remainder. Subtract lines 4a and 4b from line 4. | ||||
|
5
Remaining underdistributions for years prior to 2022, if any. Subtract lines 3g and 4a from line 2. If the amount is greater than zero, explain in Part VI. See instructions. |
||||
|
6
Remaining underdistributions for 2022. Subtract lines 3h and 4b from line 1. If the amount is greater than zero, explain in Part VI. See instructions. |
||||
|
7 Excess distributions carryover to 2023. Add lines 3j and 4c. |
||||
| 8 Breakdown of line 7: | ||||
| a Excess from 2018..... | ||||
| b Excess from 2019..... | ||||
| c Excess from 2020..... | ||||
| d Excess from 2021..... | ||||
| e Excess from 2022..... | ||||
| Facts And Circumstances Test |
|---|
| Return Reference | Explanation |
|---|---|
| SCHEDULE A, PART II, LINE 10, EXPLANATION OF OTHER INCOME: | SAVINGS BOND PAYOUT - 2021 AMOUNT: $ 7,500. |
| Software ID: | |
| Software Version: |
Attach to Form 990 or 990-EZ.
Go to www.irs.gov/Form990 for the latest information.
| Return Reference | Explanation |
|---|---|
| FORM 990, PART III, LINE 1, DESCRIPTION OF ORGANIZATION MISSION: | BRIGHTFOCUS FUNDS EXCEPTIONAL SCIENTIFIC RESEARCH WORLDWIDE TO DEFEAT ALZHEIMER'S DISEASE, MACULAR DEGENERATION, AND GLAUCOMA AND PROVIDES EXPERT INFORMATION ON THESE HEARTBREAKING DISEASES. OUR VISION IS: A WORLD FREE FROM DISEASES OF MIND AND SIGHT. COLLECTIVELY, 300 MILLION PEOPLE WORLDWIDE SUFFER FROM THESE DISEASES. BRIGHTFOCUS HAS A PROVEN TRACK RECORD OF SUPPORTING THE MOST INNOVATIVE, EARLY-STAGE RESEARCH SEEKING TO FOSTER A BETTER UNDERSTANDING OF, TREATMENTS FOR, AND ULTIMATELY, A CURE FOR, THESE AGE-RELATED DISEASES WITH NO CURE. SINCE 1973, BRIGHTFOCUS HAS AWARDED MORE THAN $287 MILLION IN RESEARCH GRANTS TO THOUSANDS OF SCIENTISTS AROUND THE WORLD. OUR RESEARCH FUNDING HAS LED TO MAJOR CONTRIBUTIONS TO UNDERSTANDING THESE DISEASES AND SUPPORT FOR SCIENTISTS WHO HAVE RECEIVED PRESTIGIOUS AWARDS, INCLUDING TWO NOBEL PRIZES. AN INDICATOR OF OUR ABILITY TO PUSH NEW BOUNDARIES OF KNOWLEDGE IS THAT BRIGHTFOCUS-SUPPORTED RESEARCH WAS RECENTLY FOUND TO HAVE HAD 10 TIMES THE IMPACT ON DRIVING FUTURE SCIENCE THAN WORK SUPPORTED BY MANY OTHER ORGANIZATIONS. THE WORLD-CLASS RESEARCH IDENTIFIED AND SUPPORTED BY BRIGHTFOCUS IS ON THE CUTTING EDGE OF THE FIGHT TO SAVE MIND AND SIGHT. OUR FUNDING ACTS AS A CATALYST IN EARLY-STAGE RESEARCH, AND BRIGHTFOCUS RESEARCH PROGRAMS ARE DESIGNED TO PROVIDE INITIAL FUNDING FOR HIGHLY INNOVATIVE EXPERIMENTAL IDEAS. DUE TO THE STRUCTURED GRANT REVIEW AND APPROVAL PROCESS, THE RESEARCH IMPACT OF BRIGHTFOCUS IS VERY HIGH. MOST RECIPIENTS OF BRIGHTFOCUS FUNDING GO ON TO RECEIVE FUTURE GRANTS FROM OTHER SOURCES THAT ARE UP TO 10 TIMES LARGER THAN THE ORIGINAL BRIGHTFOCUS AWARD. THIS HIGH RETURN ON BRIGHTFOCUS INVESTMENT SPEAKS TO OUR ABILITY TO IDENTIFY PROMISING RESEARCH IN ITS EARLIEST STAGES 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. ALONG WITH FUNDING CUTTING-EDGE RESEARCH TO FIND CURES FOR SOME OF THE WORLD'S COSTLIEST DISEASES, BRIGHTFOCUS ALSO PROVIDES FREE EDUCATIONAL MATERIALS AND SUPPORT TO HUNDREDS OF THOUSANDS OF THOSE IMPACTED BY THESE DISEASES NATIONWIDE. WE ROOT THESE EDUCATIONAL MATERIALS IN THE LATEST RESEARCH FINDINGS (VIEW OUR RESEARCH MILESTONES ON BRIGHTFOCUSBOLD.ORG.) BRIGHTFOCUS ALSO INCREASES PUBLIC AWARENESS OF ALZHEIMER'S, MACULAR DEGENERATION, AND GLAUCOMA, AND COMMUNICATES WITH THOUGHT LEADERS AND ELECTED OFFICIALS ABOUT THE IMPORTANCE OF SCIENTIFIC RESEARCH IN THESE AREAS. BRIGHTFOCUS' AWARD-WINNING PUBLIC SERVICE ANNOUNCEMENTS (PSAS) HAVE APPEARED ON TELEVISION, RADIO, AND IN PRINT THROUGHOUT THE NATION. THE IMPACT OF ALZHEIMER'S, MAKE A PLAN TODAY: GET YOUR EYES CHECKED, AND NOW IS THE MOMENT TO STOP ALZHEIMER'S DISEASE POWERFULLY SEEKS 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, SUPERMARKETS AND DIGITALLY. IN FISCAL YEAR 2023, THESE PSA MESSAGES GENERATED $25,308,680 IN DONATED MEDIA SERVICES AND GARNERED OVER 532 MILLION IMPRESSIONS. 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. PARTNERING WITH SEVERAL HIGH-PROFILE PUBLIC AND PRIVATE ORGANIZATIONS, BRIGHTFOCUS IS HELPING TO BETTER EDUCATE THE PUBLIC ON THE LATEST RESEARCH DEVELOPMENTS PERTAINING TO ALZHEIMER'S, MACULAR DEGENERATION, AND GLAUCOMA, AS WELL AS THE IMPORTANCE OF EQUITABLE PARTICIPATION IN CLINICAL RESEARCH TO ACCELERATE THE PATH TO CURES FOR NEURODEGENERATIVE DISEASES. SPECIFICALLY, BRIGHTFOCUS IS PRODUCING AND DISSEMINATING FREE PROGRAMS INCLUDING: - BRIGHTFOCUS CHATS, SINCE 2014, THESE AUDIO DISCUSSIONS HAVE BROUGHT TOGETHER PATIENTS AND CAREGIVERS FOR INTERACTIVE MONTHLY TELEPHONE FORUMS TO LEARN FROM AND ASK QUESTIONS OF LEADING VISION DISEASE EXPERTS. THE CHATS ARE ARCHIVED ON OUR WEBSITE, WITH AUDIO AND PRINT TRANSCRIPTS AVAILABLE IN SEVERAL ACCESSIBLE FORMATS ONLINE, INCLUDING AS PODCASTS ON SPOTIFY AND APPLE ITUNES. - ZOOM IN ON DEMENTIA AND ALZHEIMER'S, A MONTHLY VIRTUAL DISCUSSION OPEN TO THE PUBLIC FEATURING TOPIC EXPERTS. - BRAIN INFO LIVE, A SUSTAINED, EPISODIC VIRTUAL EDUCATION SERIES TAILORED TO DIVERSE COMMUNITIES ACROSS THE US PRODUCED IN ENGLISH, SPANISH, AND HAITIAN CREOLE. BRIGHTFOCUS IS A PRESENTING PARTNER OF AN UPCOMING DOCUMENTARY, REMEMBERING GENE WILDER, AS WELL AS A DOCUMENTARY REMEMBERING ADELE, AND WILL EXECUTE ASSOCIATED EDUCATIONAL IMPACT CAMPAIGNS. THESE FILMS WILL BE SHOWN IN COMMUNITY SETTINGS ACROSS THE COUNTRY TO INCREASE AWARENESS OF, AND PARTICIPATION IN, ALZHEIMER'S CLINICAL RESEARCH. WE HAVE EXPANDED OUR WRITTEN AND MULTIMEDIA CONTENT OF KEY RESEARCH FINDINGS, PROMOTING AND SHARING THIS INFORMATION THROUGH OUR WEBSITE AND SOCIAL MEDIA PLATFORMS, INCLUDING VIDEO AND YOUTUBE. BRIGHTFOCUS INFOGRAPHICS VISUALLY COMMUNICATE INFORMATION ON ALZHEIMER'S, MACULAR DEGENERATION, AND GLAUCOMA, AND WE PROVIDE ACCESSIBLE CONTENT TRANSCRIPTS AND RESOURCES. IN THE SPRING OF 2020, WE LAUNCHED A FULL SECTION OF OUR WEBSITE DEDICATED TO SHARING EXCLUSIVE CONTENT ON COVID-19 FOR FAMILIES IMPACTED BY DISEASES OF MIND AND SIGHT. MORE SPECIFICALLY, EACH OF BRIGHTFOCUS' THREE PROGRAM AREAS MAILS AWARENESS-RAISING MATERIALS TO HUNDREDS OF THOUSANDS OF NATIONAL HOUSEHOLDS, WITH MESSAGES FOCUSING ON: - RISK FACTORS AND SYMPTOM RECOGNITION THROUGH PUBLIC AWARENESS AND STEPS THE PUBLIC SHOULD TAKE THAT MAY HELP REDUCE THEIR RISK. - 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 ADVOCACY ORGANIZATIONS, GOVERNMENTS AT ALL LEVELS, AND MEMBERS OF THE MEDIA, TO CALL GREATER ATTENTION TO DISEASES OF MIND AND SIGHT AND SHARE THE LATEST RESEARCH AND BEST PRACTICES WITH PUBLIC FIGURES AND KEY STAKEHOLDERS. THROUGH OUR OWN OUTREACH EFFORTS, AS WELL AS VIA ACTIVE ROLES IN ADVOCACY COALITIONS, WE HELP ADVANCE THE CAUSE OF PIONEERING SCIENCE AND BETTER POSITION BRIGHTFOCUS AS A RESOURCE FOR THOSE STRUGGLING WITH AND SEARCHING FOR CURES FOR THESE TERRIBLE DISEASES. BRIGHTFOCUS IS THE PRESENTING SPONSOR OF THE HELEN KELLER PRIZE FOR VISION RESEARCH, ONE OF THE MOST PRESTIGIOUS RECOGNITIONS IN THE FIELD. SELECTED BY A PANEL OF THE WORLD'S FOREMOST VISION SCIENTISTS, EACH YEAR'S LAUREATE IS HONORED FOR A GROUNDBREAKING CONTRIBUTION OR DISCOVERY TO SAVE SIGHT. BRIGHTFOCUS BEGAN ITS SPONSORSHIP IN 2015 TO CALL GREATER ATTENTION TO VISION RESEARCH ACROSS THE PRIVATE AND PUBLIC SECTORS. BRIGHTFOCUS WAS HONORED IN 2023 FOR ITS CONTRIBUTIONS TO ADVANCING GLOBAL VISION RESEARCH BY THE ASSOCIATION FOR RESEARCH IN VISION AND OPHTHALMOLOGY (ARVO) FOUNDATION. |
| FORM 990, PART III, LINE 4A, DESCRIPTION OF PROGRAM SERVICE: | ALZHEIMER'S DISEASE RESEARCH (ADR) - ALZHEIMER'S DISEASE 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. AN ESTIMATED 55 MILLION PEOPLE WORLDWIDE HAVE ALZHEIMER'S DISEASE OR OTHER DEMENTIAS, WITH WOMEN AND OTHER MINORITY GROUPS MOST AT-RISK. BRIGHTFOCUS' ALZHEIMER'S DISEASE RESEARCH (ADR) PROGRAM FUNDS RESEARCH FOCUSED ON UNDERSTANDING THE CAUSES OF ALZHEIMER'S DISEASE, 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. SINCE ITS INCEPTION, BRIGHTFOCUS HAS CONTRIBUTED MORE THAN $175 MILLION TO THE CONQUERING OF ALZHEIMER'S DISEASE. DURING THE FISCAL YEAR THAT ENDED MARCH 31, 2023, ADR AWARDED $6,394,521 IN PEER-REVIEWED GRANT AWARDS TO 26 NEW RESEARCH PROJECTS AND 8 OTHER AWARDS TO MAKE A TOTAL OF 34 GRANTS AT $7,755,537 TOTAL IN FUNDING. NOTABLE PROJECTS INCLUDE: HYPERTENSION AND LIFESTYLE EFFECTS ON RISK OF ALZHEIMER'S (INCLUDING LIPIDS); DRUG DISCOVERY AND BIOMARKERS; THE ROLE OF INFLAMMATION, MICROGLIA, AND VASCULAR HEALTH IN DISEASE RISK; LOOKING AT THE MITOCHONDRIA AND CELL ENERGY DEFICIENCIES; THE ROLE OF SLEEP DISTURBANCES CAUSING AN INCREASED RISK OF COGNITIVE ISSUES; DIFFERENCES IN GENETICS AND DISEASE RISK FOR UNDERREPRESENTED POPULATIONS; AND BETTER USE OF MODERN TECHNOLOGIES, INCLUDING BIG DATA/AI AND SYSTEMS GENETICS ANALYSIS FOR INCREASED AND DECREASED RISKS. ADDITIONAL INFORMATION ABOUT SPECIFIC PROJECTS IS INCLUDED IN SCHEDULES F & I. BRIGHTFOCUS IS HONORED TO HAVE SUPPORTED THE EARLY RESEARCH OF TWO NOBEL PRIZE WINNERS, DR. STANLEY PRUSINER AND DR. PAUL GREENGARD, WHOSE WORK HAS BEEN INSTRUMENTAL TO OUR CURRENT UNDERSTANDING OF ALZHEIMER'S DISEASE. BRIGHTFOCUS CONTINUES ITS PARTNERSHIP WITH THE ACADEMIC JOURNAL "MOLECULAR NEURODEGENERATION," THE OFFICIAL JOURNAL OF BRIGHTFOCUS FOUNDATION AND THE NUMBER ONE OPEN-ACCESS JOURNAL IN NEUROSCIENCE. THE JOURNAL PUBLISHES TECHNICAL PAPERS RELATED TO NEURODEGENERATION IN THE THREE DISEASE AREAS. TO ACCELERATE SCIENTIFIC PROGRESS, IT IS AN "OPEN ACCESS" JOURNAL, AND ALL CONTENT IS AVAILABLE FREE OF CHARGE. THIS OPEN ACCESS ENSURES MAXIMUM REACH OF JOURNAL CONTENT TO SCIENTISTS AND HEALTH CARE PROVIDERS WORLDWIDE. IN ADDITION TO SUPPORTING CUTTING-EDGE RESEARCH, ADR PROVIDES EXCELLENT RESOURCES ON DETECTING, TREATING, AND LIVING WITH THE DISEASE. THESE ARE AVAILABLE IN BOTH PRINT AS WELL AS ON OUR WEBSITE, WWW.BRIGHTFOCUS.ORG. |
