Blocking a protein reduced nerve cell degeneration in mice
Experiments in aged mice and mouse models of amyotrophic lateral sclerosis found less nervous system inflammation and degeneration after researchers deleted or inhibited the protein.
Limit: Sample sizes and numerical effect sizes are missing from the abstract
Edited by Boris Djordjevic · AgingResearch.News
In experiments in aged mice and mice used to model amyotrophic lateral sclerosis (ALS), researchers tested OTUB2, a protein involved in inflammatory signaling. ALS is a disease that damages nerve cells controlling movement. The researchers deleted the gene for OTUB2 or used a compound to inhibit the protein.
Both approaches reduced inflammation in the nervous system and nerve cell degeneration in the ALS and aged mouse models. Biochemical tests found that OTUB2 helped assemble a protein complex that relays inflammatory signals. The authors identified OTUB2 as a potential drug target for nervous system inflammation and degeneration.
Why it matters
Chronic inflammatory signaling contributes to nerve cell degeneration during aging. This work addressed how that signaling is regulated, a question relevant to the search for ways to limit age-related nervous system damage.
Caveats
Mouse experiments do not establish whether blocking OTUB2 would benefit people. The abstract does not report sample sizes, inhibitor doses or treatment durations, or numerical effect sizes.