In individuals with dominantly inherited Alzheimer’s disease, CSF Tau begins to increase 15 years before symptom onset, while Aβ42 begins to decline over 20 years prior to symptom onset.1,2 Until a recent report of lecanemab,3 clinical trials of anti-amyloid monoclonal antibodies,4-6 secretase inhibitors,7,8 and anti-tau monoclonal antibodies9,10 have had limited success for disease modification in patients with symptomatic Alzheimer’s disease. This evidence concerns the gene MAPT and Alzheimer disease.