Project Grant F32AG099737
- The National Institute on Aging, a component of the Department of Health and Human Services, awarded Massachusetts Institute of Technology $596,050 on September 15, 2026, under the Aging Research program (CFDA 93.866) to investigate fuzzy coat dynamics of post-translationally modified tau aggregation. The project examines structural properties of tau, a microtubule-associated protein whose aggregation hallmarks Alzheimer's disease and twenty other neurodegenerative diseases. The research tests...
- The National Institute on Aging awarded The Regents of the University of California, San Francisco $663,237 on September 1, 2026, under the Aging Research program (CFDA 93.866) to support multiscale structural approaches defining tau filaments and cellular dysfunction associated with Alzheimer's disease and related dementias (ADRDs). The research integrates histological and structural imaging methods with cryo-electron microscopy to characterize tau fibril structures, aggregate morphologies, and...
- The National Institute on Aging awarded Ohio University $567,256 on February 1, 2026, under the Aging Research program (CFDA 93.866) to investigate the mechanisms of activity-dependent tau release in Alzheimer's disease pathogenesis. The research elucidates how neuronal hyperexcitability drives tau release from neurons and synapses, using a Drosophila model and human neural cell lines. Aim 1 investigates activity-dependent tau release from neurons and synapses, focusing on synaptic vesicle...
- The National Institute on Aging awarded the University of Texas Southwestern Medical Center $441,126 on July 1, 2026, under the Aging Research program (CFDA 93.866) to investigate STING regulation of tau seeding and tauopathy in Alzheimer's disease. The research will determine the molecular mechanism by which STING activation promotes tau seeding in cells and will use genetic approaches to establish the role of distinct STING functions in mouse tauopathy models. The work addresses how...
- The National Institute on Aging awarded The University of Texas Southwestern Medical Center $456,500 on February 1, 2026, under the Aging Research program (CFDA 93.866) to investigate the role of heparan sulfate proteoglycans in tau uptake in cell and mouse models as a potential treatment pathway for Alzheimer's disease. The research addresses gaps in understanding how heparan sulfate proteoglycans drive tau uptake in neurons and microglia, which are the brain cell types most affected in...
- The National Institute on Aging awarded the University of Texas Medical Branch at Galveston $1.788 million on January 1, 2026, under the Aging Research program (CFDA 93.866) to investigate the interplay between microglia and tau oligomer polymorphs in cognitive resilience among individuals with Alzheimer's disease neuropathology who remain cognitively intact. The project tests the hypothesis that brain-derived tau oligomers isolated from cognitively resilient individuals exhibit reduced toxicity...
- The National Institute on Aging awarded The Washington University $129,876 under the Aging Research program (CFDA 93.866) on June 15, 2026, to investigate the relationship between tau accumulation, white matter degeneration, and cognition in preclinical Alzheimer disease. The funded research uses autosomal dominant Alzheimer disease (ADAD) cohorts enrolled in the Dominantly Inherited Alzheimer Network (DIAN) to examine how tau tangle accumulation and white matter microstructural damage precede...
- The National Institute on Aging awarded Yale University $507,741 under the Aging Research program (CFDA 93.866) on August 1, 2026, to define the spatial relationship between early endosomal abnormalities, amyloid pathology, and early-stage tau hyperphosphorylation in primate models of sporadic Alzheimer's disease. The project addresses a gap in understanding the earliest molecular convergence points in Alzheimer's pathology. While soluble phosphorylated tau at threonine 217 (pT217tau) and...
- The National Institute on Aging awarded the University of California, Los Angeles $126,063 on August 5, 2026, under the Aging Research program (CFDA 93.866) to determine the atomic structures of amyloid-beta and tau oligomers and to characterize the molecular interaction between amyloid-beta and the TREM2 receptor on microglia. The award is classified as a Project Grant, specifically a K99/R00 award. The research develops a novel oligomer structure determination pipeline incorporating native...
- The National Institute on Aging awarded the University of Texas Medical Branch at Galveston $617,349 on June 15, 2026, under the Aging Research program (CFDA 93.866) to investigate EPAC1 signaling as a mechanism of retinal neurodegeneration during tauopathy. The research examines how activation of the cAMP/EPAC1 pathway promotes retinal neuronal injury by inducing mitochondrial dysfunction, promoting tau sumoylation and phosphorylation, and reducing clearance of tau aggregates and damaged...
The National Institute on Aging awarded $152,600 to Baylor College of Medicine on December 26, 2026, under the Aging Research program (CFDA 93.866) to investigate the synergistic mechanisms of tau and amyloid-beta aggregation in Alzheimer's disease pathology. The project, titled "Synergy in Condensation: Tau and AB in Alzheimer's Disease," employs advanced biophysical techniques including fluorescence lifetime imaging microscopy and microfluidic modulation infrared spectroscopy to characterize how tau:amyloid-beta interactions within biomolecular condensates drive pathological aggregation. The research aims to clarify the kinetics of oligomeric species formation, identify potential therapeutic targets, and determine whether reinforcing functional tau:tubulin interactions can prevent or reverse pathogenic tau:amyloid-beta assembly formation. Work is performed in Houston, Texas with a performance period through July 31, 2029. The research addresses Alzheimer's disease as the leading cause of dementia affecting over 6.7 million people in the United States, where extracellular amyloid-beta plaques and intracellular tau neurofibrillary tangles co-occur in virtually every case. Preliminary data indicate that tau condensates can adopt either a physiological state that stabilizes microtubules or a pathological state triggered by amyloid-beta recruitment, providing a mechanistic basis for investigating how interactions between these two intrinsically disordered proteins drive neuronal dysfunction.
Mod # | Description | ReasonForModification | Federal Obligation | Date |
|---|---|---|---|---|
| Not listed | $76.3k | 6/30/26 | ||
| Not listed | $0 | 6/30/26 | ||
| Not listed | $76.3k | 6/30/26 |