| FORM 990, PART III, LINE 4B, DESCRIPTION OF PROGRAM SERVICE: | MACULAR DEGENERATION RESEARCH (MDR) - 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. AT LEAST 20 MILLION AMERICANS HAVE SOME TYPE OF MACULAR DEGENERATION, INCLUDING BOTH THE EARLY AND LATER STAGES OF THE WET AND DRY TYPES. MACULAR DEGENERATION RESEARCH (MDR ), A PROGRAM OF BRIGHTFOCUS, HAS AWARDED NEARLY $50 MILLION TO SCIENTISTS STUDYING THE DISEASE. THE LATEST RESEARCH IS FOCUSED ON NOVEL TREATMENTS FOR THE DISEASE, UNDERSTANDING ITS CAUSES AND PROGRESSION, PREDICTION METHODS AND DISEASE MODELING, DRUG THERAPIES, THE ROLE OF THE METABOLISM IN DISEASE RISK, GENES, THE ROLE OF THE IMMUNE RESPONSE IN DISEASE RISK, AND NEW IMAGING, MACHINE LEARNING AND SCREENING TECHNIQUES. MDR GRANTS ARE AVAILABLE TO MACULAR DEGENERATION RESEARCHERS WORLDWIDE. MDR 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, 2023, MDR AWARDED $3,839,035 IN PEER-REVIEWED GRANT AWARDS TO 13 NEW RESEARCH PROJECTS, WITH 5 ADDITIONAL PROJECTS THAT TAKE THE TOTAL FUNDING TO 18 GRANTS AT $4,039,275. DETAILS ABOUT SPECIFIC PROJECTS ARE INCLUDED IN SCHEDULES F & I. IN ADDITION TO SUPPORTING CUTTING-EDGE RESEARCH, MDR PROVIDES EXCELLENT RESOURCES ON DETECTING, TREATING, AND LIVING WITH THIS DISEASE. THESE ARE AVAILABLE IN BOTH PRINT AS WELL AS ON OUR WEBSITE, WWW.BRIGHTFOCUS.ORG |
| FORM 990, PART III, LINE 4C, DESCRIPTION OF PROGRAM SERVICE: | NATIONAL GLAUCOMA RESEARCH (NGR) - GLAUCOMA IS THE SECOND LEADING CAUSE OF BLINDNESS WORLDWIDE. ACCORDING TO A RECENT REPORT FROM THE WORLD HEALTH ORGANIZATION, APPROXIMATELY 80 MILLION PEOPLE AROUND THE WORLD HAVE GLAUCOMA. MORE THAN THREE MILLION AMERICANS OVER THE AGE OF 40 ARE LIVING WITH GLAUCOMA, WITH AN ESTIMATED 2.7 MILLION HAVE OPEN-ANGLE GLAUCOMA, THE MOST COMMON TYPE. IN THE UNITED STATES, GLAUCOMA IS A LEADING CAUSE OF BLINDNESS AMONG BLACK AND HISPANIC AMERICANS. WITH EARLY DETECTION AND TREATMENT, GLAUCOMA OFTEN CAN BE MANAGED TO PROTECT EYES FROM MORE SERIOUS VISION LOSS. IT IS ESTIMATED THAT ONLY HALF OF THE PEOPLE LIVING WITH GLAUCOMA ARE AWARE THAT THEY HAVE THE DISEASE. BRIGHTFOCUS' NGR PROGRAM HAS AWARDED MORE THAN $49 MILLION WORLDWIDE FOR THE STUDY OF GLAUCOMA. NGR-SUPPORTED RESEARCH HAS BEEN FOCUSED ON THE EYE-BRAIN CONNECTION, HOW PRESSURE BUILDUP IN THE EYE CAN AFFECT SYNAPTIC NERVE COMMUNICATIONS, NEUROPROTECTION, AND OPTIC NERVE REGENERATION, DISCOVERING GLAUCOMA RISK GENES, AI/DEEP LEARNING AND ADAPTIVE OPTICS, SLEEP DISTURBANCE AND RISK OF DEVELOPING GLAUCOMA, DEVELOPING EARLY GLAUCOMA SCREENING, AND PURSUING NOVEL GENETIC COUNSELING AND COMMUNICATION STRATEGIES, AMONGST OTHER INNOVATIVE PURSUITS. BRIGHTFOCUS' NATIONAL GLAUCOMA RESEARCH (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, 2023, NGR AWARDED $2,034,241 IN PEER-REVIEWED GRANT AWARDS FOR 11 NEW PROJECTS AND 2 OTHER AWARDS TO MAKE A TOTAL OF 13 GRANTS AT $2,526,791 IN FUNDING. DETAILS ABOUT SPECIFIC PROJECTS ARE INCLUDED IN SCHEDULES F & I. IN ADDITION TO SUPPORTING CUTTING-EDGE RESEARCH, BRIGHTFOCUS' NGR PROGRAM PROVIDES EXCELLENT RESOURCES ON DETECTING, TREATING, AND LIVING WITH THE DISEASE. THESE ARE AVAILABLE IN BOTH PRINT AS WELL AS ON OUR WEBSITE, WWW.BRIGHTFOCUS.ORG. |
| FORM 990, PART VI, SECTION B, LINE 11B | A DRAFT OF THE FEDERAL FORM 990 IS DISTRIBUTED TO THE AUDIT COMMITTEE FOR REVIEW PRIOR TO BEING SUBMITTED TO THE INTERNAL REVENUE SERVICE. THE DRAFT FEDERAL FORM 990 IS 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 IS DISTRIBUTED TO EACH MEMBER OF THE FULL BOARD OF DIRECTORS PRIOR TO BEING FILED WITH THE INTERNAL REVENUE SERVICE. THE DRAFT OR FINAL FEDERAL FORM 990 MAY BE DISTRIBUTED IN PERSON, BY REGULAR MAIL, E-MAIL, OR FAX. |
| FORM 990, PART VI, SECTION B, LINE 12C | BRIGHTFOCUS 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 TO COMPLETE A CONFLICT OF INTEREST DISCLOSURE STATEMENT ANNUALLY. EMPLOYEES MEET ANNUALLY WITH THE BRIGHTFOCUS' CHIEF COMPLIANCE OFFICER TO REVIEW THEIR CONFLICT OF INTEREST STATEMENTS, AND GIVE 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 PRESIDENT/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 15 | BRIGHTFOCUS' BOARD OF DIRECTORS HAS OVERALL AUTHORITY AND RESPONSIBILITY FOR APPROVING THE ANNUAL BUDGET WHICH INCLUDES SALARY AND BENEFITS FOR ALL EMPLOYEES AT EVERY LEVEL INCLUDING NON-DIRECTOR OFFICERS AND KEY EMPLOYEES. 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 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. 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 PRESIDENT/CEO'S COMPENSATION, THE PRESIDENT/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. THE PRESIDENT/CEO IS CHARGED WITH THE SETTING OF SALARIES OF ALL OTHER EMPLOYEES IN ACCORDANCE WITH A COMPENSATION STRUCTURE AND BUDGET APPROVED BY THE BOARD OF DIRECTORS. THE PRESIDENT/CEO AND HUMAN RESOURCES REVIEW EMPLOYEE COMPENSATION AND BENEFITS THAT INCLUDE KEY EMPLOYEES, BY PERIODICALLY ENGAGING AN OUTSIDE CONSULTANT TO CONDUCT COMPENSATION AND BENEFIT BENCHMARKING STUDIES THAT INCLUDE VARIOUS REGIONAL AND NATIONAL NON-PROFIT COMPENSATION REPORTS AND SURVEYS. COMPENSATION DELIBERATIONS AND DECISIONS INCLUDE THE REVIEW OF SELF AND SUPERVISORY EVALUATIONS OF EMPLOYEE PERFORMANCE COMPARED TO SET INDIVIDUAL AND ORGANIZATIONAL GOALS. |
| FORM 990, PART VI, SECTION C, LINE 19 | BRIGHTFOCUS MAKES ITS GOVERNING DOCUMENTS INCLUDING ITS ARTICLES OF INCORPORATION AND BYLAWS, THE FEDERAL FORM 1023, THE 501(C)(3) LETTER OF DETERMINATION FROM THE INTERNAL REVENUE SERVICE, 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, AUDITED FINANCIAL STATEMENTS, THE 501(C)(3) LETTER OF DETERMINATION FROM THE INTERNAL REVENUE SERVICE, AND FEDERAL FORM 990 ON OUR WEBSITE. |
| FORM 990, PART XI, LINE 9: | RECOVERIES OF PRIOR YEAR GRANTS 1,028,552. CHANGE IN PRESENT VALUE OF GRANTS 267,164. |
| SCHEDULE F, PART II, LINE 1, COLUMN D: | REGION: EUROPE (D) PURPOSE OF GRANT: ALZHEIMER'S DISEASE RESEARCH BY LUCIA CHAVEZ-GUTIERREZ, PHD, ENTITLED: (A2023005S) ELUCIDATING THE MECHANISMS OF ACTION OF GAMMA-SECRETASE MODULATORS (GSMS) TO FACILITATE STRUCTURE-BASED DESIGN OF NEXT-GENERATION THERAPEUTICS. INVESTIGATOR'S SUMMARY: ALZHEIMER'S DISEASE (AD) IS LINKED TO THE BUILD-UP OF LONGER, AGGREGATION-PRONE AMYLOID-BETA (A-BETA) PEPTIDES IN THE BRAIN. GAMMA-SECRETASE DYSREGULATION LEADING TO ENHANCED PRODUCTION OF LONGER A-BETAS CAUSES AD. GAMMA-SECRETASE MODULATORS PROMOTE THE PRODUCTION OF SHORTER A-BETAS, WHILE SPARING CRITICAL (GAMMA-SECRETASE) BIOLOGICAL ROLES. THESE MOLECULES ARE PROMISING AGENTS IN THE FIGHT AGAINST AD; HOWEVER, A LACK OF UNDERSTANDING OF THEIR MODES OF ACTION HAVE LIMITED THEIR DEVELOPMENT. HERE, WE WILL DEFINE THE MODE(S) OF ACTION OF GAMMA-SECRETASE MODULATORS AND FOSTER THERAPEUTIC DEVELOPMENT. GRANT AWARDED: $300,000, FLANDERS INSTITUTE FOR BIOTECHNOLOGY, (VIB), GENT, BELGIUM. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/A2023005S REGION: EUROPE (D) PURPOSE OF GRANT: ALZHEIMER'S DISEASE RESEARCH BY MARTA CASQUERO-VEIGA, PHD, ENTITLED: (A2023012F) DEVELOPMENT OF MULTIMODAL NEUROIMAGING BIOMARKERS OF THE PRO-COAGULANT STATE IN ALZHEIMER'S DISEASE (NIPAD). INVESTIGATOR'S SUMMARY: ALZHEIMER'S DISEASE (AD) PATHOPHYSIOLOGY INCLUDES AN EARLY HEMOSTATIC DYSREGULATION, INDUCING A PRO-THROMBOTIC MILIEU. CONSEQUENTLY, AD-PATIENTS' BRAINS SHOW INCREASED FIBRIN LEVELS AND DEGRADATION-RESISTANT CLOTS, WHICH CONTRIBUTES TO NEURONAL DEATH. THESE PROCESSES APPEAR EARLY IN AD'S COURSE, BUT NOT IN ALL PATIENTS. THIS STUDY AIMS TO DEVELOP NEW GENERATION PROBES TO VISUALIZE THE PRO-COAGULANT COMPONENTS ACCUMULATED IN THE AD BRAIN, BY IN VIVO NON-INVASIVE MULTIMODAL IMAGING. ULTIMATELY, OUTCOMES WILL ENABLE CLINICIANS TO PRESCRIBE A SUITABLE TREATMENT TO AMELIORATE AD'S PROGRESSION. GRANT AWARDED: $200,000, INSTITUTO DE INVESTIGACION SANITARIA - FUNDACION JIMENEZ DIAZ, MADRID, SPAIN. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/A2023012F REGION: EUROPE (D) PURPOSE OF GRANT: ALZHEIMER'S DISEASE RESEARCH BY QI WANG, PHD, ENTITLED: (A2023018F) RESTORING MITOCHONDRIAL HOMEOSTASIS AS A THERAPY OF ALZHEIMER'S DISEASE. INVESTIGATOR'S SUMMARY: DEFECTS IN MITOCHONDRIA PRECEDE THE ONSET OF DEMENTIA BY DECADES AND ARE INVOLVED IN MULTIPLE ASPECTS OF ALZHEIMER'S DISEASE (AD) PATHOGENESIS. I AIM TO TEST WHETHER ACTIVATING THE BENEFICIAL MITOCHONDRIAL STRESS RESPONSES WITH A COMPOUND NAMED 9-TB COULD IMPROVE AD PATHOLOGIES. I WILL INVESTIGATE 9-TB'S EFFECTS ON MITOCHONDRIAL FUNCTION, MAIN COGNITIVE AND BIOMEDICAL MANIFESTATIONS OF AD IN A MOUSE MODEL. I WILL USE ADVANCED MULTI-OMICS APPROACH TO FULLY REVEAL 9-TB'S MECHANISMS OF ACTION AND VALIDATE ITS MECHANISM USING IN VITRO, EX VIVO AND IN SILICO SYSTEMS, FULFILLING THE REQUIREMENTS FOR CLINICAL TRIALS. GRANT AWARDED: $200,000, SWISS FEDERAL INSTITUTE OF TECHNOLOGY LAUSANNE, SWITZERLAND. