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• W2941035059 abstract "Abstract Aging increases the risk of Alzheimer’s disease (AD). During normal aging synapses decline and β-Amyloid (Aβ) accumulates. An Aβ defective clearance with aging is postulated as responsible for Aβ accumulation, although a role for increased Aβ production with aging can also lead to Aβ accumulation. To test this hypothesis, we established a long-term culture of primary mouse neurons that mimics neuronal aging (lysosomal lipofuscin accumulation and synapse decline). Intracellular endogenous Aβ42 accumulated in aged neurites due to increased amyloid-precursor protein (APP) processing. We show that APP processing is up-regulated by a specific age-dependent increase in APP endocytosis. Endocytosed APP accumulated in early endosomes that, in turn were found augmented in aged neurites. APP processing and early endosomes up-regulation was recapitulated in vivo. Finally, we found that inhibition of Aβ production reduced the decline in synapses in aged neurons. We propose that potentiation of APP endocytosis by neuronal aging increases Aβ production, which contributes to aging-dependent decline in synapses. Summary How aging increases the risk of Alzheimer’s disease is not clear. We show that normal neuronal aging increases the intracellular production of β-amyloid, due to an upregulation of the amyloid precursor protein endocytosis. Importantly, increased Aβ production contributes to the aging-dependent synapse loss." @default.
• W2941035059 created "2019-05-03" @default.
• W2941035059 creator A5006317491 @default.
• W2941035059 creator A5022064838 @default.
• W2941035059 creator A5063042058 @default.
• W2941035059 creator A5083395399 @default.
• W2941035059 date "2019-04-23" @default.
• W2941035059 modified "2023-09-23" @default.
• W2941035059 title "Neuronal aging potentiates beta-amyloid generation via amyloid precursor protein endocytosis" @default.
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