TDP-43 protein changes and reactivated retroviruses in Alzheimer’s and related dementias
Official title: Effects of TDP-43 Proteinopathy on Retrotransposon Activation and Cell-Type Specific Vulnerability in a Mammalian Model of Alzheimer's and Related Dementias
Funded at State University New York Stony Brook · NIH-11460985 · Data updated 2026-11-12
Researchers are looking at whether abnormal TDP-43 protein and reawakened retroviruses damage brain cells and contribute to Alzheimer’s and related dementias.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | State University New York Stony Brook NIH-funded |
| Lab location | 1 site (Stony Brook, United States) |
| Project start | December 1, 2022 |
| Project end | November 30, 2027 |
| Funding year | 2026 |
| Award (this year) | $54,984 |
| NIH project number | 3R01AG079898-04S1 |
| Project ID | NIH-11460985 on NIH RePORTER |
Who could benefit from this research
✓Could help
People with Alzheimer’s disease, related dementias, or mild cognitive impairment and those interested in contributing samples or joining future clinical work related to TDP-43 biology may find this relevant.
✕Less likely to help
Patients whose conditions are purely vascular or caused by unrelated mechanisms without TDP-43 involvement are less likely to benefit directly from these findings in the near term.
What this research studies
From my perspective as a patient, this work uses mice that carry a human TDP-43 mutation linked to dementia to model brain changes seen in Alzheimer’s and related conditions. Scientists will boost TDP-43 levels in either neurons or astrocytes using targeted viral tools to see how one cell type affects the other. They will measure whether dormant retrotransposons (endogenous viral elements) become active and whether that activation causes cell death or spreads toxicity between cells. The project aims to build the first mammalian platform to connect TDP-43 behavior, retrotransposon activation, and cell-type specific vulnerability.
Why it matters
Potential benefit: If successful, this could point to new molecular targets to block or slow neurodegeneration in Alzheimer’s and related dementias.
How similar studies have gone: Previous cell and invertebrate models have linked TDP-43 and retrotransposon activation, but applying these ideas in a mammalian (mouse) model is novel and still early-stage.
Where this research is happening
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State University New York Stony Brook
Stony Brook, United States Active
Researchers
- Principal investigator: Sher, Roger B — State University New York Stony Brook
- Study coordinator: Sher, Roger B
About this research
- This is an active NIH-funded research project — typically early-stage science, not a clinical trial accepting patient enrollment.
- Some NIH-funded labs run parallel clinical studies or seek volunteers for related work. To check, contact the principal investigator or institution listed above.
- For full project details, budget, and progress reports, visit the official NIH RePORTER page.