Targeted knockdown of mTOR specifically within touch receptor neurons in C. elegans reduced ectopic neurite sprouting—abnormal neural branch formation that occurs with aging—without affecting overall lifespan. Pan-somatic mTOR knockdown during adulthood showed no robust effects on either neuronal morphology or longevity, demonstrating that mTOR's neuronal aging effects operate through cell-intrinsic mechanisms rather than systemic pathways. This finding represents a significant advance in understanding how mTOR's dual roles—as both a longevity regulator and neuronal aging promoter—can be mechanistically separated. The research suggests that while mTOR inhibition can preserve specific aspects of neuronal health during aging, these benefits don't automatically translate to lifespan extension. This has important implications for therapeutic strategies targeting age-related neurodegeneration. The cell-type-specific approach reveals that mTOR's effects on brain aging may be more nuanced than previously understood, operating through distinct pathways in different tissues. However, the study's limitation to a simple model organism and focus on morphological rather than functional outcomes means clinical relevance remains to be established in mammalian systems.