Normally, TGFβ is involved in the self-renewal and maintenance of NSCs, but in the diseased brain, altered TGFβ levels are evident as in Alzheimer's disease where amyloid-beta plaques and tau tangles interfere with TGFβ signaling in NSCs, and reduced TGFβ signaling may lead to a decrease in the self-renewal capacity of NSCs, impairing the brain's ability to regenerate neurons and repair damaged neural tissue and contributing to the progressive loss of cognitive function (Meyers and Kessler 2017). The gene discussed is TGFB1; the disease is Alzheimer disease.