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Amyloid precursor protein (APP) is central to Alzheimer's disease (AD) by its role in Aβ build-up and in neuronal and astrocytic malfunction. The major risk factor for late-onset AD is aging, which increases APP processing in both neurons and astrocytes, and consequently increases Aβ production. This focused review covers the subjects of how aging and AD affect APP dynamics within the both cell types and how astrocytes dysfunction can enhance neuroinflammation and neuronal dysfunction and injury. We discuss the interplay between neurons and astrocytes in aging and AD brains, where bi-directional cellular interactions accelerate neurodegeneration.
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Jáuregui et al. (2025) studied this question.
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