Harmful tau protein changes after brain injury and vascular dementia
Official title: Cis proline directed proteotoxicity in the early development and therapy of traumatic brain injury and vascular dementia
Funded at Beth Israel Deaconess Medical Center · NIH-11173784 · Data updated 2026-11-12
This project will try blocking a harmful form of tau protein and boosting a protective neuron response to help people with traumatic brain injury or vascular-related dementia.
Quick facts
| Grant type | NIH-funded research |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Beth Israel Deaconess Medical Center NIH-funded |
| Lab location | 1 site (Boston, United States) |
| Project start | September 1, 2022 |
| Project end | August 31, 2027 |
| Funding year | 2025 |
| Award (this year) | $243,917 |
| NIH project number | 5R00AG076739-04 |
| Project ID | NIH-11173784 on NIH RePORTER |
Who could benefit from this research
✓Could help
People who have had a recent traumatic brain injury or who have vascular-related cognitive impairment or dementia and who are willing to provide clinical data or samples would be the best candidates to participate or contribute.
✕Less likely to help
Patients whose cognitive decline is driven by unrelated mechanisms or who cannot or will not participate in research may not directly benefit from this project.
What this research studies
Researchers are focusing on an early toxic form of the tau protein called cis P-tau that appears after traumatic brain injury or reduced blood flow to the brain. They will study how the enzyme JNK3 makes cis P-tau and how a neuron-protective response driven by REST might oppose this damage. Work will use cell experiments, mouse models of TBI and vascular dementia, and samples or data from patients across mentored (K99) and independent (R00) phases. Later work will test whether blocking JNK3 activity or restoring REST can reduce tau damage and protect brain cells in chronic stages.
Why it matters
Potential benefit: If successful, this could lead to treatments that reduce early tau-related damage and slow or prevent cognitive decline after brain injury or vascular dementia.
How similar studies have gone: Prior research has identified cis P-tau as an early toxic tau form in TBI and Alzheimer’s, but targeting JNK3 and boosting REST is a newer therapeutic approach still mainly tested in preclinical models.
Where this research is happening
-
Beth Israel Deaconess Medical Center
Boston, United States Active
Researchers
- Principal investigator: Qiu, Chenxi — Beth Israel Deaconess Medical Center
- Study coordinator: Qiu, Chenxi
Related research
Other NIH-funded projects on the same topics.
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Cis-proline tau toxicity in brain injury and dementia
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Investigating how a specific protein contributes to brain damage in Alzheimer's and related conditions
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This study is looking at how a traumatic brain injury (TBI) might increase the chances of developing dementia, and it’s for anyone who has had a TBI and wants to help us understand how it affects brain health over time.
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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.