Project Grant RF1AG076214
- This $519,750 Project Grant award from the National Institute on Aging (CFDA 93.866 - Aging Research) supports a 2-year research study by the J. David Gladstone Institutes, a non-profit biomedical research organization in San Francisco. The study aims to explore the underlying molecular mechanisms by which reducing levels of the tau protein can prevent or diminish excitation/inhibition imbalance and network hyperexcitability in the brain. This imbalance has been observed in various...
- This $1,823,353 Project Grant awarded by the National Institute on Aging (CFDA 93.866 Aging Research) to the Seattle Institute For Biomedical And Clinical Research aims to elucidate the molecular mechanisms by which pathological tau protein causes neurodegeneration in Alzheimer's disease (AD) and related tauopathy disorders. The research project will leverage a C. elegans model of tauopathy to investigate the functional role of nuclear speckles, membraneless organelles involved in RNA...
- This Project Grant award from the National Institute on Aging (CFDA 93.866 - Aging Research) will investigate the role of glial fibrillary acidic protein (GFAP) upregulation in reactive astrocytes and its impact on tripartite excitatory synapses in a tauopathy mouse model of Alzheimer's disease. Specifically, the $452,550 award to The General Hospital Corporation (dba Massachusetts General Hospital) will overexpress GFAP in astrocytes and blunt GFAP upregulation to evaluate changes in the...
- This Project Grant award from the National Institute on Aging (NIA), under the Aging Research federal grant program (CFDA 93.866), supports research to investigate the role of reactive astrocytes in the propagation and clearance of tau in Alzheimer's disease. The $487,574 award to The General Hospital Corporation, doing business as Massachusetts General Hospital (MGH), aims to elucidate how the upregulation of the glial fibrillary acidic protein (GFAP) in astrocytes may attenuate the spread of...
- This Project Grant award of $320,000 from the National Institute on Aging's Aging Research Federal Grant Program (CFDA 93.866) is supporting research at the University of Texas Medical Branch at Galveston (UTMB) to investigate the impact of pathological tau protein on alternative polyadenylation (APA) regulation in Alzheimer's disease. The study aims to comprehensively profile APA transcripts and gene expression in mouse primary hippocampal neurons expressing wild-type and mutant tau proteins....
- This Project Grant award of $816,661.00 from the National Institute on Aging (CFDA 93.866 - Aging Research) supports research to comprehensively map the impact of tau pathology on the proteome and measure the functional consequences in neurodegeneration associated with Alzheimer's disease and frontotemporal dementia. The project combines expertise in mass spectrometry-based proteomics and functional genomics to elucidate the molecular and cellular mechanisms by which pathological tau drives...
- This $165,348 Project Grant award from the National Institute on Aging (CFDA 93.866 - Aging Research) supports research to investigate the cellular and molecular mechanisms underlying neurotoxicity and cognitive deficits caused by hyperphosphorylated tau protein, a hallmark of Alzheimer's disease. The grant recipient, the Rector & Visitors of the University of Virginia, will use a combination of transcriptomic profiling and neurophysiology approaches to characterize the effects of...
- This Project Grant award from the National Institute on Aging's Aging Research program (CFDA 93.866) provides $2,181,250 in funding to the Seattle Institute For Biomedical And Clinical Research to develop small molecule inhibitors of the MSUT2 protein as a potential therapeutic approach for treating tauopathy disorders such as frontotemporal lobar degeneration, Alzheimer's disease, and related conditions. The project aims to optimize potent and brain-penetrant MSUT2 inhibitors and demonstrate...
- This $2,190,943 federal Project Grant award from the National Institute on Aging (CFDA 93.866 - Aging Research) supports a research study conducted by the University of Alabama at Birmingham (UAB) to examine the relationship between tau protein deposition and functional brain network health in individuals at risk for Alzheimer's disease (AD). The key objectives of the study are to: 1) Use tau positron emission tomography (PET) and resting-state functional magnetic resonance imaging (fMRI) to...
- This $130,302 Project Grant award from the National Institute on Aging (CFDA 93.866 - Aging Research) supports research at New York University School of Medicine to investigate the selective vulnerability of basal forebrain cholinergic neurons (BFCNs) to tau pathology in Alzheimer's disease (AD). The key products and services to be delivered include: Investigating the biochemical underpinnings and functional alterations of BFCNs with pathological tau accumulation using human induced...
