Low glucose metabolism worsened C9orf72-related ALS and FTD features in a study
Original source
Glucose hypometabolism prompts RAN translation and exacerbates C9orf72-related ALS/FTD phenotypes. (opens in a new tab)Compass summarised this from the study's abstract.
Study details
- Studied in
- Mouse, Cells
Related topics
A study found that reduced glucose metabolism activated a pathway that increased production of dipeptide repeat proteins linked to C9orf72-related amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). The changes impaired survival of neurons derived from people with C9orf72 expansions and caused motor problems in genetically modified mice.
Why this matters
The findings suggest that energy metabolism may contribute to C9orf72-related disease through a self-reinforcing process. They identify possible mechanisms for future research, but the study does not show that changing glucose metabolism benefits people or alters current treatment.
Limitations and context
The work was conducted in C9-BAC mice and patient-derived neurons, rather than in a clinical trial. It establishes a possible mechanism, not a treatment effect in people. The source is one primary research article, and the proposed therapeutic opportunities still require testing.