A single fibril study reveals that ApoE inhibits the elongation of Aβ42 fibrils in an isoform-dependent manner
Abstract ApoE-ε4 is the strongest genetic risk factor for late-onset Alzheimer’s disease (AD), linked to increased amyloid-β (Aβ) deposition in the brain. In AD mouse models, microglial expression of apoE3 reduces amyloid plaque burden through enhanced phagocytosis, whereas apoE4 is associated with...
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| Main Authors: | , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Nature Portfolio
2025-04-01
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| Series: | Communications Chemistry |
| Online Access: | https://doi.org/10.1038/s42004-025-01524-z |
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