Project Grant R01AG085933
- Federal Project Grant Award Summary Emory University received a $147,656 Project Grant award from the National Institute on Aging (NIA) under the Aging Research program (CFDA 93.866), with an award date of March 11, 2025 and project completion date of September 29, 2025. The grant supports the development of the first human locus coeruleus (LC) organoid model to advance understanding of Alzheimer's disease (AD) pathology. The research addresses a critical gap in AD knowledge by utilizing...
- Federal Project Grant Award Summary Emory University received a $149,190 Project Grant from the National Institute on Aging under the Aging Research program (CFDA 93.866) awarded August 6, 2026, with completion targeted for February 28, 2029. The funded research project, "Neuromelanin Formation and Toxicity in the Locus Coeruleus: The Role of Norepinephrine Metabolism," investigates the selective vulnerability of the locus coeruleus (LC) brain region in Alzheimer's disease (AD). The...
- This Project Grant award from the National Institutes of Health's Aging Research program (CFDA 93.866) will support research to identify early transcriptional and pathological changes in brain regions vulnerable to Alzheimer's disease (AD). The $459,076 award, granted to Trustees of Boston University, will use single-nucleus RNA sequencing and targeted mass spectrometry to profile cell type-specific gene expression and tau/amyloid beta proteoforms in the transentorhinal cortex, entorhinal...
- 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...
- Federal Project Grant Award Summary Weill Medical College of Cornell University received a $1,399,657 Project Grant from the National Institute on Aging (CFDA 93.866 – Aging Research) awarded June 1, 2025, with completion targeted for March 31, 2030. The grant supports research titled "Mapping Proteomic Changes of Tauopathy in Human Neurons," which aims to elucidate the cellular mechanisms underlying tau aggregate propagation in Alzheimer's disease (AD) and frontotemporal dementia...
- 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...
- Federal Project Grant Award Summary New York University School of Medicine received a $390,906 Project Grant from the National Institute on Aging (NIA) under the Aging Research program (CFDA 93.866), awarded July 15, 2025, with completion targeted for March 31, 2030. This award funds a comprehensive research initiative titled "Deciphering the Selective Vulnerability of Basal Forebrain Cholinergic Neurons to Tauopathy," which investigates the molecular mechanisms underlying tau...
- 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...
- This three-year, $5.782 million project grant from the National Institute on Aging, part of the Department of Health and Human Services, will support research into single-cell characterization of frontotemporal lobar degeneration caused by mutations in the progranulin gene. The University of California, San Francisco will map the transcriptome and gene regulatory networks that define glial pathology and neuronal vulnerability in the frontal cortex and thalamus of progranulin-deficient...
- Federal Project Grant Award Summary Brigham & Women's Hospital Inc. (Department of Faulkner Pathology) received a $3.67 million Project Grant from the National Institute on Aging under the Aging Research program (CFDA 93.866) for a four-year research initiative spanning September 1, 2025, through August 31, 2029. The award supports investigation into the role of transfer RNA-derived fragments (tRFs) in tau pathology associated with Alzheimer's disease and related dementias. The research aims...
