Although these disturbances can often be compensated, at least for a while, to maintain homeostasis, they also profoundly impair the cellular stress responses leading to vulnerability toward other non-specific (e.g., neuroinflammation) and “AD-specific” (Aβ peptides, p-tau) toxicity, with the caveat that the term “AD-specific” may be misleading, as accumulation of Aβ plaques and p-tau tangles appear to be part of the normal aging process and are not necessarily tightly associated with dementia (Braak and Braak, 1997; Price et al., 2009; Rodrigue et al., 2012). The gene discussed is MAPT; the disease is dementia.