For example, neuronal stress imposed by a variety of neurological conditions [32], which are associated with increased risk for development of AD, results in overexpression of APP, release of sAPP, glial activation, and overexpression of IL-1 for genesis of each of the precursors of the neuropathological changes of AD, implying that overexpression of APP starts a cascade of events that gives rise to Aβ deposition rather than Aβ being seminal in Alzheimer pathogenesis. The gene discussed is IL1A; the disease is Alzheimer disease.