Many researches have indicated that APα promoted the proliferation of neural progenitor cells (NPCs) and restored the cognitive function of Alzheimer’s disease (AD) mice, as well as prevented the loss of tyrosine hydroxylase (TH, a rate-limiting enzyme for dopamine biosynthesis)-positive neurons in the SN pars compacta (SNpc) and their neural fibers in the striatum and ameliorated the deficits of motor performance in MPTP-injected mice (Wang et al., 2005, 2010; Wang and Brinton, 2008; Adeosun et al., 2012; Singh et al., 2012; Sun et al., 2012; Wang, 2014; Zhang et al., 2015). The gene discussed is TH; the disease is Alzheimer disease.