Amyloid-β, which is implicated in the pathogenesis of Alzheimer's disease, is generated from the sequential cleavage of the amyloid precursor protein (APP) by β- and γ-secretase, aprocessthatisbelievedtooccurinendosomes. Neuronalactivitycanincreaseamyloid-β generationbuttheunderlyingmechanismisunclear. Here, theauthorsshowthatdepletionofactivity-regulatedcytoskeleton-associatedprotein (ARC) inAlzheimer'sdiseasemicepreventsactivity-inducedamyloid-β production. Moreover, ARCcausesincreasedcolocalizationofAPPandγ-secretaseinpostsynapticendosomes, potentiallyfacilitatingAPPcleavageandhenceamyloid-β production.
ORIGINAL RESEARCH PAPER
Wu, J. et al. Arc/Arg3.1 regulates an endosomal pathway essential for activity-depedent β-amyloid generation. Cell 147, 615–628 (2011)
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Yates, D. A pathogenic role for ARC?. Nat Rev Neurosci 12, 706 (2011). https://doi.org/10.1038/nrn3147
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DOI: https://doi.org/10.1038/nrn3147
