Grants and Contracts Details
Description
Alzheimer’s disease (AD) is a devastating neurodegenerative disease with no cure. It is characterized by β-amyloid (Aβ)-containing senile plaques and tau-containing neurofibrillary tangles in the brain. Among many mechanisms contributing to AD, excessive deposition of toxic Aβ peptides is considered to play a key role. Recent studies have demonstrated that Aβ deposition in the brain triggers robust morphological and transcriptomic changes in astrocytes. How these alterations of astrocyte functions may contribute to the development of AD remains poorly characterized. Evidence from our lab strongly suggest that astrocyte-derived ATP may play critical roles in amyloid deposition in the brain and pathogenesis of Alzheimer's disease. With a unique genetic mouse model to eliminate ATP exocytosis in astrocytes, we will explore the functional significance of astrocytic ATP exocytosis in Alzheimer's disease progression, in hopes of identifying novel and effective therapeutic strategies to treat Alzheimer's disease. This project is currently funded by an NIH R03 grant (AG083363).
Status | Active |
---|---|
Effective start/end date | 9/1/23 → 8/31/25 |
Fingerprint
Explore the research topics touched on by this project. These labels are generated based on the underlying awards/grants. Together they form a unique fingerprint.