How SUMO protein changes affect Tau, brain energy, and connections in frontotemporal dementia

Role of SUMOylation in Mitochondrial/Synaptic Axis Dysfunction Induced by Abnormal Tau in FTD

NIH-funded research Columbia University Health Sciences · NIH-11169869

The team will test whether changing small SUMO protein tags can reduce harmful Tau clumping and improve brain cell energy and connections in frontotemporal dementia using animal models and neurons made from patient cells.

Quick facts

Grant typeNIH-funded research
Study typeNIH-funded research
Funding institutionColumbia University Health Sciences NIH-funded
Lab location1 site (New York, United States)
Project IDNIH-11169869 on NIH RePORTER

What this research studies

Researchers will use mice that carry a disease-causing Tau mutation and neurons grown from people with Tau mutations to study how SUMO protein tagging changes Tau behavior. They will compare the effects of different SUMO types (SUMO1 versus SUMO2/3) on Tau clumping, mitochondrial respiratory chain enzyme activities, and synaptic signaling. The team will boost SUMO2 in models that show reduced SUMO2 and increased SUMO1 to see if that restores mitochondrial and synaptic function. Findings from these experiments could guide approaches that target SUMOylation in human disease.

Who could benefit from this research

Good fit: People with frontotemporal dementia, especially those known to carry Tau (MAPT) mutations or who are willing to provide cells or biospecimens for research, would be the most directly relevant group.

Not a fit: People whose dementia is not driven by Tau-related problems or who do not carry Tau mutations may be less likely to benefit directly from this line of work.

Why it matters

Potential benefit: If successful, this work could point to new strategies to reduce harmful Tau aggregation and improve brain energy use and connectivity for people with frontotemporal dementia.

How similar studies have performed: Prior laboratory and animal-model work indicates SUMO1 can promote Tau aggregation while SUMO2 can reduce it and improve mitochondrial measures, but applying these findings toward human treatments remains novel.

Where this research is happening

New York, United States

Researchers

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 below.
Conditions Alzheimer disease dementiaAlzheimer syndromeAlzheimer's Disease
Last reviewed 2026-06-13 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.