Intraneuronal accumulation of Aβ in the basal forebrain has been suggested to be an early event in the progression of AD-associated neuropathology (Arendt et al., 1988; Billings et al., 2005; LaFerla et al., 2007; Gouras et al., 2010; Baker-Nigh et al., 2015; Takahashi et al., 2017), and we report that reduction of ChAT expression in the post-mortem human basal forebrain of individuals with AUD was accompanied by increased Aβ1–42 immunoreactive cells, consistent with increased intraneuronal expression of Aβ1–42 in cholinergic neurons. This evidence concerns the gene CHAT and Alzheimer disease.