Human blood marker points to a compound that slows ALS in mice
Amyotrophic lateral sclerosis (ALS) is a severe neurological disease that destroys nerve cells responsible for muscle movement. The disease typically begins with limb or bulbar weakness and progresses to respiratory failure. Current treatments only modestly slow progression, underscoring the urgent need for more effective therapies.
A blood marker called N-acyl taurines (NATs) has been linked to the progression of amyotrophic lateral sclerosis (ALS), a severe neurological disease that destroys nerve cells responsible for muscle movement. Researchers at Nagoya University in Japan discovered that higher levels of NATs correlate with faster disease progression and shorter survival times in ALS patients.
They also found that PF-04457845, a compound already deemed safe for human use, can slow motor decline in ALS mouse models. This compound, which blocks an enzyme that breaks down NATs, reduced neurodegeneration, improved motor function, and extended the lifespan of ALS mice. The study, published in JCI Insight, suggests that boosting NAT levels with medication could help protect nerve cells and that PF-04457845 and other medications targeting NATs and the endocannabinoid system could be potential therapies for ALS.
Further research is planned to assess NAT as a practical biomarker for disease severity and treatment response.
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