Given that only a small portion (∼10%) of early‐onset amyloid‐positive AD (EOAD, <65 years age of onset) is accounted for by identified pathogenic variants in the amyloid precursor protein (APP), presenilin 1 (PSEN1), or presenilin 2 (PSEN2) genes, a proportion of EOAD cases may be attributed to an extreme enrichment of late‐onset AD (LOAD, ≥65 years age of onset) genetic risk factors, leading to younger age of onset.5, 11. This evidence concerns the gene PSEN1 and amyloid positivity.