In our earlier study [25], we started to assess the effects of chronic SHS exposure (10 months to ~30 mg/m3) on behavioral and cognitive performance, metabolism, and neuropathology in 2-month-old wild-type (WT) mice and mice expressing wild-type human tau, a genetic model pertinent to Alzheimer’s disease in which there is a spread of neurofibrillary tangles, consisting of hyperphosphorylated tau aggregates, that is associated with disease severity [26,27]. The gene discussed is MAPT; the disease is Alzheimer disease.