A neuron-specific interaction between Alzheimer’s disease risk factors SORL1, APOE, and CLU
Pranav Preman,
Amaia M. Arranz
Affiliations
Pranav Preman
VIB Center for Brain & Disease Research, Leuven, Belgium; Laboratory for the Research of Neurodegenerative Diseases, Department of Neurosciences, Leuven Brain Institute (LBI), KU Leuven (University of Leuven), Leuven, Belgium
Amaia M. Arranz
Achucarro Basque Center for Neuroscience, Leioa, Spain; Ikerbasque Basque Foundation for Science, Bilbao, Spain; Corresponding author
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.