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/A2023018F REGION: MIDDLE EAST (D) PURPOSE OF GRANT: ALZHEIMER'S DISEASE RESEARCH BY ARIEL GILAD, PHD, ENTITLED: (A2023024S) BRAIN-WIDE NETWORK DYSFUNCTIONS IN ALZHEIMER'S DISEASE OF INDIVIDUAL MICE. INVESTIGATOR'S SUMMARY: A HALLMARK OF ALZHEIMER'S DISEASE (AD) IS ABNORMAL BRAIN-WIDE NETWORKS THAT DIFFER ACROSS AND WITHIN PATIENTS. HERE, WE AIM TO USE AN AD MOUSE MODEL TO RECORD BRAIN-WIDE NETWORKS IN MICE DURING AD-RELATED COGNITIVE TASKS. BY USING AN INDIVIDUAL APPROACH AND TRACK EACH MOUSE THROUGHOUT ITS LIFESPAN, WE BELIEVE THAT EACH MOUSE WILL DISPLAY BRAIN-WIDE DYSFUNCTION THAT IS MODULATED BASED ON AD PROGRESSION AND INDIVIDUAL TRAITS. WE AIM TO OUTLINE KEY BRAIN AREAS THAT MAY BE TARGETED IN INDIVIDUAL HUMAN PATIENTS USING DEEP-BRAIN STIMULATION, THUS INCREASING THE QUALITY OF LIFE FOR MILLIONS OF PEOPLE GRANT AWARDED: $300,000, HEBREW UNIVERSITY OF JERUSALEM, ISRAEL. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/A2023024S REGION: EUROPE (D) PURPOSE OF GRANT: ALZHEIMER'S DISEASE RESEARCH BY LOUISE VAN DER WEERD, PHD, ENTITLED: (A2023026S) IRON SPREADING PATTERNS IN ALZHEIMER'S DISEASE. INVESTIGATOR'S SUMMARY: WE KNOW THAT IRON ACCUMULATES IN THE BRAINS OF PATIENTS WITH ALZHEIMER'S DISEASE (AD). THIS PROCESS STRONGLY PREDICTS HOW FAST A PATIENT'S COGNITIVE FUNCTION WILL DECLINE. HOWEVER, WE DO NOT YET KNOW WHERE IN THE BRAIN THE ACCUMULATION STARTS, AND HOW THE ACCUMULATION SPREADS. THAT MAKES IT DIFFICULT TO DEVELOP MEASUREMENTS THAT CAN HELP TO PREDICT THE DISEASE COURSE FOR INDIVIDUAL PATIENTS. IN THIS PROJECT WE WILL DEVELOP AN ATLAS OF THE BRAIN THAT SHOWS HOW IRON ACCUMULATES AS AD PROGRESSES OVER TIME. WE DO THAT BY STUDYING HUNDREDS OF BRAIN DONORS WITH VARYING DEGREES OF AD. GRANT AWARDED: $299,354, LEIDEN UNIVERSITY MEDICAL CENTER, LEIDEN, NETHERLANDS. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/A2023024S REGION: EUROPE (D) PURPOSE OF GRANT: ALZHEIMER'S DISEASE RESEARCH CONFERENCE SUPPORT. GRANT AWARDED: $99,353, THE 2023 INTERNATIONAL CONFERENCE ON ALZHEIMER'S & PARKINSON'S DISEASES, GOTHENBURG, SWEDEN. REGION: EUROPE (D) PURPOSE OF GRANT: ALZHEIMER'S DISEASE RESEARCH TRAVEL GRANTS FOR CONFERENCE ATTENDANCE. GRANT AWARDED: $10,000, FINGERS BRAIN HEALTH INSTITUTE, STOCKHOLM, SWEDEN. REGION: EUROPE (D) PURPOSE OF GRANT: ALZHEIMER'S DISEASE RESEARCH BY DR. GAELLE CHETELAT ENTITLED: (CA2021013) SEX DIFFERENCES IN RISK PROFILES ACROSS THE ALZHEIMER'S DISEASE CONTINUUM. INVESTIGATOR'S SUMMARY: THIS PROJECT WILL AIM TO MODEL COGNITIVE RESILIENCE IN RODENTS BY COMBINING A RAT MODEL OF SUCCESSFUL AGING WITH A MODEL OF EARLY ALZHEIMER'S DISEASE (AD). THE HYPOTHESIS TESTS WHETHER THESE RATS ARE RESILIENT TO AD PATHOLOGY, RESULTING IN INTACT COGNITION COMPARED TO AD RATS. THE INVOLVEMENT OF THE SEROTONERGIC SYSTEM WILL BE EVALUATED TO DETERMINE POTENTIAL THERAPEUTIC TARGETS THAT MAY PROMOTE RESILIENCE TO AD. GRANT AWARDED: $25,000, FONDATION VAINCRE ALZHEIMER, PARIS, FRANCE. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/CA2021013 |
| SCHEDULE F, PART II, LINE 1, COLUMN D, CONTINUED: | REGION: EUROPE (D) PURPOSE OF GRANT: NATIONAL GLAUCOMA RESEARCH BY KAREN PEYNSHAERT, PHD, ENTITLED: (G2023002F) EXPLORING ICG-MEDIATED ILM PHOTODISRUPTION AS A TOOL TO BOOST RETINAL GANGLION CELL ENGRAFTMENT. INVESTIGATOR'S SUMMARY: THIS PROJECT EXPLORES AN INNOVATIVE BIOPHOTONIC APPROACH TO MANIPULATE THE INNER LIMITING MEMBRANE (ILM), A BARRIER WHICH GREATLY HINDERS THE RETINAL ENTRY OF DONOR RGCS FOLLOWING INTRAVITREAL INJECTION. BY CONTROLLED PERFORATION OF THE ILM, WE AIM TO ENHANCE THE MIGRATION OF RGCS INTO THE RETINA WHILE MAINTAINING ILM'S CUES NECESSARY FOR THEIR SUBSEQUENT DEVELOPMENT. GRANT AWARDED: $150,000, GHENT UNIVERSITY, GENT, BELGIUM. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/G2023002F REGION: NORTH AMERICA (D) PURPOSE OF GRANT: NATIONAL GLAUCOMA RESEARCH BY ADRIANA DI POLO, PHD, ENTITLED: (G2023005S) DISEASE-MODIFYING MITOCHONDRIAL UNCOUPLERS: A NEW THERAPEUTIC STRATEGY FOR GLAUCOMA. INVESTIGATOR'S SUMMARY: MITOCHONDRIAL DYSFUNCTION IS A KEY FEATURE OF NEURONAL DAMAGE IN GLAUCOMA. THIS PROPOSAL WILL TEST THE POTENTIAL OF MILD MITOCHONDRIA UNCOUPLERS AS DISEASE-MODIFYING AGENTS TO REDUCE OXIDATIVE STRESS, IMPROVE CALCIUM HOMEOSTASIS, AND PROMOTE REPAIR PATHWAYS. THE OUTCOME OF THIS STUDY WILL PROVIDE ROBUST PROOF-OF-PRINCIPLE DATA AND OPEN NEW OPPORTUNITIES FOR CLINICAL TESTING IN GLAUCOMA PATIENTS. GRANT AWARDED: $200,000, UNIVERSITY OF MONTREAL, CANADA. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/G2023005S REGION: EUROPE (D) PURPOSE OF GRANT: NATIONAL GLAUCOMA RESEARCH BY SILVIA MARINELLI, PHD, ENTITLED: (G2023006S) A NEW OPTIMIZED FORM OF NERVE GROWTH FACTOR: AN ANTI-INFLAMMATORY AND NEUROPROTECTIVE DRUG CANDIDATE FOR GLAUCOMA. INVESTIGATOR'S SUMMARY: WE DEVELOPED AN OPTIMIZED NERVE GROWTH FACTOR, PAINLESS NGF (NGFP), THAT HAS THE SAME NEUROPROTECTIVE PROPERTIES AS NATURAL NGF BUT LACKS ADVERSE EFFECTS, SUCH AS PAIN AND CELL DEATH SIGNALLING. NGFP, WITHOUT THE PITFALLS OF NATURAL NGF, IS A PROMISING THERAPEUTIC CANDIDATE FOR GLAUCOMA, ABLE TO RESCUE RGC DEGENERATION THROUGH A SYNERGISTIC ACTION OF NEUROPROTECTION AND INFLAMMATORY MODULATION GRANT AWARDED: $200,000, FONDAZIONE EBRI "RITA LEVI-MONTALCINI", ROME, ITALY. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/G2023006S REGION: EUROPE (D) PURPOSE OF GRANT: NATIONAL GLAUCOMA RESEARCH BY DARRYL OVERBY, PHD, ENTITLED: (G2023011S) MICROENVIRONMENTAL REGULATION OF BARRIER FUNCTION IN SCHLEMM'S CANAL ENDOTHELIAL CELLS. INVESTIGATOR'S SUMMARY: THE ONLY WAY TO TREAT GLAUCOMA IS TO REDUCE EYE PRESSURE, BUT THE FACTORS CONTROLLING EYE PRESSURE ARE NOT UNDERSTOOD. OUR LAB HAS SHOWN THAT EYE PRESSURE IS PARTLY REGULATED BY A LAYER OF SPECIALISED CELLS THAT CREATE A BARRIER AGAINST FLUID DRAINAGE FROM THE EYE. WE AIM TO RECREATE THIS CELLULAR BARRIER IN THE LAB, WHICH WILL OPEN NEW AVENUES FOR RESEARCH AND DEVELOPMENT TARGETING THIS BARRIER. GRANT AWARDED: $184,242, IMPERIAL COLLEGE OF SCIENCE, TECHNOLOGY AND MEDICINE, LONDON, UNITED KINGDOM. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/G2023011S REGION: EUROPE (D) PURPOSE OF GRANT: NATIONAL GLAUCOMA RESEARCH BY DARRYL OVERBY, PHD, ENTITLED: (CG2020003) DEVELOPING NEW DRUGS TO LOWER EYE PRESSURE IN GLAUCOMA. INVESTIGATOR'S SUMMARY: OUR RESEARCH HAS IDENTIFIED A PARTICULAR CELL TYPE (SCHLEMM'S CANAL CELLS) THAT REGULATE EYE PRESSURE BY CONTROLLING THE DRAINAGE OF AQUEOUS HUMOR FROM THE EYE. IN THIS PROJECT, WE WILL DEVELOP AND APPLY NOVEL SCREENING TECHNOLOGIES TO IDENTIFY NEW DRUGS TO LOWER EYE PRESSURE BY IMPROVING AQUEOUS HUMOR DRAINAGE ACROSS SCHLEMM'S CANAL CELLS. GRANT AWARDED: $97,975, IMPERIAL COLLEGE OF SCIENCE, TECHNOLOGY AND MEDICINE, LONDON, UNITED KINGDOM. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/CG2020003 REGION: EAST ASIA & PACIFIC (D) PURPOSE OF GRANT: MACULAR DEGENERATION RESEARCH BY MATTHEW RUTAR, PHD, ENTITLED: (M2023009N) INVESTIGATING THE ROLE OF NEUTROPHIL EXTRACELLULAR TRAPS IN NEOVASCULAR AMD. INVESTIGATOR'S SUMMARY: NEOVASCULAR AMD (NAMD) IS A MAJOR CAUSE OF BLINDNESS WITH FEW AVAILABLE TREATMENTS. OUR CENTRAL HYPOTHESIS IS THAT DYSREGULATION OF NEUTROPHIL EXTRACELLULAR TRAPS (NETS) PROMOTES INFLAMMATION AND DEGENERATION IN NAMD, THUS REPRESENTING A NOVEL TARGET FOR DIAGNOSTIC BIOMARKERS AND THERAPEUTIC INTERVENTIONS. WE DETERMINE A ROLE FOR NETS USING EXPERIMENTAL MODELS AND AMD DONOR TISSUE, AND EVALUATE THE POTENTIAL OF FIRST-GENERATION INHIBITORS OF NET ACTIVITY IN CURTAILING INFLAMMATION AND PATHOLOGY IN CNV. GRANT AWARDED: $334,938, UNIVERSITY OF CANBERRA, BRUCE, AUSTRALIA. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/M2023009N |
