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Elucidating the role of SORL1 as an APOE receptor using iPSC‐derived astrocytes

Apolipoprotein E (APOE), the strongest genetic risk factor in late‐onset AD (LOAD), encodes a protein that can interact with Aβ and regulate its clearance. Interestingly, SORL1, another AD risk gene, belongs to the family of APOE receptors involved in Aβ clearance. SORL1 is the only APOE receptor gene that has been identified as a genetic risk factor in LOAD. Recent studies identified SORL1 loss‐of‐function variants in familial AD patients, suggesting that SORL1 may be a causal gene for AD. Here, we investigated the potential convergent mechanisms of APOE and SORL1 function in the brain by examining the novel function of SORL1 in human astrocytes in Aβ clearance.