How TBK1 helps neurons clear damaged proteins in dementia and ALS
Defining TBK1-associated autophagy networks in neurons
This project looks at how a protein called TBK1 helps brain cells clear damaged proteins and how that relates to frontotemporal dementia, ALS, and related Alzheimer-type conditions.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of California, San Francisco NIH-funded |
| Lab location | 1 site (San Francisco, United States) |
| Project ID | NIH-11314614 on NIH RePORTER |
What this research studies
Researchers will map how TBK1 controls autophagy, the cell's cleanup process, in neurons. They will use lab-grown neurons and detailed protein-level mapping (phospho-proteomics) to find which proteins and pathways change when TBK1 function is reduced. The team will study interactions with proteins like optineurin that guide selective autophagy and test how these changes lead to neuron damage. Results are intended to reveal the molecular steps that cause neuron loss in FTD and ALS and point to possible targets for future therapies.
Who could benefit from this research
Good fit: People with frontotemporal dementia, ALS, or known TBK1 or OPTN genetic changes, and those willing to donate blood or tissue samples for research, would be most relevant.
Not a fit: Patients without FTD/ALS or without TBK1/OPTN-related disease are unlikely to see direct benefits from this basic laboratory research in the near term.
Why it matters
Potential benefit: If successful, this work could reveal targets or strategies to slow or prevent neuron loss in FTD, ALS, and related dementias.
How similar studies have performed: Prior research has linked TBK1 and optineurin to neurodegeneration and autophagy, but detailed maps of TBK1-controlled networks in neurons remain novel and are still being developed.
Where this research is happening
San Francisco, United States
- University of California, San Francisco — San Francisco, United States (Active)
Researchers
- Principal investigator: Mordes, Daniel Adam — University of California, San Francisco
- Study coordinator: Mordes, Daniel Adam
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 below.