Abstract
Recent evidence implicated aberrant mammalian target of rapamycin (mTOR)-dependent signaling in both Alzheimer's disease (AD) and brain tumors. This review focuses on the potential mechanisms shared by both neurodegeneration and carcinogenesis. In particular, attention was paid to the possible roles of mTOR-dependent signaling in these two fundamental pathophysiological processes. We hypothesize that common stresses could lead either to progressive degeneration or uncontrolled carcinogenesis via cell type specific upregulation of mTOR-dependent signaling in the central nervous system while mTOR-mediated carcinogenesis might permit glial cells to escape from degeneration.