FUNCTIONAL ANALYSIS OF GLIA IN TAUOPATHY - ALZHEIMER'S DISEASE IS THE MOST COMMON NEURODEGENERATIVE DISORDER AND IS CHARACTERIZED CLINICALLY BY COGNITIVE DYSFUNCTION. CLASSIC NEUROPATHOLOGICAL FEATURES OF THE DISEASE INCLUDE THE FORMATION OF EXTRACELLULAR AMYLOID PLAQUES, INTRANEURONAL DEPOSITION OF ABNORMALLY PHOSPHORYLATED AND AGGREGATED TAU PROTEIN INTO NEUROFIBRILLARY TANGLES, AND GLIOSIS. GLIAL PATHOLOGY HAS GENERALLY BEEN CONSIDERED A SECONDARY, OR REACTIVE, CHANGE. HOWEVER, RECENT ADVANCES IN UNDERSTANDING NORMAL AND PATHOLOGICAL GLIAL BIOLOGY HAVE INSTEAD SUGGESTED THAT GLIA MAY PLAY AN ACTIVE ROLE IN NEUROLOGICAL DISORDERS, INCLUDING ALZHEIMER'S DISEASE. HERE WE TAKE A GENETIC APPROACH TO DEFINE PROTEINS AND PATHWAYS MEDIATING THE INFLUENCE OF GLIA ON ALZHEIMER'S-ASSOCIATED NEURODEGENERATION. TAKING ADVANTAGE OF THE ADVANCED MOLECULAR AND GENETIC TOOLS, SHORT LIFESPAN, AND CONSERVED GLIAL BIOLOGY IN DROSOPHILA WE WILL IDENTIFY GLIAL PROTEINS AND PATHWAYS THAT CAN INFLUENCE TAU NEUROTOXICITY IN AGING ADULT BRAINS. IN PROOF OF PRINCIPLE STUDIES, WE HAVE VALIDATED A NOVEL SYSTEM FOR STUDYING NON-CELL AUTONOMOUS NEURODEGENERATION IN TAUOPATHY AND SHOW THAT OUR ASSAY SYSTEM WORKS IN THE CONTEXT OF UNBIASED SCREENING. IN ADDITION, BASED ON THE OBSERVATION THAT MANY GENES IMPLICATED IN ALZHEIMER'S DISEASE THROUGH GENOME WIDE GENETIC ASSOCIATION STUDIES (GWAS) ARE EXPRESSED PREDOMINANTLY OR SUBSTANTIALLY IN GLIAL CELLS, WE WILL TEST THE EFFECT OF UPREGULATING AND DOWNREGULATING THESE GWAS-DERIVED GENE CANDIDATES IN FLY GLIA ON TAU-INDUCED NEUROTOXICITY. TO ADDITIONALLY CONNECT OUR GENETIC MODEL EXPERIMENTS WITH THE AUTHENTIC HUMAN DISEASE, WE WILL USE STATE-OF-THE-ART INFORMATICS TOOLS TO INTEGRATE FUNCTIONAL GENETIC DATA WITH ALZHEIMER'S DISEASE TRANSCRIPTOMICS AND PROTEOMICS. SINCE OUR SYSTEMS ANALYSIS WILL BE PERFORMED ON A GLIAL SUBTYPE-SPECIFIC BASIS OUR STUDIES CAN NOT ONLY OUTLINE GLIAL NETWORKS MODULATING THE TOXICITY OF TAU TO NEURONS, BUT ALSO PROVIDE FUNCTIONAL INSIGHT INTO NEWLY DEFINED GLIAL SUBTYPES. OUR STUDIES WILL DEVELOP FUNDAMENTAL INSIGHTS INTO GLIA CELL BIOLOGY IN HEALTH AND DISEASE AND WILL EXPAND THE ARRAY OF CELLULAR AND MOLECULAR TARGETS RELEVANT FOR THERAPY DEVELOPMENT IN ALZHEIMER'S DISEASE AND RELATED NEURODEGENERATIVE DISORDERS.
Mod # | Description | ReasonForModification | Federal Obligation | Date |
|---|---|---|---|---|
| Not listed | $1.6m | 9/5/25 | ||
| Not listed | $2.5m | 8/31/22 | ||
| Not listed | $2.5m | 8/31/22 |
GrantNumber | Description | Subgrantee | Prime Award | Dollars Obligated | Updated At |
|---|---|---|---|---|---|
127862S | Massachusetts Institute Of Technology | Project Grant RF1AG076214 | $667.4k | 12/21/22 |