Chronic apigenin exposure extended median lifespan in wild-type C. elegans and improved multiple healthspan markers — pharyngeal pumping rate, locomotor activity, and macromolecular damage accumulation — according to this new study. RNA-seq transcriptomic profiling revealed that apigenin primarily modulated redox-sensitive stress signalling and cellular homeostasis pathways. Crucially, in transgenic worms engineered to express human amyloid-beta or tau proteins, apigenin similarly extended lifespan and attenuated the functional impairments caused by Alzheimer's-associated proteotoxicity.
Apigenin is a flavone found abundantly in parsley, celery, chamomile tea, and other common foods, and has attracted growing interest as a senolytic and anti-inflammatory nutraceutical. This C. elegans work adds mechanistic detail — pointing to oxidative stress reduction as a core pathway — consistent with earlier mammalian cell and rodent findings. However, the gulf between a nematode and a human brain is enormous: C. elegans lacks a vascular system, an adaptive immune response, and the neuroanatomical complexity relevant to Alzheimer's disease. Effect sizes and optimal dosages in humans remain entirely unknown. This is also a preprint posted on bioRxiv and has not yet undergone peer review, meaning findings and interpretations may change substantially. For now, the work is hypothesis-generating rather than practice-changing — reinforcing apigenin as a compound worth investigating in higher organisms, but offering no grounds for supplementation recommendations.