| SCHEDULE I, PART II, LINE 1, COLUMN (H): | NAME OF ORGANIZATION OR GOVERNMENT: MASSACHUSETTS GENERAL HOSPITAL. (H) PURPOSE OF GRANT: ALZHEIMER'S DISEASE RESEARCH BY ZAHRA SHIRZADI, PHD, ENTITLED: (A2023001F) NOVEL TOOLS TO DISSECT THE MULTI-FACTORIAL ETIOLOGIES OF WHITE MATTER INJURY IN AGING AND ALZHEIMER'S DISEASE. INVESTIGATOR'S SUMMARY: THE BRAIN'S WHITE MATTER IS COMPOSED OF MILLIONS OF BUNDLES OF NERVE FIBERS THAT CONNECT NEURONS IN DIFFERENT BRAIN REGIONS INTO FUNCTIONAL CIRCUITS. THEREFORE, ANY DAMAGE TO THESE FIBERS CAN AFFECT NORMAL BRAIN FUNCTION. IT IS VERY COMMON TO OBSERVE SIGNS OF WHITE MATTER INJURY IN BRAIN IMAGES OF PRECLINICAL AND SYMPTOMATIC ALZHEIMER'S DISEASE (AD) PATIENTS, YET IT IS UNCLEAR WHY THIS INJURY OCCURS. FOLLOWING UP ON OUR RECENT STUDIES IN FAMILIAL AD, WE WILL INVESTIGATE WHETHER AD MARKERS INCLUDING AMYLOID ACCUMULATION AND BRAIN TISSUE LOSS CAN DESCRIBE WHITE MATTER INJURY IN AD. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/A2023001F NAME OF ORGANIZATION OR GOVERNMENT: BAYLOR COLLEGE OF MEDICINE. (H) PURPOSE OF GRANT: ALZHEIMER'S DISEASE RESEARCH BY DAHEUN CHUNG, PHD, ENTITLED: (A2023002F) EXPLORING THE PROTECTIVE ROLE OF THE BIG TAU ISOFORM IN ALZHEIMER'S DISEASE. INVESTIGATOR'S SUMMARY: AS COGNITIVE DECLINE IS HIGHLY CORRELATED WITH THE SEVERITY OF TAU PATHOLOGY IN ALZHEIMER'S DISEASE, PROTECTING TAU FROM ABNORMAL CHANGES MAY BRING THERAPEUTIC BENEFITS. WHILE THERE IS NO EFFECTIVE TAU-TARGETING TREATMENT, I RECENTLY DISCOVERED THAT AN UNDERSTUDIED TAU ISOFORM, ABUNDANT IN THE BRAIN REGION SPARED FROM TAU PATHOLOGY, IS LESS LIKELY TO BECOME PATHOLOGICALLY ALTERED. AS SUCH, I PROPOSE TO EXAMINE IF THIS TAU ISOFORM IS CRUCIAL IN PREVENTING THE DEVELOPMENT OF TAU PATHOLOGY IN THE BRAIN, AND IF IT HAS ANY UNIQUE INTERACTING PROTEIN PARTNERS THAT FACILITATE SUCH A PHENOMENON. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/A2023002F NAME OF ORGANIZATION OR GOVERNMENT: NORTHWESTERN UNIVERSITY FEINBERG SCHOOL OF MEDICINE. (H) PURPOSE OF GRANT: ALZHEIMER'S DISEASE RESEARCH BY DAVID GATE, PHD, ENTITLED: (A2023003S) PROTEOGENOMICS TO STUDY ADAPTIVE IMMUNITY IN NEURODEGENERATIVE DISEASE. INVESTIGATOR'S SUMMARY: THIS PROPOSAL WILL UTILIZE A NOVEL PROTEOGENOMICS APPROACH TO EXPLORE THE ROLE OF ADAPTIVE IMMUNE T CELLS IN THE PATHOPHYSIOLOGY OF AGE-RELATED NEURODEGENERATION. THIS APPROACH AIMS TO IDENTIFY NEUROIMMUNOLOGIC DISEASE MECHANISMS AND THERAPEUTIC TARGETS FOR THESE DEVASTATING DISEASES. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/A2023003S NAME OF ORGANIZATION OR GOVERNMENT: JOHNS HOPKINS UNIVERSITY SCHOOL OF MEDICINE. (H) PURPOSE OF GRANT: ALZHEIMER'S DISEASE RESEARCH BY MEAGHAN MORRIS, MD, PHD, ENTITLED: (A2023004S) EXPLORING THE ORIGINS OF TAU PATHOLOGY IN HUMAN BRAIN: MOLECULAR SIGNATURES OF AGING AND NEURODEGENERATION IN THE LOCUS CERULEUS. INVESTIGATOR'S SUMMARY: THE SPREAD OF TAU PATHOLOGY IN ALZHEIMER'S DISEASE IS ASSOCIATED WITH PROGRESSIVE COGNITIVE DECLINE. HOWEVER, THE MOLECULAR EVENTS SURROUNDING THE EARLIEST FORMATION AND SPREAD OF TAU PATHOLOGY IN THE HUMAN BRAIN ARE LARGELY UNEXPLORED. THIS STUDY WILL EXAMINE THE MOLECULAR ENVIRONMENT ASSOCIATED WITH AGING AND EARLY ACCUMULATION OF TAU PATHOLOGY IN HUMAN BRAIN, AS WELL AS THE EARLIEST SPREAD OF TAU PATHOLOGY IN AGING AND ALZHEIMER'S DISEASE. INSIGHT INTO THIS EARLY TAU FORMATION COULD PROVIDE TARGETABLE PATHWAYS TO PREVENT THE FORMATION OR SPREAD OF TAU PATHOLOGY IN THE BRAIN. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/A2023004S NAME OF ORGANIZATION OR GOVERNMENT: CORNELL UNIVERSITY. (H) PURPOSE OF GRANT: ALZHEIMER'S DISEASE RESEARCH BY MATTHEW ISAACSON, PHD, ENTITLED: (A2023006F) IMAGING NEURAL ACTIVITY CHANGES UNDERLYING THE ACUTE RESCUE OF MEMORY FUNCTION AFTER IMPROVING CEREBRAL BLOOD FLOW IN ALZHEIMER'S DISEASE MOUSE MODELS. INVESTIGATOR'S SUMMARY: USING VISUAL AND SPATIAL BEHAVIORAL TASKS DURING FUNCTIONAL BRAIN IMAGING, WE WILL CHARACTERIZE LEARNING AND MEMORY DEFICITS AND THEIR NEURAL CORRELATES IN AN ALZHEIMER'S DISEASE MOUSE MODEL. WITH A PREVIOUSLY ESTABLISHED ACUTE TREATMENT TO IMPROVE BLOOD FLOW IN THE BRAIN THAT IMPROVES MEMORY, WE WILL GAIN NEW INSIGHT INTO HOW IMPROVED COGNITIVE ABILITY MANIFESTS IN NEURAL ACTIVITY CHANGES AND UNCOVER DISEASE-RELEVANT FAILURE MODES OF NEURAL CIRCUITRY THAT WILL INFORM HOW THESE CIRCUITS COULD BE THERAPEUTICALLY MANIPULATED TO RESTORE COGNITIVE ABILITY IN NEURODEGENERATIVE DISORDERS. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/A2023006F NAME OF ORGANIZATION OR GOVERNMENT: MASSACHUSETTS GENERAL HOSPITAL. (H) PURPOSE OF GRANT: ALZHEIMER'S DISEASE RESEARCH BY JOOST RIPHAGEN, MD, PHD, ENTITLED: (A2023007F) MEYNERT TO MAYHEM? THE TEMPORAL-SPATIAL EVOLUTION OF EARLY TAU PATHOLOGY IN ALZHEIMER'S DISEASE. INVESTIGATOR'S SUMMARY: FOR OPTIMAL TREATMENT OF ALZHEIMER'S DISEASE (AD) IT IS CRUCIAL TO IDENTIFY PEOPLE AT RISK OF AD EARLY, BEFORE IRREVERSIBLE BRAIN DAMAGE OCCURS. A SMALL REGION AT THE BOTTOM OF THE BRAIN (BASAL FOREBRAIN) IS ONE OF THE FIRST REGIONS TO ACCUMULATE MISFOLDED AD TAU PROTEINS AND IS CRITICAL FOR MEMORY FUNCTION. WE WILL USE ADVANCED BRAIN IMAGING METHODS (MRI AND PET) TO DETECT SUBTLE CHANGES IN THIS REGION AND PREDICT DISEASE PROGRESSION. FINDINGS FROM THIS STUDY HAVE THE POTENTIAL TO UNDERSTAND MECHANISMS OF DISEASE PROGRESSION AND MOVE DETECTION AND TREATMENT TO EARLIER STAGES OF THE DISEASE. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/A2023007F NAME OF ORGANIZATION OR GOVERNMENT: WEILL MEDICAL COLLEGE OF CORNELL UNIVERSITY. (H) PURPOSE OF GRANT: ALZHEIMER'S DISEASE RESEARCH BY TILL ZIMMER, PHD, ENTITLED: (A2023008F) MOLECULAR MECHANISMS AND EFFECTS OF ALZHEIMER'S-RELATED LIPID DYSREGULATION IN ASTROCYTES. INVESTIGATOR'S SUMMARY: THE BRAIN IS FULL OF FATS, ALSO CALLED LIPIDS, WHICH ARE DYSREGULATED IN ALZHEIMER'S DISEASE (AD). LIPID SUPPLY BY ASTROCYTES IS VITAL TO THE FUNCTION AND SURVIVAL OF NEURONS AND NEURONAL DEGENERATION IS THOUGHT TO CAUSE AD-RELATED SYMPTOMS. IMPROPER LIPID SUPPORT BY ASTROCYTES IN AD COULD CAUSE NEURONS TO BE DYSFUNCTIONAL OR DEGENERATE. TO BETTER UNDERSTAND THESE MECHANISMS, WE WILL STUDY HOW ALZHEIMER'S-ASSOCIATED DISEASE MECHANISMS LIKE NEUROINFLAMMATION AND ACCUMULATION OF A-BETA PROTEIN AFFECT LIPID METABOLISM IN ASTROCYTES AND HOW THESE ASTROCYTE LIPIDS ALTER NEURONAL FUNCTION. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/A2023008F NAME OF ORGANIZATION OR GOVERNMENT: UNIVERSITY OF SOUTH FLORIDA. (H) PURPOSE OF GRANT: ALZHEIMER'S DISEASE RESEARCH BY ARI SUDWARTS, PHD, ENTITLED: (A2023009F) IDENTIFYING THE INTERACTOME AND NON-AUTONOMOUS SIGNALLING OF RISK-GENE BIN1 IN AMYLOID-RESPONSIVE MICROGLIA. INVESTIGATOR'S SUMMARY: GENES EXPRESSED IN MICROGLIA - THE IMMUNE CELL OF THE BRAIN - HAVE COME TO LIGHT AS KEY RISK FACTORS FOR LATE-ONSET ALZHEIMER'S DISEASE (LOAD). THE BIN1 GENE CONTAINS THE SECOND-MOST COMMON RISK FOR LOAD, AND BIN1 IS INTEGRAL FOR MICROGLIAL RESPONSES TO INFLAMMATION AND DISEASE. MY PROJECT WILL IDENTIFY WHICH GENES BIN1 INTERACTS WITH IN MICROGLIA, PROVIDING CRUCIAL INSIGHT INTO BIN1 FUNCTION. ADDITIONALLY, I FOUND BIN1 IS INVOLVED IN MICROGLIA SIGNALLING TO OTHER CELLS. THIS WILL BE EXPLORED USING A COMBINATION OF CUTTING-EDGE TECHNOLOGIES TO IDENTIFY CELL RECIPIENTS OF MICROGLIAL SIGNALS. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/A2023009F NAME OF ORGANIZATION OR GOVERNMENT: UNIVERSITY OF CALIFORNIA, LOS ANGELES. (H) PURPOSE OF GRANT: ALZHEIMER'S DISEASE RESEARCH BY DAVID BOYER, PHD, ENTITLED: (A2023010F) ATOMIC STRUCTURE DETERMINATION OF A-BETA OLIGOMERS ASSOCIATED WITH ALZHEIMER'S DISEASE. INVESTIGATOR'S SUMMARY: THE FORMATION OF AMYLOID FIBRILS IN THE BRAINS OF PATIENTS IS THE DEFINING CHARACTERISTIC OF ALZHEIMER'S DISEASE AND RELATED DEMENTIA (ADRD). EXPERIMENTS DETAILING THE STRUCTURES OF AMYLOID FIBRILS HAVE GREATLY ADVANCED OUR UNDERSTANDING OF ADRD AND OFFER ROUTES TO THERAPEUTIC DEVELOPMENT; HOWEVER, WE ARE CURRENTLY HINDERED IN THE FIGHT TO CURE ADRD DUE TO THE LACK OF STRUCTURES OF INTERMEDIATES ON THE PATHWAY TO FIBRILS - TERMED AMYLOID OLIGOMERS. HERE I PROPOSE TO OBTAIN THE STRUCTURES OF AMYLOID OLIGOMERS USING CRYO-ELECTRON MICROSCOPY TO DEEPEN OUR KNOWLEDGE OF THE MOLECULAR BASIS OF ADRD. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/A2023010F |
| SCHEDULE I, PART II, LINE 1, COLUMN (H), CONTINUED: | NAME OF ORGANIZATION OR GOVERNMENT: MASSACHUSETTS GENERAL HOSPITAL. (H) PURPOSE OF GRANT: ALZHEIMER'S DISEASE RESEARCH BY JINGYUAN CHEN, PHD, ENTITLED: (A2023011S) WHOLE-BRAIN SLEEP-WAKE ENERGETICS IN SUBJECTS AT GENETIC RISK FOR ALZHEIMER'S DISEASE. INVESTIGATOR'S SUMMARY: RECENT RODENT STUDIES HAVE SUGGESTED THAT DISRUPTED SYNAPTIC ACTIVITY ACROSS SLEEP-WAKE CYCLES PLAYS AN IMPORTANT ROLE IN CAUSING ALZHEIMER'S DISEASE (AD). IN THIS PROPOSAL, WE WILL LEVERAGE CUTTING-EDGE HUMAN IMAGING TECHNIQUES TO TEST WHETHER SUCH ABNORMALITIES OF CYCLIC NEURONAL ACTIVITY ACROSS SLEEP-WAKE CYCLES CAN BE IDENTIFIED IN SUBJECTS AT GENETIC RISK FOR AD. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/A2023011S NAME OF ORGANIZATION OR GOVERNMENT: NORTHWESTERN UNIVERSITY FEINBERG SCHOOL OF MEDICINE. (H) PURPOSE OF GRANT: ALZHEIMER'S DISEASE RESEARCH BY ARUN UPADHYAY, PHD, ENTITLED: (A2023013F) STABLE ISOTOPE-BASED DATING OF THE AMYLOID FIBRIL PROTEOME. INVESTIGATOR'S SUMMARY: THE RECENT SUCCESS OF ANTIBODY-BASED THERAPEUTICS TARGETING VARIOUS FORMS OF A-BETA PEPTIDES HIGHLIGHTS THE IMPORTANCE OF AMYLOID FIBRILS IN AD PATHOLOGY. NOTABLY, FIBRIL DYNAMICS IS ONE OF THE MOST CRUCIAL FACTORS AFFECTING AMYLOID DEPOSITION DURING AD PROGRESSION. IN THIS APPLICATION, I PROPOSE TO (1) IDENTIFY PROTEINS ASSOCIATED WITH NEWLY FORMED AMYLOID FIBRILS IN THE BRAIN; (2) INVESTIGATE IF MANIPULATING THESE PROTEINS INFLUENCES THE ONSET OF AMYLOID PATHOLOGY. ULTIMATELY, THIS PROJECT WILL UNCOVER NEW ASPECTS OF AMYLOID KINETICS AND MAY PROVIDE NEW TARGETS FOR REDUCING AMYLOID PATHOLOGY. