AD is characterized by the accumulation of abnormal proteins, including amyloid beta (Aβ) and phosphorylated tau (p-tau), in addition to total tau (t-tau), a marker of neurodegeneration in the brain.4 Recently, disease-modifying therapies have been approved for treatment of early AD, with demonstrated efficacy in reducing amyloid burden.5 With AD being the most frequent form of dementia and the most common neurodegenerative disease worldwide,6 these therapies provide hope for patients and clinicians, with potential public health implications.7 This evidence concerns the gene MAPT and Alzheimer disease.