GENETIC AND SINGLE-CELL MULTI-OMIC CHARACTERIZATION OF ALZHEIMER'S DISEASE RISK AND RESILIENCE PATHWAYS - P…
Federal financial assistance recorded from USAspending. This is not a procurement contract.
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ASST_NON_R00AG086583_075 · WASHINGTON UNIVERSITY, THE · Department of Health and Human Services
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- Assistance award identifier
- ASST_NON_R00AG086583_075
- FAIN
- R00AG086583
- Recipient
- WASHINGTON UNIVERSITY, THE
- Awarding agency
- Department of Health and Human Services
- Funding agency
- Department of Health and Human Services
- Assistance listing (CFDA)
- 93.866
- Total obligated
- $248,999
- Period
- Jul 15, 2024 – Jun 30, 2029
- Fiscal year
- 2026
- Place of performance state
- MO
- Source file
- FY2026_All_Assistance_Full_20261006.zip
Description
GENETIC AND SINGLE-CELL MULTI-OMIC CHARACTERIZATION OF ALZHEIMER'S DISEASE RISK AND RESILIENCE PATHWAYS - PROJECT SUMMARY ALZHEIMERâS DISEASE (AD) IS A DEVASTATING AND COMPLEX NEURODEGENERATIVE DISORDER WITH A CRUSHING SOCIAL AND ECONOMIC BURDEN CURRENTLY AFFECTING MORE THAN 6 MILLION PATIENTS IN THE US. WITH THE NUMBER OF AFFECTED INDIVIDU- ALS PROJECTED TO INCREASE, IDENTIFYING DISEASE-MODIFYING TREATMENTS AND INTERVENTIONS FOR AD REMAINS ONE OF THE MOST CRITICAL UNDERTAKINGS IN MODERN BIOMEDICAL RESEARCH. A CRITICAL STEP TO THE DEVELOPMENT OF THESE INTERVEN- TIONS INVOLVES CHARACTERIZING THE GENES AND PATHWAYS MEDIATING AD RISK AND RESILIENCE. THE OBJECTIVE OF THIS PROPOSAL IS TO EXPLORE THE MODULATION OF AD GENETIC RISK BY AGE AND EXAMINE HOW CALORIC RESTRICTION (CR), A LIFESPAN-INCREASING INTERVENTION, CAN BE HARNESSED TO COUNTER AD RISK. THE PROPOSAL WILL UTILIZE STATE-OF- THE-ART SINGLE-NUCLEI MULTI-OMIC FUNCTIONAL GENOMIC ANALYSES OF HEALTHY AND AD HUMAN BRAIN TISSUE, AS WELL AS TRANSGENIC AD MOUSE MODELS, TO PERFORM DEEP MOLECULAR CHARACTERIZATION OF AD RISK AND RESILIENCE ACROSS THE GENETIC, EPIGENOMIC, AND TRANSCRIPTOMIC LAYERS. AIM 1 WILL DISSECT NON-CODING AD GENETIC RISK THROUGH INTENSIVE MULTI-OMIC MOLECULAR PROFILING OF HEALTHY AND AD BRAINS, ALLOWING THE NOMINATION OF CAUSAL VARIANTS, CELL TYPES, AND PATHWAYS MEDIATING RISK. AIM 2 WILL IDENTIFY PROTECTIVE MECHANISMS IN COGNITIVELY HEALTHY, LONG-LIVED INDIVID- UALS, INCLUDING CENTENARIANS, AND DETERMINE WHETHER AD RESILIENCE MANIFESTS BY MAINTAINING A âYOUNGâ STATE OR BY COMPENSATING FOR DETRIMENTAL AGE-RELATED EFFECTS AND AD GENETIC RISK. THIS WILL INVOLVE COMPARISON ACROSS A BROAD AGE SPECTRUM, INCLUDING MOLECULAR PROFILES OF YOUNG CONTROLS (AGED 18-35) AND AD PATIENTS. AIM 3 WILL CHARACTERIZE THE INTERPLAY BETWEEN CR AND NEURODEGENERATION IN GENETICALLY DIVERSE AD MOUSE MODELS. THIS WILL PROVIDE INSIGHT INTO THE PATHWAYS MEDIATING LIFESPAN-INCREASING INTERVENTIONS IN THE BRAIN, THEIR INTERAC