Recent efforts to study age-related neurodegeneration using hPSC-derived MGLs rely on inserting genetic Alzheimer’s disease risk variants into the genome of hiPSCs before differentiating them into MGLs, or coculturing MGLs with brain organoids derived from hiPSCs with APP mutations for extended culture periods, resulting in overt amyloid pathology (Table 3). The gene discussed is APP; the disease is amyloidosis.