Specifically, the LC has been suggested to be one of the initial sites of appearance of pathologically altered tau aggregates in preclinical stages of Alzheimer’s disease (AD) (Braak et al., 2011; Braak & Del Tredici, 2015; Zarow et al., 2003), leading to compensatory increases in α2A adrenergic receptor levels in regions receiving noradrenergic input (Andrés-Benito et al., 2017). This evidence concerns the gene MAPT and Alzheimer disease.