Apigenin in C. elegans: longer median lifespan and protection in Alzheimer's protein models
In the abstract, chronic apigenin exposure extended median lifespan and improved healthspan readouts in wild-type C. elegans and in worms expressing amyloid-beta or tau; effects are described as partly linked to reduced oxidative stress signaling. [1]
Automatic summary · not editorially reviewed
The key findings
In wild-type C. elegans, chronic apigenin exposure extended median lifespan and improved pharyngeal pumping, locomotor activity and age-related macromolecular damage measures. [1]
Reporter strains and RNA-seq indicated apigenin mainly modulated redox-sensitive stress signaling and cellular homeostasis pathways in aging animals. [1]
In transgenic strains expressing amyloid-beta or tau, apigenin showed similar benefits on lifespan, healthspan and proteotoxicity-linked impairments. [1]
The source at a glance
- Study type / format
- Preclinical animal study (abstract)
- Population / context
- Wild-type and transgenic C. elegans strains, including strains expressing amyloid-beta or tau
- Summary based on
- Study abstract
- Publication status
- Preprint · peer-review status not confirmed
- Original publication
- September 29, 2026
Apigenin tested in wild-type C. elegans lifespan assays
The abstract describes apigenin as an abundant plant compound with reported neuroprotective effects in age-related disease models, but says its healthspan effects and mechanisms were not thoroughly studied. The researchers ran lifespan assays together with measures of aging-relevant physiological function in wild-type C. elegans. Chronic exposure extended median lifespan and improved several healthspan readouts: pharyngeal pumping, locomotor activity and accumulation of age-related macromolecular damage.
Supporting source [1]
Redox signaling and Alzheimer's protein strains in the abstract
Reporter strains and RNA-seq profiling indicated that apigenin mainly modulated redox-sensitive stress signaling and pathways tied to cellular homeostasis in aging animals. In transgenic strains expressing the Alzheimer's-associated proteins amyloid-beta or tau, apigenin showed similar beneficial effects on lifespan, healthspan and functional impairments linked to proteotoxicity. The abstract frames apigenin as a potential healthspan-promoting intervention acting in part through reduced oxidative stress-associated signaling.
Supporting source [1]
Worm-only evidence; abstract scope limits conclusions
All reported results come from C. elegans, a nematode worm, not from humans. The abstract does not report sample sizes, follow-up durations, effect sizes or statistical uncertainty. It was the only text reviewed; the full text was not reviewed. The findings are associations in an animal model and do not establish that apigenin prevents Alzheimer's disease or extends human lifespan.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. All results are from C. elegans; sample sizes, follow-up, effect sizes and statistical uncertainty are not reported. Animal-model associations do not show human benefit.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Grant RA, Park LHE, Wahl D, LaRocca TJ. · europepmc.org · September 29, 2026