A study links higher neuronal TAF15 to oxidative stress in ALS and FTD
Original source
Elevated neuronal TAF15 expression induces oxidative stress and anxiety-related behavioral deficits. (opens in a new tab)Compass summarised this from the study's abstract.
Study details
- Studied in
- Human, Mouse
Population inferred from the title and abstract by Compass.
Higher levels of the protein TAF15 were found in prefrontal cortex neurons from people with multiple frontotemporal dementia and amyotrophic lateral sclerosis subtypes. In cell and mouse experiments, increasing neuronal TAF15 caused oxidative stress, nerve-cell toxicity and inflammation-like changes in supporting brain cells. An antioxidant, N-acetylcysteine amide, reversed these effects in the experiments. [S1]
Why this matters
The findings identify a possible link between TAF15 and oxidative stress in neurodegeneration. However, the treatment-related result was shown in laboratory and mouse experiments, not in people, so it does not currently change ALS treatment. [S1]
Limitations and context
This is one primary research report. The experimental results came from cells and mice, and the human finding was an observation of TAF15 levels in brain tissue. The study does not establish that TAF15 causes ALS in people or that N-acetylcysteine amide is safe or effective as an ALS treatment. [S1]