Targeting of GSK3 as a treatment for AD has been the focus of a number of investigations, given that chronically high levels of GSK3 activation have been detected in AD, and that elevated levels of GSK3 activity lead to pathogenic hyperphosphorylation of Tau protein (and in turn the deposition of neurofibrillary tangles), Aβ production, and marked cognitive deficits [176–180]. The gene discussed is MAPT; the disease is Cognitive impairment.