Schematic illustration of a hypothetic biological model for the inverse epidemiological association between Alzheimer’s disease (AD) and cancer in the elderly. In AD, degenerative as well as aberrant proliferative/regenerative responses are enhanced in the brain relative to normal aging. The former manifests as neuronal death and synaptic loss, which may be caused by neurotoxic molecules (e.g., Aβ and phosphorylated tau, inflammatory factors) overproduced in the brain. The later could be derived from maladapted regenerative changes including cell cycle reentry, glial proliferation and aberrant neuroplasticity, which can lead to the production of the above-mentioned neurotoxic products or may directly cause neuronal death. The vicious neuropathological cycle is maintained in the brain at the expense of body’s biosynthetic resources (energy and nutrients) for other cellular system, which can reduce the propensity for tumorogenesis because of a mutual competition (the balance point shifting to a pro-AD pathogenic trend). An opposite flow of the body’s biosynthetic resources occurs in the event of cancer development. The propensity of uncontrolled cancer cell replication deprives the body’s biosynthetic resources, including that for the anabolic activity driving the aberrant regenerative burden (the balance point shifting to pro-cancer pathogenic tendency). Consistent with the above biological mechanism, anti-cancer drugs may mitigate AD-type neuropathology, given that their anti-proliferative pharmacological efficacy would relieve the burden of aberrant neural regeneration, and thus slows down vicious pathogenic cycle.