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A neuron-specific interaction between Alzheimer's disease risk factors SORL1, APOE, and CLU
Pranav Preman1, Amaia M Arranz2
1VIB 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.
Abstract:
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.
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