Supplementation with S-adenosylhomocysteine (SAH) extends the lifespan of model organisms. To explore the impact of SAH on aging, we generated a Caenorhabditis elegans model with increased SAH levels through pathogenic mutation in the S-adenosylhomocysteine hydrolase (AHCY), which impairs SAH hydrolysis to adenosine and homocysteine. We showed that animals with an endogenous mutation leading to pathogenic AHCY Y145C exhibited delayed aging accompanied by increased SAH and reduced SAM levels. The extended longevity of these animals required AMP-activated protein kinase (AMPK). Our results demonstrate the potential of AHCY mutant worms as a tool to study SAH influence on aging and point to the SAM:SAH ratio as a potential determinant of C. elegans lifespan.