Aβ42 oligomers trigger synaptic loss through CAMKK2-AMPK-dependent effectors coordinating mitochondrial fission and mitophagy

During the early stages of Alzheimer's disease (AD) in both mouse models and human patients, soluble forms of Amyloidβ1-42 oligomers (Aβ42o) trigger loss of excitatory synapses (synaptotoxicity) in cortical and hippocampal pyramidal neurons (PNs) prior to the formation of insoluble Aβ plaques....

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Bibliographic Details
Published in:	bioRxiv
Main Authors:	Lee, Annie, Kondapalli, Chandana, Virga, Daniel M, Lewis, Tommy L, Koo, So Yeon, Ashok, Archana, Mairet-Coello, Georges, Herzig, Sebastien, Shaw, Reuben, Sproul, Andrew, Polleux, Franck
Format:	Paper
Language:	English
Published:	Cold Spring Harbor Cold Spring Harbor Laboratory Press 14.05.2019 Cold Spring Harbor Laboratory
Edition:	1.1
Subjects:	Alzheimer's disease Animal models Cortex (entorhinal) CRISPR Dendrites Genomes Hippocampus Homeostasis Mitochondria Mitophagy Neurodegenerative diseases Neuroscience Pyramidal cells Senile plaques Serine Tau protein
ISSN:	2692-8205, 2692-8205
Online Access:	Get full text
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