NIH-funded research R01 grant

How the Sec20 protein affects nerve cells and may relate to ALS and frontotemporal dementia

Official title: Functional role of Sec20, a BH3 and Secretory (Sec) domain protein, in neurons and its relevance to a motor neuron disease in Drosophila

Funded at University of Alabama at Birmingham · NIH-10829253 · Data updated 2026-11-12

This project looks at whether changes in the Sec20 protein cause nerve cell damage through mitochondrial and recycling (autophagy) problems that link to adult-onset ALS and frontotemporal dementia.

More Motor Neuron Disease research and trials

Quick facts

Grant typeR01 grant
Study typeNIH-funded research
Funding institutionUniversity of Alabama at Birmingham
NIH-funded
Lab location1 site (Birmingham, United States)
Project startApril 15, 2023
Project endMarch 31, 2028
Funding year2026
Award (this year)$469,350
NIH project number4R01NS131315-03
Project IDNIH-10829253 on NIH RePORTER

Who could benefit from this research

Could help

Adults with ALS or frontotemporal dementia, especially those known to carry the C9orf72 repeat expansion, would be most directly relevant to these findings.

Less likely to help

People without ALS/FTD or whose disease is driven by unrelated causes are unlikely to see direct benefit from this laboratory research in the near term.

What this research studies

From a patient's perspective, researchers are using fruit flies to see how Sec20 works in nerve cells and why losing it leads to motor problems and neuron loss. They will compare those effects to damage caused by the C9orf72 G4C2 repeat expansion, a common genetic cause of ALS-FTD, to see how the two interact. The team will study mitochondria, autophagy pathways, and neuronal survival using genetic and molecular experiments in the lab. Results will be used to connect fly findings to the human BNIP1/Sec20 pathway and help explain disease mechanisms.

Why it matters

Potential benefit: If successful, this could reveal a new disease pathway and point to targets for therapies that protect motor neurons in ALS and FTD.

How similar studies have gone: Previous studies have linked mitochondrial and autophagy dysfunction and C9orf72 repeats to ALS/FTD, but the specific role of Sec20/BNIP1 in this pathway is a newer and less-tested area.

Where this research is happening

  • University of Alabama at Birmingham
    Birmingham, United States
    Active

Researchers

  • Principal investigator: Bhat, Krishna Moorthi — University of Alabama at Birmingham
  • Study coordinator: Bhat, Krishna Moorthi

Related research

Other NIH-funded projects on the same topics.

About this research

  1. This is an active NIH-funded research project — typically early-stage science, not a clinical trial accepting patient enrollment.
  2. Some NIH-funded labs run parallel clinical studies or seek volunteers for related work. To check, contact the principal investigator or institution listed above.
  3. For full project details, budget, and progress reports, visit the official NIH RePORTER page.
Last reviewed 2026-11-14 by the Find a Trial editorial team. Information on this page is for educational purposes and is not medical advice. Always consult qualified healthcare professionals about clinical trial participation.