Project Grant R01AG092547

Award Date 5/15/25
Completion Date 2/28/30
Dollars Obligated $622K
Federal Grant Program
93.866
Assistance Type
Project Grant
Place of Performance
Baltimore, MD 21205, USA
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This federal Project Grant award from the National Institute on Aging (CFDA 93.866 - Aging Research) to the J. David Gladstone Institutes is focused on exploring the role of the NOX2 enzyme in mediating brain dysfunction associated with Alzheimer's disease (AD). The $842,175 award, spanning December 2024 to November 2029, aims to investigate how inhibiting NOX2 could mitigate AD-related pathologies such as amyloid-beta and tau protein accumulation, network hyperactivity, glucose...
The Project Grant award for "NEURODEGENERATIVE REPROGRAMING OF MICROGLIA IN ALZHEIMER'S DISEASE" was provided by the National Institute on Aging (CFDA 93.866 Aging Research) in the amount of $442,357.00. The grant, awarded to the Research Foundation of the City University of New York (RFCUNY), aims to elucidate the molecular mechanisms underlying a specific subset of stressed "dark" microglia and their neurodegenerative impact in Alzheimer's disease (AD) models. The...
This $2,119,771 Project Grant award from the National Institute on Aging (under CFDA 93.866 - Aging Research) will fund research at the University of Massachusetts Medical School (UMass Medical) to investigate the role of peripheral insulin resistance and inflammation in Alzheimer's disease (AD) pathogenesis. The project aims to define age-related changes in metabolism and inflammation in peripheral organs, particularly the liver, and examine how these processes impact AD-relevant...
This Project Grant award from the National Institute on Aging's Aging Research federal grant program (CFDA 93.866) provides $871,419 to the University of Washington to conduct research on the role of microglia, the brain's immune cells, in the pathogenesis of Alzheimer's disease. The research aims to characterize molecular profiles and spatial organization of microglia across the adult age spectrum, both with and without Alzheimer's disease, through single-nucleus RNA sequencing of over 5,000...
This $125,896 Project Grant, awarded by the National Institute on Aging under the Aging Research program (CFDA 93.866), supports a research project led by The Washington University in St. Louis. The project aims to utilize state-of-the-art single-nuclei multi-omic functional genomic analyses of healthy and Alzheimer's disease (AD) human brain tissue, as well as transgenic AD mouse models, to perform deep molecular characterization of AD risk and resilience pathways across genetic, epigenomic,...
This federal Project Grant award, provided by the National Institute on Aging (NIA) under the Aging Research program (CFDA 93.866), aims to develop and apply advanced statistical methods to improve scientific inferences in Alzheimer's disease (AD) research. The key products and services to be delivered through this $455,274 award made to The Johns Hopkins University include: Developing efficient and statistically proper methods to better model, estimate, and predict the risk of AD incidence...
This $445,625 federal Project Grant award from the National Institute on Aging (CFDA 93.866 - Aging Research) supports research to develop an innovative nanotechnology approach to interrupt amyloid-beta (Aβ)-scavenger receptor (SR) signaling and mitigate neuroinflammation in Alzheimer's disease (AD). The research aims to: (1) elucidate how SR-targeted nanoparticles can ameliorate Aβ-mediated glial cell dysfunction and inflammatory pathways; and (2) evaluate the long-term neuroprotective...
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This federal Project Grant award of $622,086 from the National Institute on Aging (CFDA 93.866 - Aging Research) aims to elucidate the role of the NOD2/RIPK2 signaling pathway in microglial activation and its implications for neuroinflammation and neurodegeneration in Alzheimer's disease (AD). The study, conducted by The Johns Hopkins University, involves molecular and biophysical analyses to understand the mechanisms of amyloid-beta oligomer (ABO)-induced microglial activation and the involvement of the NOD2/RIPK2 signaling axis. Additionally, the research will utilize genetically modified AD mouse models to evaluate the impact of selectively removing microglial NOD2 or RIPK2 on ABO-induced pathology, neuroinflammation, and neurodegeneration. The project will also investigate the neuroprotective effects of a RIPK2 inhibitor, CMPD0673, in the AD mouse model. The findings from this comprehensive study could pave the way for novel therapeutic strategies targeting microglial NOD2/RIPK2 signaling in Alzheimer's disease and related dementias.

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