In humans, genetic variation in Cntnap5 is associated with risk for Alzheimer's disease and bipolar disorder, while its deletion is associated with autism and dyslexia, suggesting the possibility that common pathways may come into play among different neurobiological disorders (Pagnamenta et al., 2010; Xu et al., 2014; Schott et al., 2016). This evidence concerns the gene CNTNAP5 and early-onset autosomal dominant Alzheimer disease.