IMPACT OF NEUROMELANIN AND TAU ACCUMULATION DURING AGING AND DISEASE ON LOCAL GENE EXPRESSION IN THE HUMAN LOCUS COERULEUS USING SPATIALLY-RESOLVED TRANSCRIPTOMICS WITH PROTEIN DETECTION - PROJECT SUMMARY THE LOCUS COERULEUS (LC) IS A SMALL BILATERAL NUCLEUS LOCATED IN THE DORSAL PONS OF THE BRAINSTEM, AND SERVES AS THE BRAIN'S PRIMARY SITE FOR PRODUCING THE NEUROMODULATOR NOREPINEPHRINE (NE). NE-PRODUCING NEURONS IN THE LC PROJECT TO MANY REGIONS OF THE CENTRAL NERVOUS SYSTEM TO MODULATE HIGHLY DIVERGENT FUNCTIONS INCLUDING COGNITION, AROUSAL, AND MOOD. THE LC IS ONE OF THE EARLIEST SITES OF DEGENERATION IN ALZHEIMER'S DISEASE (AD), AND PROFOUND LOSS OF LC-NE NEURONS ACCELERATES WITH DISEASE PROGRESSION. SEVERAL UNIQUE ANATOMICAL, MORPHOLOGICAL AND NEUROCHEMICAL PROPERTIES LIKELY CONTRIBUTE TO VULNERABILITY OF LC-NE NEURONS. FIRST, LC-NE NEURONS SYNTHESIZE NEUROMELANIN (NM), A PROPERTY SHARED BY ONLY A FEW CELL TYPES IN THE HUMAN BRAIN. NM ACCUMULATES WITH AGING, AND ONE HYPOTHESIS IS THAT IT INITIALLY PROTECTS LC-NE NEURONS BY SEQUESTERING OR CHELATING NEUROTOXIC SUBSTANCES. HOWEVER, IN LATE LIFE AND DISEASE STATES, NM DEPOSITION MAY BE DETRIMENTAL WHEN IT OVERWHELMS CELLULAR MACHINERY, AND ACCUMULATED TOXINS ARE RELEASED FROM DEGENERATING CELLS. SECOND, ACCUMULATION OF PHOSPHORYLATED TAU (PTAU), A PRIMARY AD NEUROPATHOLOGY, IS DETECTED IN THE LC PRIOR TO ANY OTHER BRAIN REGION. IN THIS APPLICATION, WE GENERATE TRANSCRIPTOMIC-SCALE SPATIAL MAPS THAT INCORPORATE LOCALIZATION OF NM AND PTAU IN THE HUMAN LC IN BRAIN DONORS DIAGNOSED WITH AD AND CONTRAST THESE EXPRESSION PATTERNS TO BOTH MIDDLE-AGED AND AGE-MATCHED ELDERLY NEUROTYPICAL DONORS. WE WILL USE THE 10X GENOMICS VISIUM SPATIAL GENE EXPRESSION AND THE VISIUM SPATIAL PROTEOGENOMICS PLATFORMS, WHICH COMBINE TRANSCRIPTOME-WIDE RNA SEQUENCING WITH DETAILED HIGH-RESOLUTION HISTOLOGY AND IMMUNOFLUORESCENCE IMAGING TO SEGMENT AND QUANTIFY NM AND PTAU, RESPECTIVELY. WE WILL COMPUTATIONALLY ALIGN ADJACENT TISSUE SECTIONS FROM THE SAME DONOR ACROSS PLATFORMS TO DETERMINE HOW JOINT ACCUMULATION OF NM AND PTAU DURING AGING AND DISEASE IMPACTS THE LOCAL TISSUE MICROENVIRONMENT IN THE HUMAN LC. RESULTS WILL BE VALIDATED AND EXTENDED USING COMPLEMENTARY IN SITU HYBRIDIZATION PLATFORMS WITH CELLULAR RESOLUTION AND SIMULTANEOUS PROTEIN DETECTION. ACCUMULATION OF NM AND PTAU REPRESENT TWO KEY BIOLOGICAL HYPOTHESES UNDERLYING THE VULNERABILITY AND RESILIENCY OF LC-NE NEURONS TO NEURODEGENERATION IN THE HUMAN BRAIN. HENCE, GENERATION OF THESE DATA ARE IMPORTANT BECAUSE UNDERSTANDING THE MOLECULAR SEQUELAE DOWNSTREAM OF THIS ACCUMULATION IS CRITICAL TO DEVELOP STRATEGIES TO TARGET CELLS IN THE LC FOR DISEASE TREATMENT OR PREVENTION.
Mod # | Description | ReasonForModification | Federal Obligation | Date |
|---|---|---|---|---|
| Not listed | $838.2k | 3/20/26 | ||
| Not listed | $67.8k | 6/13/25 | ||
| Not listed | $763.0k | 3/27/25 | ||
| Not listed | $763.0k | 3/27/25 | ||
| Not listed | $867.3k | 5/1/24 |