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/A2023013F NAME OF ORGANIZATION OR GOVERNMENT: WEILL MEDICAL COLLEGE OF CORNELL UNIVERSITY. (H) PURPOSE OF GRANT: ALZHEIMER'S DISEASE RESEARCH BY SUNG JI AHN, PHD, ENTITLED: (A2023014F) NEUROVASCULAR AND NEURONAL NETWORK DYSFUNCTION IN TAUOPATHY MOUSE MODELS. INVESTIGATOR'S SUMMARY: ALZHEIMER'S DISEASE (AD) IS THE LEADING CAUSES OF DEMENTIA, CURRENTLY UNTREATABLE. A MAJOR CULPRIT THAT DAMAGES THE BRAIN IN AD IS THE PROTEIN "TAU." TAU MOLECULES ARE NORMAL CONSTITUENTS OF BRAIN CELLS BUT WHEN CHEMICALLY ALTERED FORM CLUMPS THAT CLOG UP IN THE CELLS. WE SEEK TO FIND OUT IF TAU CLUMPS ARE DAMAGING BY STARVING THE BRAIN OF ITS BLOOD SUPPLY, WHICH CARRIES VITAL OXYGEN AND NUTRIENTS NECESSARY FOR NORMAL BRAIN FUNCTION AND SURVIVAL. WE WILL ALSO TEST IF PROVIDING EXTRA OXYGEN TO THE BRAIN CAN OVERCOME THE BRAIN DYSFUNCTION CAUSED BY TAU, WHICH COULD HAVE THERAPEUTIC IMPLICATIONS. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/A2023014F NAME OF ORGANIZATION OR GOVERNMENT: JOHNS HOPKINS UNIVERSITY SCHOOL OF MEDICINE. (H) PURPOSE OF GRANT: ALZHEIMER'S DISEASE RESEARCH BY ALYSSA COYNE, PHD, ENTITLED: (A2023015S) ESCRT-III NUCLEAR SURVEILLANCE IN CHMP2B FTD. INVESTIGATOR'S SUMMARY: MAINTENANCE OF THE PROTEIN COMPLEXES THAT CONTROL COMMUNICATION BETWEEN THE NUCLEAR AND CYTOPLASMIC COMPARTMENTS OF CELLS IS ESSENTIAL FOR PROPER NEURONAL FUNCTION AND SURVIVAL. RECENT WORK HAS DEMONSTRATED THAT DEFECTS IN A NUCLEAR SURVEILLANCE PATHWAY INITIATE DAMAGE TO THESE CELLULAR COMMUNICATION CHANNELS AS AN EARLY AND SIGNIFICANT EVENT IN LOU GEHRIG'S DISEASE. THIS PROPOSAL WILL EXAMINE THE CONTRIBUTION OF IMPAIRED NUCLEAR SURVEILLANCE AND NUCLEAR-CYTOPLASMIC COMPARTMENTALIZATION TO A GENETICALLY LINKED FORM OF DEMENTIA. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/A2023015S NAME OF ORGANIZATION OR GOVERNMENT: UNIVERSITY OF SOUTHERN CALIFORNIA. (H) PURPOSE OF GRANT: ALZHEIMER'S DISEASE RESEARCH BY PAUL SEIDLER, PHD, ENTITLED: (A2023016S) UNFOLDING ALZHEIMER'S TAU THERAPIES: APPROACHES FOR THE NEAR- AND LONG-TERM. INVESTIGATOR'S SUMMARY: BY NO MISTAKE, NATURAL PRODUCT CHEMICALS IN THE FORMS OF VITAMINS AND DIETARY SUPPLEMENTS HAVE LONG PLAYED A ROLE IN SUPPORTING HUMAN HEALTH. IN THE CONTEXT OF AGING, PLANT NATURAL PRODUCTS EVOLVED ALONGSIDE MICROBIAL PROTEINS THAT BEAR STRUCTURAL SIMILARITY TO PROTEINS FROM THE HUMAN BRAIN THAT BECOME TANGLED WITH AGE. WE LEVERAGE THESE REALIZED STRUCTURAL AND CHEMICAL SIMILARITIES TO DEVELOP DIETARY SUPPLEMENTS AND PHARMACEUTICAL-GRADE MEDICINES TO SUPPORT HEALTHIER AGING AND TO TREAT AD, RESPECTIVELY. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/A2023016S NAME OF ORGANIZATION OR GOVERNMENT: SHRINERS HOSPITALS FOR CHILDREN - NORTHERN CALIFORNIA. (H) PURPOSE OF GRANT: ALZHEIMER'S DISEASE RESEARCH BY OLGA CHECHNEVA, PHD, ENTITLED: (A2023017S) NUCLEAR MATERIAL TRANSFER IN PATHOGENIC PROTEIN SPREADING. INVESTIGATOR'S SUMMARY: SPREADING OF PATHOGENIC PROTEIN AGGREGATES IN NEURONS CAUSES PROGRESSION OF ALZHEIMER'S DISEASE AND MANY GENETIC AND AGE-RELATED NEUROLOGICAL DISORDERS. THIS PROJECT WILL INVESTIGATE A PREVIOUSLY UNRECOGNIZED POPULATION OF SOX-10 LINEAGE CELLS THAT TRANSFER NUCLEAR AND RIBOSOMAL MATERIAL TO NEURONS AND THEIR ROLE IN PATHOGENIC PROTEIN SPREADING. OUR RESEARCH WILL ADVANCE OUR UNDERSTANDING OF THE MECHANISMS UNDERLYING PATHOGENIC PROTEIN SPREADING WITH THE AIM TO DEVELOP NOVEL THERAPIES TO TREAT ALZHEIMER'S DISEASE AND OTHER DEVASTATING DISORDERS OF THE NERVOUS SYSTEM. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/A2023017S NAME OF ORGANIZATION OR GOVERNMENT: UNIVERSITY OF CALIFORNIA, SAN FRANCISCO. (H) PURPOSE OF GRANT: ALZHEIMER'S DISEASE RESEARCH BY HENRY PAN, PHD, ENTITLED: (A2023019F) FIDELITY OF TAU STRAIN TRANSMISSION: A FLUORESCENCE IN SITU AND CRYO-EM STRUCTURAL CHARACTERIZATION STUDY. INVESTIGATOR'S SUMMARY: ALZHEIMER'S DISEASE AND ALZHEIMER'S RELATED DISEASES (ADRD) ARE PROTEIN CONFORMATIONAL DISEASES, WHERE THE SAME PROTEIN SUCH AS TAU CAN TAKE ON A DIVERSE RANGE OF CONFORMATIONAL STRAINS EACH ONE ASSOCIATED WITH A DIFFERENT DISEASE. MODELING TAU STRAINS CORRECTLY IS IMPORTANT FOR MECHANISTIC BIOLOGICAL STUDIES AND PRECLINICAL DRUG DEVELOPMENT STUDIES. THIS PROPOSAL SEEKS TO DEVELOP METHODS THAT CAN RAPIDLY SCREEN FOR FIBRIL STRAINS IN CELL AND TRANSGENIC RODENT MODELS TO ISOLATE STRAINS OF INTEREST FROM HETEROGENEOUS SAMPLES FOR CRYO-EM STRUCTURAL CHARACTERIZATION. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/A2023019F NAME OF ORGANIZATION OR GOVERNMENT: UNIVERSITY OF KENTUCKY. (H) PURPOSE OF GRANT: ALZHEIMER'S DISEASE RESEARCH BY KATE FOLEY, PHD, ENTITLED: (A2023020F) DETERMINING THE MECHANISMS OF ANTI-A-BETA IMMUNOTHERAPY ON CEREBROVASCULAR DYSFUNCTION. INVESTIGATOR'S SUMMARY: WITH RECENT FDA APPROVAL OF ANTI-A-BETA IMMUNOTHERAPIES TO TREAT ALZHEIMER'S DISEASE, IT IS IMPERATIVE TO UNDERSTAND HOW TO MITIGATE THE CEREBROVASCULAR SIDE EFFECTS CAUSED BY THESE THERAPIES. THIS PROPOSAL WILL CHARACTERIZE THE CELLULAR RESPONSE TO ANTI-A-BETA ANTIBODY TREATMENT, AS WELL AS DETERMINE THE ROLE OF A VASCULAR DAMAGING PROTEIN, MMP9, IN PREVENTING THE CEREBROVASCULAR DEFICITS THAT RESULT FROM ANTI-A-BETA ANTIBODY THERAPY. THIS PROJECT WILL IDENTIFY TARGETABLE PATHWAYS TO HELP REDUCE CEREBROVASCULAR ADVERSE EVENTS ASSOCIATED WITH ANTI-A-BETA IMMUNOTHERAPIES. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/A2023020F NAME OF ORGANIZATION OR GOVERNMENT: MASSACHUSETTS GENERAL HOSPITAL. (H) PURPOSE OF GRANT: ALZHEIMER'S DISEASE RESEARCH BY MARIA VIRTUDES SANCHEZ MICO, PHD, ENTITLED: (A2023021F) IN VIVO IMAGING OF ASTROGLIAL DYSFUNCTION IN A MOUSE MODEL OF ALZHEIMER'S DISEASE. INVESTIGATOR'S SUMMARY: ASTROCYTES PLAY AN ESSENTIAL METABOLIC ROLE TO SUPPORT ENERGY REQUIREMENTS OF BRAIN CELLS. IMPAIRMENT OF ASTROGLIAL METABOLISM IS THOUGHT TO ACCELERATE NEURONAL DEGENERATION AND WORSEN ALZHEIMER'S DISEASE (AD). THUS, THERE IS AN URGENT NEED TO FULLY UNDERSTAND ASTROGLIAL METABOLIC DYSFUNCTION. HERE, WE WILL IMAGE THE ASTROGLIAL METABOLISM IN THE BRAINS OF LIVING AD MOUSE MODEL USING FLUORESCENT REPORTER MOLECULES AND MULTIPHOTON MICROSCOPY. THE OUTCOME OF OUR EXPERIMENTS WOULD FACILITATE THE DEVELOPMENT OF NEW THERAPEUTIC STRATEGIES TO PREVENT OR REVERSE THE PROGRESSION OF THIS DEVASTATING DISEASE FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/A2023021F |
| SCHEDULE I, PART II, LINE 1, COLUMN (H), CONTINUED: | NAME OF ORGANIZATION OR GOVERNMENT: YALE UNIVERSITY. (H) PURPOSE OF GRANT: ALZHEIMER'S DISEASE RESEARCH BY CARLA ROTHLIN, PHD, ENTITLED: (A2023022S) FUNCTIONAL UNDERSTANDING OF AXL EFFECTOR ROLE(S) IN MICROGLIA TOWARDS DEVELOPING DISEASE MODIFYING THERAPIES IN ALZHEIMER'S DISEASE. INVESTIGATOR'S SUMMARY: WE HAVE IDENTIFIED A PROTEIN EXPRESSED IN BRAIN IMMUNE CELLS THAT MAKES THESE CELLS BETTER AT PROTECTING AGAINST ALZHEIMER'S DISEASE (AD). HERE WE ENVISION TO UNDERSTAND EXACTLY HOW THIS PROTEIN FUNCTIONS BY ENGULFING AND REMOVING A-BETA PLAQUES OR BY DAMPENING INFLAMMATION TO PREVENT AD-ASSOCIATED NEUROINFLAMMATION. WE WILL ALSO BETTER UNDERSTAND THE SEQUENCE OF EVENTS LEADING TO THE IMPROVED ACTIVITY OF THIS PROTEIN THAT PROTECTS AGAINST COGNITIVE DECLINE. THIS KNOWLEDGE WILL ENABLE US TO DEVELOP THERAPEUTICS TO IMPROVE DISEASE OUTCOME IN AD. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/A2023022S NAME OF ORGANIZATION OR GOVERNMENT: UNIVERSITY OF CALIFORNIA, SAN DIEGO. (H) PURPOSE OF GRANT: ALZHEIMER'S DISEASE RESEARCH BY SUBHOJIT ROY, MD, PHD, ENTITLED: (A2023023S) THERAPEUTIC GENE-EDITING IN ALZHEIMER'S DISEASE. INVESTIGATOR'S SUMMARY: OUR OVERALL GOAL IS TO TAKE A CRISPR BASED GENE THERAPY FOR ALZHEIMER'S DISEASE (AD) TO THE CLINIC. BROADLY SPEAKING, OUR APPROACH RESTORES THE PHYSIOLOGIC BALANCE OF THE AMYLOID PATHWAY DECREASING NEUROTOXIC PROTEIN FRAGMENTS, WHILE PROMOTING NEUROPROTECTIVE PROTEIN FRAGMENTS. THERE ARE OVER 100 ONGOING CLINICAL TRIALS WORLDWIDE USING CRISPRS, AND THE RESULTS SO FAR WITH NON-NEUROLOGIC DISORDERS HAVE SHOWN UNPRECEDENTED (ALMOST 100%) EFFICACY. OUR BROAD VISION IS TO APPLY CRISPRS FOR DEVASTATING NEUROLOGIC ILLNESSES LIKE AD. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/A2023023S NAME OF ORGANIZATION OR GOVERNMENT: UNIVERSITY OF KENTUCKY. (H) PURPOSE OF GRANT: ALZHEIMER'S DISEASE RESEARCH BY DANIEL C. LEE, PHD, ENTITLED: (A2023025S) CITRULLINATED TAU AS A THERAPEUTIC TARGET IN TAUOPATHIES. INVESTIGATOR'S SUMMARY: ALZHEIMER'S DISEASE (AD) CONTINUES TO IMPACT NEURONAL HEALTH. TAU PATHOLOGY IS DIVERSE DESPITE BEING A SINGLE PROTEIN AND ALSO REMAINS THE CLOSET COROLLARY TO MEMORY LOSS AND NEURODEGENERATION. TAU DIVERSITY LIKELY COMES FROM DIFFERENT CELLULAR MODIFICATIONS ON THE TAU PROTEIN. WE DISCOVERED A NEW MODIFICATION ON TAU CALLED CITRULLINATION WHICH CHANGES THE AMINO ACID ARGININE TO A CITRULLINE. WE HYPOTHESIZE THAT CITRULLINATION TO TAU CAUSES MORE TOXICITY IN THE BRAIN. WE WILL TEST CITRULLINATION INHIBITORS AND VACCINES AGAINST CITRULLINATED TAU IN MICE THAT DEVELOP HALLMARKS OF AD. