Genetic deletion of phosphatidylinositol transfer protein-1 (pitp-1) extended lifespan in C. elegans worms while improving age-related mobility decline and oxidative stress resistance. The longevity benefits occurred specifically when pitp-1 was suppressed in neurons during early adulthood, working through reduced TOR signaling activity as measured by decreased S6 kinase phosphorylation. The protein also enhanced proteostasis by reducing toxic polyglutamine aggregation in neuronal models. This discovery illuminates a previously unknown intersection between lipid metabolism and aging regulation. PITP-1 appears to function as a molecular hub where insulin/IGF-1 signaling converges with mTOR pathways—two of the most conserved longevity mechanisms across species. The neuronal specificity suggests brain lipid metabolism may be particularly crucial for systemic aging control, challenging traditional views that peripheral tissues drive longevity. While conducted in worms, the conservation of both insulin/IGF-1 and mTOR pathways across evolution makes this finding potentially translatable. The protein's role in coordinating multiple aging pathways rather than operating independently represents a more sophisticated model of longevity regulation, though human relevance requires validation in mammalian systems.