A neuron-specific interaction between Alzheimer’s disease risk factors SORL1, APOE, and CLU
Lee et al.1 report that loss of the Alzheimer's disease risk factor SORL1 results in neuron-specific reduction in APOE and CLU, altered lipid homeostasis, and increased Aβ levels and phosphorylated Tau, both rescued by stabilizing retromer or enhancing autophagy.