Alzheimer disease (AD),1,2 the most common cause of cognitive impairment, is characterized by β-amyloid (Aβ) plaques and tau neurofibrillary tangles, which lead to neuroinflammation, neurodegeneration, and cognitive decline.3,4 Although recent Aβ-targeting therapies offer hope,5 the complex nature of AD requires additional pharmacological and nonpharmacological interventions to prevent or delay cognitive impairment. This evidence concerns the gene MAPT and Cognitive impairment.