Editing Openai/692df380-fd64-8008-b788-94e93ef3ff89 (section)

===== 3.3 Aging, neuromuscular function, and geroscience-specific data =====
* In a chronic inflammation/aging mouse model, elevated neurotoxic kynurenines (3-HK, QUIN) were shown to mediate neuromuscular dysfunction; treating motor neurons with these metabolites induced neurite degeneration. JCI Insight<ref>{{cite web|title=JCI Insight|url=https://insight.jci.org/articles/view/136091|publisher=JCI Insight|access-date=2025-12-28}}</ref>
* A 2025 review argues that age-related KP dysregulation—shifting toward the KMO branch—may be a driver of habituation and learning deficits with aging. MDPI<ref>{{cite web|title=MDPI|url=https://www.mdpi.com/2073-4409/14/22/1786|publisher=mdpi.com|access-date=2025-12-28}}</ref>
* In C. elegans, downregulation of several KP enzymes (TDO, KYNU, HAAO) extends lifespan and improves late-life function; the common theme is reduced production of downstream oxidative/excitotoxic metabolites. Nature<ref>{{cite web|title=Nature|url=https://www.nature.com/articles/s41467-023-43527-1|publisher=nature.com|access-date=2025-12-28}}</ref>

But: there is no direct demonstration that KMO inhibition in otherwise healthy mammals extends lifespan or compresses morbidity.