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/A2023025S NAME OF ORGANIZATION OR GOVERNMENT: MAYO CLINIC, JACKSONVILLE. (H) PURPOSE OF GRANT: ALZHEIMER'S DISEASE RESEARCH BY ENTITLED: (CA2021010) MOLECULAR NEURODEGENERATION JOURNAL. INVESTIGATOR'S SUMMARY: THE AIM OF MOLECULAR NEURODEGENERATION (MN) JOURNAL (HTTPS://MOLECULARNEURODEGENERATION.BIOMEDCENTRAL.COM/) IS TO SERVE THE SCIENTIFIC COMMUNITY BY PUBLISHING HIGH-IMPACT, HIGH-QUALITY, AND FRONT-LINE RESEARCH DISCOVERIES IN DIVERSE AREAS OF NEURODEGENERATIVE DISEASES INCLUDING ALZHEIMER'S DISEASE AND EYE-RELATED DEGENERATIVE CONDITIONS. MN IS THE OFFICIAL JOURNAL OF THE BRIGHTFOCUS FOUNDATION. ALL ARTICLES ARE FREE AND PERMANENTLY ACCESSIBLE ONLINE, WITHOUT SUBSCRIPTION CHARGES OR REGISTRATION BARRIERS. THE JOURNAL HAS SEEN FURTHER GROWTH IN RECENT YEARS IN PARTICULAR IN THE AREA OF SCIENTIFIC IMPACT AND REPUTATION. SOME OF THESE ARE REFLECTED IN THE FOLLOWING METRICS: 1) THE IMPACT FACTOR OF MOLECULAR NEURODEGENERATION, THE OFFICIAL SCIENTIFIC JOURNAL OF BRIGHTFOCUS FOUNDATION, HAS RISEN TO 18.879, ACCORDING TO ITS PUBLISHER, UP FROM 14.195 A YEAR AGO (33% INCREASE).; 2) IT IS NOW THE TOP-RANKED OPEN-ACCESS PUBLICATION IN ITS FIELD, ON PAR WITH OTHER HIGH-IMPACT JOURNALS INCLUDING NEURON, JOURNAL OF EXPERIMENTAL MEDICINE AND NATURE COMMUNICATIONS. A SCIENTIFIC JOURNAL'S IMPACT FACTOR IS DERIVED FROM HOW OFTEN ITS ARTICLES ARE CITED IN SCIENTIFIC LITERATURE DURING A PARTICULAR TIME PERIOD AND REFLECTS THE JOURNAL'S INFLUENCE IN SHAPING AND LEADING SCIENTIFIC PROGRESS. JOURNALS WITH HIGHER IMPACT FACTORS ARE CONSIDERED MORE PRESTIGIOUS AND HAVE HIGHER STANDARDS FOR PUBLICATION.; 3) THE JOURNALHAS BEEN RANKED AS THENUMBER ONE OPEN-ACCESS JOURNALIN THE NEUROSCIENCE CATEGORY FOR NINE YEARS IN A ROW (2013 PRESENT) AND IS RANKED NO. 7 AMONGALL274 NEUROSCIENCE JOURNALS. AMONG THE TOP 10, MOLECULAR NEURODEGENERATION IS THE ONLY OPEN-ACCESS JOURNAL. NAME OF ORGANIZATION OR GOVERNMENT: LUMIND IDSC. (H) PURPOSE OF GRANT: ALZHEIMER'S DISEASE RESEARCH ENTITLED: MODELING THE IMPACT OF RESEARCH INVESTMENT ON ALZHEIMER'S DISEASE IN DOWN SYNDROME: CAREGIVING AND SOCIETAL COSTS. NAME OF ORGANIZATION OR GOVERNMENT: INTERNATIONAL SOCIETY FOR MOLECULAR NEURODEGENERATION. (H) PURPOSE OF GRANT: ALZHEIMER'S DISEASE RESEARCH TRAVEL GRANTS FOR CONFERENCE ATTENDANCE. NAME OF ORGANIZATION OR GOVERNMENT: INTERNATIONAL SOCIETY FOR MOLECULAR NEURODEGENERATION. (H) PURPOSE OF GRANT: ALZHEIMER'S DISEASE RESEARCH BY ENTITLED: (CA2021011) MOLECULAR NEURODEGENERATION JOURNAL. INVESTIGATOR'S SUMMARY: THIS AWARD IS FOR THE CREATION, AND GROWTH OF, THE "INTERNATIONAL SOCIETY FOR MOLECULAR NEURODEGENERATION (ISMND) AND SUPPORT OF ITS BI-ANNUAL MEETINGS AND EDUCATIONAL AND SCIENTIFIC PURPOSES. IN ACCORDANCE WITH SECTION 501(C)(3) OF THE INTERNAL REVENUE CODE AND THE PROVISIONS OF THE FLORIDA NOT FOR PROFIT CORPORATION ACT. THE INTERNATIONAL SOCIETY FOR MOLECULAR NEURODEGENERATION (ISMND) SHALL BE ORGANIZED AND OPERATED PRIMARILY AND EXCLUSIVELY FOR EDUCATIONAL AND SCIENTIFIC PURPOSES. THE INTERNATIONAL SOCIETY FOR MOLECULAR NEURODEGENERATION'S MISSION IS TO SERVE AS AN ACCELERATOR FOR THE CONTINUOUS IMPROVEMENT OF BRAIN AND EYE HEALTH AND WELL-BEING BY CREATING A MULTIDISCIPLINARY GLOBAL PLATFORM FOR SCIENTISTS, PHYSICIANS, AND THE PUBLIC FROM DIFFERENT FACETS AND SCIENTIFIC DISCIPLINES TO MORE READILY CONNECT, SHARE AND COMMUNICATE SCIENTIFIC DISCOVERIES, AND DEVELOP CURES FOR NEURODEGENERATIVE DISEASES, IN THE HOPES OF A WORLD FREE OF BRAIN AND EYE DISEASES. NAME OF ORGANIZATION OR GOVERNMENT: UNIVERSITY OF CALIFORNIA, IRVINE. (H) PURPOSE OF GRANT: ALZHEIMER'S DISEASE RESEARCH TRAVEL GRANTS FOR CONFERENCE ATTENDANCE. NAME OF ORGANIZATION OR GOVERNMENT: FOUNDATION FOR THE NATIONAL INSTITUTES OF HEALTH. (H) PURPOSE OF GRANT: ALZHEIMER'S DISEASE RESEARCH BY SJOERD FINNEMA, PHD, ENTITLED: (CA2021012) SV2A PET AS A BIOMARKER OF SYNAPTIC DENSITY. INVESTIGATOR'S SUMMARY: THE FOUNDATION FOR THE NATIONAL INSTITUTES OF HEALTH (FNIH) BIOMARKERS CONSORTIUM (BC) HAS LAUNCHED A PROJECT THAT SIGNALS A PARADIGM SHIFT IN OUR METHODS TO IMAGE THE BRAIN. USING ADVANCES IN PET (POSITRON EMISSION TOPOGRAPHY) TECHNOLOGY, THE PROJECT WILL FOCUS ON MEASURING THE INTEGRITY OF SYNAPSESTINY GAPS THAT CONNECT NEURONS AND COMMUNICATE INFORMATION TO THE BRAIN. LOSS OF THESE SYNAPSE CONNECTIONS STRONGLY CORRELATES WITH COGNITIVE DECLINE IN ALZHEIMER'S DISEASE (AD). A NEW IMAGING TOOL TO TRACK THIS BIOLOGICAL INDICATOR OF DISEASE PROGRESSION AND OF PATIENT RESPONSE TO THERAPEUTIC INTERVENTIONS WOULD BE A CATALYST IN THE DEVELOPMENT OF CLINICALLY EFFECTIVE TREATMENTS FOR AD. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/CA2021012 |
| SCHEDULE I, PART II, LINE 1, COLUMN (H), CONTINUED: | NAME OF ORGANIZATION OR GOVERNMENT: UNIVERSITY OF COLORADO. (H) PURPOSE OF GRANT: ALZHEIMER'S DISEASE RESEARCH BY LOTTA GRANHOLM, PHD, ENTITLED: (CA2018010) INTERNATIONAL BRAIN BANK FOR DOWN SYNDROME-RELATED ALZHEIMER'S DISEASE. EMERGENCY RELIEF SUPPLEMENT DUE TO COVID-19. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/CA2018010 NAME OF ORGANIZATION OR GOVERNMENT: UNIVERSITY OF SOUTHERN CALIFORNIA. (H) PURPOSE OF GRANT: ALZHEIMER'S DISEASE RESEARCH BY JINKOOK LEE, PHD, ENTITLED: (CA2023001) EXPANDING AND ENHANCING LASI-DAD FOR BETTER UNDERSTANDING OF ALZHEIMER'S DISEASE AND DEMENTIA. INVESTIGATOR'S SUMMARY: THIS PROJECT WILL EXPAND AND ENHANCE THE ONGOING LONGITUDINAL AGING STUDY IN INDIA DIAGNOSTIC ASSESSMENT OF DEMENTIA (LASI-DAD) BY EXPLORING HOW DNA METHYLATION OF ALZHEIMER'S ASSOCIATED GENES IS ASSOCIATED WITH COGNITION AND DEMENTIA. IT WILL FURTHER VALIDATE PREVIOUS FINDINGS FROM THE LASI-DAD TO COMPARE THE ACCURACY OF FINDINGS WITH GOLD STANDARD MEASURES OF COGNITION AND BLOOD BIOMARKERS. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/CA2023001 NAME OF ORGANIZATION OR GOVERNMENT: UNIVERSITY OF CALIFORNIA, BERKELEY. (H) PURPOSE OF GRANT: NATIONAL GLAUCOMA RESEARCH BY SHUBHAM MAURYA, PHD, ENTITLED: (G2023001F) REGULATION OF MICROGLIAL PHENOTYPE BY NEUROPROTECTIVE LXB4 IN OCULAR HYPERTENSION-INDUCED NEUROPATHY. INVESTIGATOR'S SUMMARY: WE HAD IDENTIFIED A NOVEL WAY TO STOP THE DEATH OF RETINAL CELLS IN MICE GLAUCOMATOUS EYES USING SMALL MOLECULE LIPID MEDIATORS. THESE LIPID MEDIATORS HAVE BIOACTIONS IN MODULATING THE FUNCTIONS OF A RESIDENT IMMUNE CELL TYPE IN THE RETINA, I.E., MICROGLIA. THIS PROJECT INTENDS TO STUDY THE REGULATION OF MICROGLIA BY LIPIDS MEDIATORS DURING GLAUCOMA PROGRESSION TO STOP OR PREVENT THE DISEASE. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/G2023001F NAME OF ORGANIZATION OR GOVERNMENT: UNIVERSITY OF WISCONSIN-MADISON. (H) PURPOSE OF GRANT: NATIONAL GLAUCOMA RESEARCH BY KAZUYA OIKAWA, PHD, BVSC, ENTITLED: (G2023003F) MODULATION OF NEUROINFLAMMATION IN GLAUCOMA BY GLP-1R AGONIST. INVESTIGATOR'S SUMMARY: INFLAMMATION OF THE NERVOUS SYSTEM TISSUE CONTRIBUTES TO BLINDING LOSS OF NERVE CELLS IN THE EYE AND BRAIN IN GLAUCOMA. IN THIS PROJECT, WE AIM TO REPURPOSE AN EXISTING FDA-APPROVED DRUG TO MODIFY THIS INFLAMMATORY RESPONSE WITH THE GOAL OF IDENTIFYING A POTENTIAL NEW THERAPY TO HELP PRESERVE VISION IN PATIENTS WITH GLAUCOMA. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/G2023003F NAME OF ORGANIZATION OR GOVERNMENT: UNIVERSITY OF CALIFORNIA, BERKELEY. (H) PURPOSE OF GRANT: NATIONAL GLAUCOMA RESEARCH BY KARTHIK SHEKHAR, PHD, ENTITLED: (G2023004S) A SPATIAL TRANSCRIPTOMICS APPROACH TO IDENTIFY MOLECULAR CHANGES AND MULTICELLULAR INTERACTIONS UNDERLYING RETINAL NEURODEGENERATION IN GLAUCOMA. INVESTIGATOR'S SUMMARY: TO IDENTIFY NOVEL MOLECULAR TARGETS THAT CAN SLOW DOWN RELENTLESS RETINAL GANGLION CELL (RGC) DEATH IN GLAUCOMA, WE NEED TO UNDERSTAND MOLECULAR PATHWAYS AND MULTI-CELLULAR INTERACTIONS THAT UNDERLIE RGC SUSCEPTIBILITY. WE WILL COMBINE INNOVATIVE SPATIAL PROFILING TECHNOLOGIES, MOUSE MODELS, AND MACHINE LEARNING TO UNDERSTAND RGC DEGENERATION AND THE ROLE OF THE MICROENVIRONMENT IN GLAUCOMA. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/G2023004S NAME OF ORGANIZATION OR GOVERNMENT: GEORGIA TECH RESEARCH CORPORATION. (H) PURPOSE OF GRANT: NATIONAL GLAUCOMA RESEARCH BY MARK PRAUSNITZ, PHD, ENTITLED: (G2023007S) NON-DRUG, NON-SURGICAL HYDROGEL-BASED TREATMENT OF GLAUCOMA. INVESTIGATOR'S SUMMARY: REDUCING INTRAOCULAR PRESSURE (IOP) IS THE ONLY GLAUCOMA TREATMENT, BUT IS OFTEN INEFFECTIVE DUE TO POOR PATIENT COMPLIANCE AND SURGICAL COMPLICATIONS. WE DEVELOPED A NON-DRUG, NON-SURGICAL METHOD TO LOWER IOP BY INJECTING A HYDROGEL TO EXPAND THE SUPRACHOROIDAL SPACE OF THE EYE. HERE WE OPTIMIZE THE HYDROGEL TO PROLONG IOP LOWERING, EVALUATE ITS SAFETY AND EFFICACY AND STUDY MECHANISMS OF ACTION. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/G2023007S NAME OF ORGANIZATION OR GOVERNMENT: DUKE UNIVERSITY SCHOOL OF MEDICINE. (H) PURPOSE OF GRANT: NATIONAL GLAUCOMA RESEARCH BY RUPALATHA MADDALA, PHD, ENTITLED: (G2023008S) ROLE OF SEPTIN CYTOSKELETON IN TRABECULAR MESHWORK, IOP AND GLAUCOMA. INVESTIGATOR'S SUMMARY: STUDIES DESCRIBED IN THIS PROPOSAL ARE FOCUSED ON INVESTIGATING THE ROLE OF SEPTINS WHICH ARE IDENTIFIED AS THE RISK LOCI FOR OCULAR HYPERTENSION AND GLAUCOMA IN THE HOMEOSTASIS OF AQUEOUS HUMOR OUTFLOW AND INTRAOCULAR PRESSURE. AS WE LACK AN UNDERSTANDING OF HOW SEPTINS MAY INFLUENCE OCULAR PRESSURE, COMPLETION OF THE STUDIES PLANED IN THIS APPLICATION ARE EXPECTED TO SHED LIGHT ON THIS QUESTION. