CELLULAR REPROGRAMMING TO PROMOTE LONGEVITY, RESILIENCE, AND REPAIR IN MOTOR UNIT DEGENERATION - PROJECT SU…
Federal financial assistance recorded from USAspending. This is not a procurement contract.
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ASST_NON_K00AG079815_075 · PRESIDENT AND FELLOWS OF HARVARD COLLEGE · Department of Health and Human Services
Compare Multiple AI Models with SmartSoloExplore CaptureIQ IntelligenceAssistance award details
- Assistance award identifier
- ASST_NON_K00AG079815_075
- FAIN
- K00AG079815
- Recipient
- PRESIDENT AND FELLOWS OF HARVARD COLLEGE
- Awarding agency
- Department of Health and Human Services
- Funding agency
- Department of Health and Human Services
- Assistance listing (CFDA)
- 93.866
- Total obligated
- $459,856
- Period
- Dec 1, 2022 – Apr 30, 2027
- Fiscal year
- 2023
- Place of performance state
- MA
- Source file
- FY2023_All_Assistance_Full_20261006.zip
Description
CELLULAR REPROGRAMMING TO PROMOTE LONGEVITY, RESILIENCE, AND REPAIR IN MOTOR UNIT DEGENERATION - PROJECT SUMMARY/ABSTRACT THE GLOBAL POPULATION IS AGING RAPIDLY â THE NUMBER OF ADULTS OVER 65 IS EXPECTED TO DOUBLE BY 2050. CHRONOLOGICAL AGING IS AN ESTABLISHED RISK FACTOR FOR NEURODEGENERATION AND LEADS TO DYSFUNCTION AND LOSS OF THE MOTOR UNIT (MU; A MOTOR NEURON AND ALL THE MYOFIBERS IT INNERVATES). FURTHER, GENETIC VARIANTS MAY ACCELERATE BIOLOGICAL AGING AND ACQUIRED CELLULAR DAMAGE IN THE NERVOUS SYSTEM. HOWEVER, AGED MAMMALIAN TISSUES RETAIN AN EPIGENETIC SIGNATURE, AND RECENT PUBLICATIONS HIGHLIGHT STRATEGIES SUCH AS CELLULAR REPROGRAMMING TO RESTORE YOUTHFUL TISSUE RESILIENCE. MY LONG-TERM CAREER GOAL IS TO OBTAIN A TENURE-TRACK CLINICIAN-SCIENTIST POSITION AT AN ACADEMIC INSTITUTION AND ESTABLISH A TRANSLATIONAL RESEARCH PROGRAM. SUCH A POSITION WILL ALLOW ME TO ACHIEVE MY LONG-TERM SCIENTIFIC GOAL TO INVESTIGATE CELLULAR AGING OF THE NERVOUS SYSTEM IN THE SETTING OF GENETIC PREDISPOSITION. MY SHORT-TERM SCIENTIFIC GOAL AND THE FOUNDATION OF THIS PROPOSAL IS TO TEST THE HYPOTHESIS THAT TARGETING BIOLOGICAL AGING PATHWAYS INDEPENDENTLY AND IN CONJUNCTION WITH DISEASE-SPECIFIC GENE THERAPIES MAY PROVIDE A PROMISING AVENUE TO DEVELOP NEW THERAPEUTIC STRATEGIES TARGETING NEURODEGENERATION. MY DOCTORAL PROJECT INVESTIGATES KINESIN-1 FAMILY MEMBER 5A (KIF5A), A KNOWN SUSCEPTIBILITY GENE FOR THE NEURODEGENERATIVE DISEASE AMYOTROPHIC LATERAL SCLEROSIS (ALS). MUTANT KIF5A MICE DEMONSTRATE LOSS OF FUNCTIONAL MUS IN THE CONTEXT OF INJURY AND AGING, WITH OBSERVABLE PATHOLOGICAL CORRELATES. THESE DATA SUPPORT A PROMINENT ROLE OF KIF5A IN MU MAINTENANCE, SUGGESTING MUTANT KIF5A IS UNABLE TO COMBAT BIOLOGICAL CHALLENGES SUCH AS INJURY OR AGE. THE F99 PHASE OF THIS AWARD WILL TEST THE HYPOTHESIS THAT ALS-ASSOCIATED KIF5A MUTATIONS LEAD TO HAPLOINSUFFICIENCY AND USE VIRAL VECTORS TO MANIPULATE KIF5A EXPRESSION. THE K00 PHASE WILL BUILD UPON MY EXPERIENCE WITH MU PHYSIOLOG