Project Grant RF1AG078351
- 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...
- CHCHD10 in Tauopathy in Alzheimer's Disease and Related Dementias Research Project Case Western Reserve University's Office of Research Administration, in affiliation with University Hospitals of Cleveland, received a $431,750 Project Grant award from the National Institute on Aging (Aging Research program, CFDA 93.866) effective January 1, 2026, through December 31, 2027. The award funds biomedical research investigating the role of CHCHD10 (coiled-coil-helix-coiled-coil-helix domain containing...
- Grant Award Summary The National Institute on Aging (NIA) awarded $3,147,477 to The Regents of the University of California, San Francisco under the Aging Research program (CFDA 93.866) for the project "Aberrant Proteomes in Tauopathy: Revealing Functional Consequences via Multimodal Proteomics." The award period extends from June 1, 2025, through February 28, 2030. This research project combines mass spectrometry-based proteomics and functional genomics expertise to comprehensively...
- 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 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....
- Federal Grant Award Summary The National Institute on Aging (NIA) awarded a Project Grant totaling $433,125.00 to The University of Texas Health Science Center at San Antonio effective September 15, 2025, through August 31, 2027, under the Aging Research program (CFDA 93.866). This exploratory/developmental grant funds research investigating whether extracellular tau protein modulates neurogenesis through the low-density lipoprotein receptor-related protein 1 (LRP1) pathway in adult-born granule...
- 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 Project Grant award, with a total funding amount of $431,750, was provided by the National Institute on Aging (NIA) under the Aging Research federal grant program (CFDA 93.866). The award is for the development and evaluation of a novel immuno-gene therapy approach using a single-chain fragment variable (scFv) derived from an anti-tau oligomeric complex 1 (TOC1) antibody. The key objectives are to: 1) generate and validate the TOC1-scFv-HaloTag-Proteasome Degradation Signal (PDS)...
- This Project Grant award from the National Institute on Aging (CFDA 93.866 - Aging Research) totaling $433,125 will fund a study to investigate the relationship between microglia, neurons, and tau pathology in Alzheimer's disease. The research will utilize a novel model system of microglial co-cultures with hippocampal assembloids derived from patient-derived induced pluripotent stem cell (iPSC) lines with MAPT mutations and healthy controls. The goal is to explore how bidirectional changes...
- Federal Grant Award Summary The National Institute on Aging (NIA) awarded Massachusetts General Hospital $975,148 on May 15, 2025, under the Aging Research program (CFDA 93.866) to investigate the role of reactive astrocytes in tau protein propagation and clearance in Alzheimer's disease. The research project, which extends through February 28, 2030, will generate scientific knowledge regarding the mechanisms by which glial fibrillary acidic protein (GFAP) upregulation in astrocytes may...
TAU CLEARANCE AND SYNAPTIC AND COGNITIVE FUNCTION RESCUE BY ACTIVATION OF MITOCHONDRIAL CLEARANCE IN TAUOPATHY MODEL - SUMMARY: MICROTUBULE ASSOCIATED PROTEIN TAU (MAPT) PLAYS A MAJOR ROLE IN ALZHEIMER'S DISEASE (AD) AND RELATED DISORDER (ADRD) AND HAVE DELETERIOUS EFFECTS ON MITOCHONDRIAL AND SYNAPTIC FUNCTION AND NEUROINFLAMMATION. TAU OLIGOMERS, PRIOR TO NEUROFIBRILLARY TANGLE (NFT) FORMATION, ARE TOXIC SPECIES RESPONSIBLE FOR TAU TOXICITY, MITOCHONDRIAL AND SYNAPTIC DAMAGE, AND MEMORY IMPAIRMENT. HOWEVER, THE UNDERLYING MECHANISMS OF ABNORMAL TAU ACCUMULATION AND STRATEGIES TO ELIMINATE THEM REMAIN LARGELY UNKNOWN. THERE IS LIMITED MECHANISTIC STUDY INVESTIGATING THE LIKELY INTERPLAYS BETWEEN MITOCHONDRIAL DYSFUNCTION AND NEUROINFLAMMATION AND THEIR CONTRIBUTION TO SYNAPTIC DAMAGE AND TAUOPATHY IN AD AND RELATED DISORDER (ADRD). PTEN-INDUCED PUTATIVE KINASE 1 (PINK1) IS IMPORTANT FOR THE MAINTENANCE OF MITOCHONDRIAL INTEGRITY AND QUALITY CONTROL VIA MITOPHGY. PINK1 WAS SIGNIFICANTLY DECREASED IN AD-AFFECTED BRAINS, AD MICE, INCLUDING WIDELY USED TAUOPATHY MICE, SUGGESTING DEFECTIVE MITOPHAGY IN AD AND ADRD. DEVELOPMENT AND VALIDATION OF BIOLOGICAL ACTIVITY OF PINK1 ENHANCER REMAINS TO BE EXPLORED. THIS PROPOSAL WILL ADDRESS THE FUNDAMENTAL UNEXPLORED QUESTIONS OF WHETHER PINK1 IS A KEY PLAYER IN TAU-RELATED ABERRANT MITOCHONDRIA AND SYNAPTIC INJURY AND MITOCHONDRIA-MEDIATED NEUROINFLAMMATION AND WHETHER GENETIC AND PHARMACOLOGICAL ENHANCEMENT OF PINK1 PROVES BENEFICIAL FOR TAU CLEARANCE, MITOCHONDRIAL QUALITY CONTROL, AND COGNITIVE FUNCTION AS A POTENTIAL THERAPEUTIC STRATEGY IN AD AND ADRD. WE WILL ELUCIDATE PINK1-DEPENDENT NEW MECHANISMS UNDERLYING TAU PATHOLOGY AND CLEARANCE, PROPER MITOCHONDRIAL AND SYNAPTIC FUNCTION VIA PINK1/MITOCHONDRIA/NEUROINFLAMMATION AXIS RELEVANT TO THE PATHOGENESIS OF NEURODEGENERATION BY EMPLOYING PINK1 NOVEL GENETICALLY MANIPULATED TRANSGENIC MOUSE MODELS AND PHARMACOLOGICAL PINK1 ENHANCER IN TAU-RICH ENVIRONMENT, AND HUMAN NEURONAL CELLS CONTAINING PATIENT AD- AND NON-AD-DERIVED MITOCHONDRIA.
Mod # | Description | ReasonForModification | Federal Obligation | Date |
|---|---|---|---|---|
| Not listed | $0 | 1/27/26 | ||
| Not listed | $1.1m | 9/3/25 | ||
| Not listed | $1.1m | 9/3/25 | ||
| Not listed | $1.7m | 9/15/22 | ||
| Not listed | $1.7m | 9/15/22 |