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/G2023008S NAME OF ORGANIZATION OR GOVERNMENT: INDIANA UNIVERSITY, INDIANAPOLIS. (H) PURPOSE OF GRANT: NATIONAL GLAUCOMA RESEARCH BY WEIMING MAO, PHD, ENTITLED: (G2023009S) A NOVEL MOUSE ANTERIOR SEGMENT PERFUSION CULTURE MODEL FOR MEASURING OUTFLOW FACILITY AND LONG-TERM PERFUSION CULTURE. INVESTIGATOR'S SUMMARY: GLAUCOMA IS A LEADING CAUSE OF BLINDNESS. THE MOST IMPORTANT RISK FACTOR OF GLAUCOMA IS HIGH PRESSURE INSIDE THE EYE. THIS PRESSURE ELEVATION IS DUE TO HIGH DRAINAGE RESISTANCE OF THE FLUID THAT FILLS THE EYE. TO BETTER UNDERSTAND THIS PRESSURE ELEVATION, LAB MICE HAVE BEEN WIDELY USED AS A RESEARCH MODEL. WE WILL DEVELOP A NOVEL METHOD TO MEASURE THIS DRAINAGE RESISTANCE IN MOUSE EYES. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/G2023009S NAME OF ORGANIZATION OR GOVERNMENT: JOHNS HOPKINS UNIVERSITY SCHOOL OF MEDICINE. (H) PURPOSE OF GRANT: NATIONAL GLAUCOMA RESEARCH BY JITHIN YOHANNAN, MD, ENTITLED: (G2023010S) DEVELOPING DEEP LEARNING APPROACHES TO REDUCE THE BURDEN OF GLAUCOMA CLINICAL TRIALS. INVESTIGATOR'S SUMMARY: CLINICAL TRIALS OF NEW GLAUCOMA DRUGS (NEUROPROTECTIVE AGENTS) ARE DIFFICULT BECAUSE THE WORSENING OF GLAUCOMA MUST BE TRACKED WITH VISUAL FIELD TESTING, WHICH IS VARIABLE AND ONEROUS. IN THIS PROPOSAL, WE DEVELOP AI MODELS THAT WILL REDUCE TRIAL TIME, COST, AND BURDEN BY 1) IDENTIFYING THE BEST CANDIDATES TO ENROLL IN TRIALS AND 2) USING DATA BEYOND THE VISUAL FIELD TO DETECT WORSENING. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/G2023010S |
| SCHEDULE I, PART II, LINE 1, COLUMN (H), CONTINUED: | NAME OF ORGANIZATION OR GOVERNMENT: INTERNATIONAL SOCIETY FOR EYE RESEARCH. (H) PURPOSE OF GRANT: NATIONAL GLAUCOMA RESEARCH TRAVEL GRANTS FOR CONFERENCE ATTENDANCE. NAME OF ORGANIZATION OR GOVERNMENT: GEORGIA INSTITUTE OF TECHNOLOGY. (H) PURPOSE OF GRANT: NATIONAL GLAUCOMA RESEARCH BY C. ROSS ETHIER, PHD, ENTITLED: (CG2020001) SELECTIVE TARGETING OF SCHLEMM'S CANAL INNER WALL FOR NEXT-GENERATION GLAUCOMA DRUGS: SUBPART A. INVESTIGATOR'S SUMMARY: ALL TREATMENTS FOR GLAUCOMA SEEK TO LOWER INTRAOCULAR PRESSURE (IOP), YET EXISTING APPROACHES ARE INSUFFICIENT. WE NOW UNDERSTAND THAT ENDOTHELIAL CELL OF THE INNER WALL OF SCHLEMM'S CANAL (SC) PLAY A KEY ROLE IN HOMEOSTATIC CONTROL MECHANISMS THAT MAINTAIN IOP WITHIN A TARGET RANGE. HOWEVER, TOOLS FOR DIRECTLY ASSESSING SC INNER WALL ENDOTHELIAL FUNCTION ARE LACKING, AS ARE MOLECULAR APPROACHES FOR DIRECTLY TARGETING AND INTERROGATING THESE CELLS. THE LONG-TERM GOAL OF THIS INTER-DEPENDENT, MULTIPLE PRINCIPAL INVESTIGATOR AND GRANTEE INSTITUTION-ASSOCIATED PROJECT IS TO DEVELOP NOVEL THERAPIES THAT DIRECTLY TARGET SC CELLS TO IMPROVE IOP CONTROL. THESE TARGETED THERAPIES WILL BE HIGHLY EFFECTIVE DUE THEIR SPECIFICITY, AND WILL THUS GREATLY BENEFIT GLAUCOMA PATIENTS. TO ACCOMPLISH THIS GOAL, WE HAVE ASSEMBLED AN OUTSTANDING TEAM THAT BRINGS TOGETHER ALL NECESSARY EXPERTISE TO INTERVENE IN THIS COMPLEX SYSTEM. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/CG2020001 NAME OF ORGANIZATION OR GOVERNMENT: DUKE UNIVERSITY. (H) PURPOSE OF GRANT: NATIONAL GLAUCOMA RESEARCH BY W. DANIEL STAMER, PHD, ENTITLED: (CG2020002) SELECTIVE TARGETING OF SCHLEMM'S CANAL INNER WALL FOR NEXT-GENERATION GLAUCOMA DRUGS: SUBPART B. INVESTIGATOR'S SUMMARY: FOR THE PROJECT, WE WILL SCREEN CANDIDATE ADENO ASSOCIATED VIRUSES AND ENGINEERED PROMOTERS CLONED INTO LENTIVIRUSES OBTAINED FROM COLLABORATORS IN HUMAN SCHLEMM'S CANAL CELLS IN VITRO AND ANTERIOR SEGMENTS EX VIVO FOR SELECTIVE TROPISM TO/ACTIVITY IN TRABECULAR MESHWORK VERSUS SCHLEMM'S CANAL. WE WILL UTILIZE RECENTLY VALIDATED VIRUS TECHNOLOGY (ENOS PROMOTERS DRIVING XFP OR SEAP REPORTER PROTEINS) TO TRANSDUCE SCHLEMM'S CANAL IN HUMAN ANTERIOR SEGMENTS AND MONITOR SHEAR STRESS LEVELS AND LOCATION THROUGHOUT SCHLEMM'S CANAL. WE WILL PROVIDE A STEADY SUPPLY OF SCHLEMM'S CANAL CELLS FOR DEVELOPMENT AND TESTING OF DRUG SCREENING PLATFORMS. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/CG2020002 NAME OF ORGANIZATION OR GOVERNMENT: COLUMBIA UNIVERSITY. (H) PURPOSE OF GRANT: NATIONAL GLAUCOMA RESEARCH BY SIMON JOHN, PHD, ENTITLED: (CG2020004) SELECTIVE TARGETING OF SCHLEMM'S CANAL INNER WALL FOR NEXT-GENERATION GLAUCOMA DRUGS: SUBPART D. INVESTIGATOR'S SUMMARY: THE PROJECT AIMS TO DEVELOP AND TEST RESOURCES FOR SCHLEMM'S CANAL SPECIFIC TARGETING AND EXPRESSION OF GENES FOR GENE THERAPY. SUCCESSFUL DEVELOPMENT OF THIS TARGETED THERAPY WILL HELP CONTROL EYE PRESSURE MORE EFFECTIVELY AND PROVIDE BETTER TREATMENT OPTIONS FOR GLAUCOMA PATIENTS. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/CG2020004 NAME OF ORGANIZATION OR GOVERNMENT: STANFORD UNIVERSITY. (H) PURPOSE OF GRANT: NATIONAL GLAUCOMA RESEARCH BY JEFFREY GOLDBERG, PHD, ENTITLED: (CG2022001) A RANDOMIZED, SHAM CONTROLLED, MASKED PHASE II STUDY TO EVALUATE THE SAFETY AND EFFICACY OF DUAL INTRAVITREAL IMPLANTATION OF NEUROPROTECTIVE CELL THERAPY FOR THE TREATMENT OF GLAUCOMA. INVESTIGATOR'S SUMMARY: THE PROPOSED PROJECT IS AN EXTENSION OF THE CURRENT PHASE 2 CLINICAL TRIAL, TO ASSESS AND VALIDATE THE USE OF DUAL NT-501 CNTF ENCAPSULATED CELL THERAPY (ECT) ON VISUAL IMPAIRMENT RELATED TO GLAUCOMA, IN HUMAN SUBJECTS. THE PROPOSED STUDY IS DESIGNED TO EXPAND OUR KNOWLEDGE OF THE DOSE-DEPENDENT EFFECT OF CNTF IN GLAUCOMA THROUGH DUAL IMPLANTATION OF NT-501 ECT. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/CG2022001 NAME OF ORGANIZATION OR GOVERNMENT: THE JACKSON LABORATORY. (H) PURPOSE OF GRANT: MACULAR DEGENERATION RESEARCH BY NAVDEEP GOGNA, PHD, ENTITLED: (M2023001F) MITOCHONDRIAL DYSFUNCTION AS A KEY MEDIATOR OF AMD-LIKE PHENOTYPES IN HUMANIZED ARMS2A69S MICE. INVESTIGATOR'S SUMMARY: VARIATIONS IN THE PRIMATE SPECIFIC GENE ARMS2 ARE IMPLICATED IN AGE-RELATED MACULAR DEGENERATION (AMD). HOWEVER, THE MECHANISMS BY WHICH ARMS2 INCREASES AMD RISK ARE NOT KNOWN. THE NISHINA LAB HAS DEVELOPED NEW HUMANIZED MOUSE MODELS TO STUDY THE ROLE OF ARMS2 IN AMD. PRELIMINARY RESULTS SUGGEST EARLY CHANGES IN MITOCHONDRIAL GENES, ALTERED LIPID METABOLISM AND AGE-ASSOCIATED AMD-LIKE PHENOTYPES IN THE MODEL. THIS STUDY WILL IDENTIFY ALTERATIONS IN MITOCHONDRIA AND LIPID METABOLISM DUE TO ARMS2A69S RISK VARIANT, IN AMD DEVELOPMENT, THAT COULD BE TARGETED FOR THERAPEUTIC BENEFIT. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/M2023001F NAME OF ORGANIZATION OR GOVERNMENT: UNIVERSITY OF PENNSYLVANIA. (H) PURPOSE OF GRANT: MACULAR DEGENERATION RESEARCH BY CATHARINA GRUBAUGH, PHD, ENTITLED: (M2023002F) MICROSOMAL TRANSFER PROTEIN IN RETINAL LIPID HOMEOSTASIS, IMPLICATIONS FOR AMD. INVESTIGATOR'S SUMMARY: RECENT RESEARCH HAS INCREASINGLY LINKED AGE-RELATED MACULAR DEGENERATION (AMD) TO LIPID DYSREGULATION IN THE EYE. ONE OF THE MOST IMPORTANT ROLES OF THE RETINAL PIGMENT EPITHELIUM (RPE) IS THE PROCESSING AND TRANSPORT OF LIPIDS. MICROSOMAL TRIGLYCERIDE TRANSFER PROTEIN (MTP), ENCODED BY THE MTTP GENE, REGULATES LIPID PACKAGING IN THE RPE. WE HAVE GENERATED THE RPEDELMTTP MOUSE, IN WHICH MTTP IS KNOCKED OUT IN THE RPE BUT EXPRESSED NORMALLY IN OTHER TISSUES. WE WILL TEST THE HYPOTHESIS THAT MTP-MEDIATED LIPID PACKAGING IN THE RPE IS NECESSARY TO MAINTAIN RETINAL HEALTH AND VISUAL FUNCTION. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/M2023002F NAME OF ORGANIZATION OR GOVERNMENT: UNIVERSITY OF CALIFORNIA, SAN DIEGO. (H) PURPOSE OF GRANT: MACULAR DEGENERATION RESEARCH BY JACLYN SWAN, PHD, ENTITLED: (M2023003F) THE GLYCANS OF THE HUMAN RETINA AND THEIR INTERACTION WITH COMPLEMENT FACTOR H. INVESTIGATOR'S SUMMARY: ALL CELLS IN THE HUMAN BODY ARE COVERED IN A COMPLEX SUGAR COAT, THE GLYCOCALYX. THIS MOLECULAR COAT IS CRUCIAL FOR CELL-TO-CELL COMMUNICATION AND IMMUNE SURVEILLANCE. AN UNDERLYING MECHANISM OF AGE-RELATED MACULAR DEGENERATION (AMD) IS THE DYSREGULATION OF THE INNATE IMMUNE SYSTEM. THE GLYCOCALYX IS INVOLVED IN REGULATING THESE SYSTEMS. CURRENTLY, WE DON'T KNOW THE PRECISE COMPOSITION OF THE SUGAR COATS ON CELLS IN THE EYE AT THE SITE WHERE AMD OCCURS. WE WILL CHARACTERIZE THE GLYCOCALYX OF DISEASED AND HEALTHY EYES TO TEST WHETHER DIFFERENCES CONTRIBUTE TO IMMUNOLOGICAL CONSEQUENCES. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/M2023003F |
| SCHEDULE I, PART II, LINE 1, COLUMN (H), CONTINUED: | NAME OF ORGANIZATION OR GOVERNMENT: UNIVERSITY OF WASHINGTON. (H) PURPOSE OF GRANT: MACULAR DEGENERATION RESEARCH BY RAYNE LIM, PHD, ENTITLED: (M2023004F) FACTOR H-LIKE PROTEIN 1 INSUFFICIENCY IN RETINAL PIGMENT EPITHELIUM. INVESTIGATOR'S SUMMARY: EARLY ONSET MACULAR DRUSEN (EOMD) IS AN INHERITED, SEVERE FORM OF AGE-RELATED MACULAR DEGENERATION (AMD). WE FOUND THAT RETINAL PIGMENTED EPITHELIUM (RPE) CELLS MADE FROM EOMD PATIENTS HAVE DECREASED (ABOUT 50%) EXPRESSION OF TWO IMPORTANT COMPLEMENT PROTEINS, CFH AND FHL-1. THIS SIGNIFICANT DECREASE MAY ALTER LOCAL COMPLEMENT ACTIVITY AND RPE METABOLISM. WE WILL STUDY EOMD PATIENT RPE, THEIR GENE-EDITED CONTROLS, AND DETERMINE WHETHER ADDING THE FHL-1 GENE BACK TO THE EOMD CELLS WILL HELP ATTENUATE THESE PATHOGENIC CHANGES. THIS PROJECT WILL HELP OUR UNDERSTANDING OF AMD DISEASE PATHOGENESIS AND TREATMENT. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/M2023004F NAME OF ORGANIZATION OR GOVERNMENT: UNIVERSITY OF CALIFORNIA, SAN FRANCISCO. (H) PURPOSE OF GRANT: MACULAR DEGENERATION RESEARCH BY SANGEETHA KANDOI, PHD, ENTITLED: (M2023005F) PHOTORECEPTOR REMODELING IN THE HIBERNATING CONE-DOMINANT 13-LINED GROUND SQUIRREL AS A MODEL FOR MACULAR DEGENERATION IN HUMANS. INVESTIGATOR'S SUMMARY: THE CONE PHOTORECEPTORS EXCLUSIVELY POPULATE THE SMALL CENTRAL REGION WITHIN THE HUMAN RETINA AND PROVIDE HIGH ACUITY, AND COLOR VISION. THE LOSS OF CONES IS AN ENDPOINT OF AGE-RELATED MACULAR DEGENERATION (AMD), THE LEADING CAUSE OF BLINDNESS IN INDIVIDUALS >50 YEARS OLD. OUR STUDY UTILIZES 13-LINED GROUND SQUIRREL (13-LGS), WHICH HAS 85% CONES OVERALL AND HIBERNATES IN WINTER. THE ABUNDANCE OF CONES, AND EVOLVED PROTECTION AGAINST HIBERNATION STRESS ON CONES SUGGEST THAT THE 13-LGS COULD BE A CLINICALLY RELEVANT MODEL FOR EXPLORING INNOVATIVE THERAPIES FOR CATASTROPHIC VISION LOSS IN AMD. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/M2023005F NAME OF ORGANIZATION OR GOVERNMENT: WASHINGTON UNIVERSITY IN ST. LOUIS. (H) PURPOSE OF GRANT: MACULAR DEGENERATION RESEARCH BY JAMES WALSH, MD, PHD, ENTITLED: (M2023006F) DYSREGULATED CHOROIDAL ADAPTIVE IMMUNITY EXACERBATES MACULAR DEGENERATION PATHOLOGY. INVESTIGATOR'S SUMMARY: MACULAR DEGENERATION IS ONE OF THE LEADING CAUSES OF BLINDNESS IN THE US, YET THE EXACT DISEASE PROCESS THAT LEADS TO THE FINDINGS OF THIS DISEASE ARE NOT KNOWN. THERE HAVE BEEN CONSISTENT STUDIES THAT SHOW THAT THE ADAPTIVE IMMUNE SYSTEM IS ALTERED SYSTEMICALLY, BUT BECAUSE THE EYE HAS A REPUTATION FOR BEING IMMUNE PRIVILEGED, THE ROLE OF THE LOCAL ADAPTIVE IMMUNE SYSTEM IN THIS PROCESS HAS NOT BEEN EXPLORED. WE RECENTLY DISCOVERED THAT THERE IS A RICH ADAPTIVE LYMPHOID ENVIRONMENT IN THE CHOROID THAT COULD CONTRIBUTE TO THE DISEASE PROCESS, AND WILL EXPLORE THIS FURTHER IN THIS PROPOSAL. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/M2023006F NAME OF ORGANIZATION OR GOVERNMENT: THE UNIVERSITY OF IOWA. (H) PURPOSE OF GRANT: MACULAR DEGENERATION RESEARCH BY NARENDRA PANDALA, PHD, ENTITLED: (M2023007F) AUTOLOGOUS CHOROIDAL ENDOTHELIAL CELL REPLACEMENT FOR THE TREATMENT OF AMD. INVESTIGATOR'S SUMMARY: AGE RELATED MACULAR DEGENERATION IS A LEADING CAUSE OF BLINDNESS IN THE U.S. IN THE DRY FORM OF THE DISEASE, THE MACULA, WHICH IS THE CENTRAL MOST PART OF THE RETINA THAT IS RESPONSIBLE FOR HIGH ACUITY VISION, DETERIORATES. RECENT STUDIES HAVE SHOWN THAT THE CAPILLARIES PRESENT UNDERNEATH THE RETINA IN THE CHOROID ARE LOST BEFORE RETINAL DEGENERATION. IN THIS PROJECT, WE PROPOSE TO DEVELOP AN EARLY INTERVENTION STRATEGY TO TRANSPLANT PATIENT-DERIVED CHOROIDAL STEM CELLS USING A BIOMATERIAL TO REPOPULATE THE LOST CAPILLARIES IN THE CHOROID AND THUS PREVENT FURTHER DAMAGE TO THE RETINA. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/M2023007F NAME OF ORGANIZATION OR GOVERNMENT: OREGON HEALTH & SCIENCE UNIVERSITY. (H) PURPOSE OF GRANT: MACULAR DEGENERATION RESEARCH BY YALI JIA, PHD, ENTITLED: (M2023008I) IMAGING CHORIOCAPILLARIS HEMODYNAMIC DEFECTS IN AGE-RELATED MACULAR DEGENERATION. INVESTIGATOR'S SUMMARY: AGE-RELATED MACULAR DEGENERATION IS A LEADING CAUSE OF BLINDNESS. ADVANCED FORMS OF THE DISEASE THAT INCLUDE GEOGRAPHIC ATROPHY REMAIN WITHOUT TREATMENT OPTIONS. NEW THERAPIES ARE REQUIRED, BUT RESEARCH EFFORTS ARE STYMIED BY AN INABILITY TO ASSESS PRECURSOR PATHOLOGIES ADEQUATELY. IN PARTICULAR, METHODS FOR IMAGING THE HEALTH OF BLOOD VESSELS THAT SUPPLY REGIONS THREATENED BY DEGENERATION COULD PROVIDE A MEANS OF IDENTIFYING NEW THERAPEUTIC TARGETS. THIS PROPOSAL MEETS THIS NEED BY DEVELOPING A NEW INSTRUMENT THAT WILL BE ABLE TO CHARACTERIZE VASCULAR FUNCTION IN UNSURPASSED DETAIL. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/M2023008I NAME OF ORGANIZATION OR GOVERNMENT: UNIVERSITY OF WISCONSIN-MADISON. (H) PURPOSE OF GRANT: MACULAR DEGENERATION RESEARCH BY FREYA MOWAT, PHD, ENTITLED: (M2023010N) RELEVANT GENE-DIET INTERACTIONS IN AMD: USE OF A MOUSE MODEL TO STUDY THE COMBINED EFFECTS OF AGE, HIGH GLYCEMIC DIET AND PGC1A INSUFFICIENCY. INVESTIGATOR'S SUMMARY: HUMAN AGE-RELATED MACULAR DEGENERATION (AMD) HAS MANY RISK FACTORS INCLUDING AGE, GENETICS, AND UNHEALTHY LIFESTYLE. COMBINING RISK FACTORS INCREASES THE CHANCE OF AMD. WE WILL STUDY THE COMBINED EFFECTS OF RISK FACTORS (AGING, GENETIC VARIANT IN A MITOCHONDRIAL REGULATOR, AND HIGH DIETARY GLUCOSE) IN AN ANIMAL MODEL. WE WILL DETERMINE THE EFFECT ON VISION, RETINAL STRUCTURE, DNA METHYLATION, GENE EXPRESSION, AND METABOLIC FUNCTION IN THE EYE. WE PREDICT THAT A COMBINATION OF ALL 3 RISK FACTORS WILL CAUSE THE DEVELOPMENT OF AMD-LIKE DISEASE, AND WE WILL DEFINE BIOLOGICAL PATHWAYS THAT ACT IN CONCERT TO INCREASE AMD RISK. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/M2023010N NAME OF ORGANIZATION OR GOVERNMENT: THE UNIVERSITY OF IOWA. (H) PURPOSE OF GRANT: MACULAR DEGENERATION RESEARCH BY KELLY MULFAUL, PHD, ENTITLED: (M2023011N) INVESTIGATING HUMAN CHOROIDAL MACROPHAGE RECRUITMENT AND ACTIVATION IN AGE-RELATED MACULAR DEGENERATION. INVESTIGATOR'S SUMMARY: AGE-RELATED MACULAR DEGENERATION (AMD) IS A LEADING CAUSE OF BLINDNESS WORLDWIDE. THE BACK OF THE EYE IS MADE UP OF CELL LAYERS THAT SUPPORT ONE ANOTHER SUPPLYING NUTRIENTS AND IMPORTANT MOLECULES THAT ARE REQUIRED FOR NORMAL VISION. IN AMD, THE OUTER SUPPORTING LAYER, THE CHOROID, IS DAMAGED. IMMUNE CELLS MOVE FROM THE CIRCULATION INTO CHOROID TISSUE IN RESPONSE TO DAMAGE TO PROTECT THE TISSUE. WE PREDICT THAT RECRUITED IMMUNE CELLS DO MORE DAMAGE THAN GOOD AND MAY BE INVOLVED IN THE DEATH OF THE CHOROID. WE AIM TO UNDERSTAND HOW THESE IMMUNE CELLS MOVE FROM THE CIRCULATION INTO THE TISSUE. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/M2023011N NAME OF ORGANIZATION OR GOVERNMENT: THE UNIVERSITY OF TEXAS AT AUSTIN. (H) PURPOSE OF GRANT: MACULAR DEGENERATION RESEARCH BY LYNDSAY LEACH, PHD, ENTITLED: (M2023012N) TOWARD UNCOVERING THE INTRICACIES OF INTRINSIC RPE REPAIR: IDENTIFYING IMMUNE-RELATED PRO-REGENERATIVE FACTORS USING ZEBRAFISH RPE INJURY PARADIGMS. INVESTIGATOR'S SUMMARY: MAMMALS, INCLUDING HUMANS, HAVE A LIMITED ABILITY TO REPAIR RPE TISSUE LOST TO INJURY OR DEGENERATIVE DISEASES LIKE AGE-RELATED MACULAR DEGENERATION. CONSEQUENTLY, LITTLE IS KNOWN ABOUT WHAT CELLULAR AND MOLECULAR PROCESSES DRIVE RPE REGENERATION. THIS STUDY UTILIZES ZEBRAFISH, A VERTEBRATE MODEL CAPABLE OF ROBUST TISSUE REPAIR, TO BETTER UNDERSTAND THE IMMUNE-RELATED RESPONSES UNDERLYING RPE REGENERATION AND CHRONIC RPE DAMAGE. THE PROPOSED RESEARCH WILL UNCOVER NOVEL RPE PRO-REGENERATIVE FACTORS, WHICH HOLD POTENTIAL AS FUTURE THERAPEUTIC TARGETS TO QUELL, OR EVEN REVERSE, RPE LOSS. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/M2023012N NAME OF ORGANIZATION OR GOVERNMENT: YALE UNIVERSITY. (H) PURPOSE OF GRANT: MACULAR DEGENERATION RESEARCH BY ABDELILAH MAJDOUBI, PHD, ENTITLED: (M2023013F) DECIPHERING THE INFLAMMATORY PATHWAYS TRIGGERING AGE-RELATED MACULAR DEGENERATION. INVESTIGATOR'S SUMMARY: THE FACTORS THAT LEAD TO CHRONIC INFLAMMATION AND VISION LOSS IN AGE-RELATED MACULAR DEGENERATION ARE NOT WELL UNDERSTOOD. PREVIOUS GENETIC STUDIES HIGHLIGHTED THE ROLE OF INFLAMMATORY MICROGLIA IN THE DISEASE. HOWEVER, AS THESE CELLS ARE RARE IN THE RETINA, DEEP GENETIC ANALYSIS IS NEEDED TO UNDERSTAND THE MECHANISM BY WHICH THESE CELLS CONTRIBUTE TO THE DISEASE. THE AIM OF THIS STUDY IS TO IDENTIFY DISTINCT SUBPOPULATIONS OF MICROGLIA AND DEFINE THE GENETIC FACTORS THAT REGULATE OR REINFORCE THEIR ROLE IN THE RETINAL INFLAMMATION, WHICH CAN HELP IDENTIFY POTENTIAL THERAPEUTIC TARGETS. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/M2023013F |
| SCHEDULE I, PART II, LINE 1, COLUMN (H), CONTINUED: | NAME OF ORGANIZATION OR GOVERNMENT: UNIVERSITY OF CALIFORNIA, IRVINE. (H) PURPOSE OF GRANT: MACULAR DEGENERATION RESEARCH BY DOROTA SKOWRONSKA-KRAWCZYK, PHD, ENTITLED: (M2020271) ROLE OF ELOVL2 IN AGE RELATED CHANGES IN THE EYE. EMERGENCY RELIEF SUPPLEMENT DUE TO COVID-19. FOR MORE INFORMATION, VISIT THE BRIGHTFOCUS WEBSITE: WWW.BRIGHTFOCUS.ORG/GRANT/M2020271 NAME OF ORGANIZATION OR GOVERNMENT: HELEN KELLER FOUNDATION FOR RESEARCH & EDUCATION. (H) PURPOSE OF GRANT: 2022 HELEN KELLER PRIZE FOR VISION RESEARCH PARTNERSHIP. THE HELEN KELLER PRIZE FOR VISION RESEARCH RECOGNIZES SIGNIFICANT ACCOMPLISHMENTS IN VISION RESEARCH, AND PROVIDES FUNDS FOR CONTINUANCE OF THOSE STUDIES. NAME OF ORGANIZATION OR GOVERNMENT: HELEN KELLER FOUNDATION FOR RESEARCH & EDUCATION. (H) PURPOSE OF GRANT: 2022 CONFERENCE SUPPORT. NAME OF ORGANIZATION OR GOVERNMENT: ARVO FOUNDATION FOR EYE RESEARCH. (H) PURPOSE OF GRANT: 2022 EYEFIND RESEARCH GRANT SPONSORSHIP NAME OF ORGANIZATION OR GOVERNMENT: ARVO FOUNDATION FOR EYE RESEARCH. (H) PURPOSE OF GRANT: 2022 TRAVEL GRANTS FOR CONFERENCE ATTENDEES |
| Software ID: | |
| Software Version: |