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...
Saved in:
| Main Authors: | Sourav Dasadhikari, Shamasree Ghosh, Sudip Pal, Tuomas P. J. Knowles, Kanchan Garai |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Nature Portfolio
2025-04-01
|
| Series: | Communications Chemistry |
| Online Access: | https://doi.org/10.1038/s42004-025-01524-z |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
Similar Items
-
An O-glycopeptide participates in the formation of distinct Aβ42 fibril structures and attenuates Aβ42 neurotoxicity
by: Qijia Wei, et al.
Published: (2025-07-01) -
Identification of the primary peptide contaminant that inhibits fibrillation and toxicity in synthetic amyloid-β42.
by: Daniel J Adams, et al.
Published: (2017-01-01) -
Spectral Heterogeneity of Thioflavin T Binding to Aβ42:Aβ40 Mixed Fibrils: Implications for Alzheimer’s Disease Screening
by: Kiyo Fukase, et al.
Published: (2025-04-01) -
The p3 peptides (Aβ17-40/42) rapidly form amyloid fibrils that cross-seed with full-length Aβ
by: Yao Tian, et al.
Published: (2025-02-01) -
Bushen-Tiansui Formula Improves Cognitive Functions in an Aβ1–42 Fibril-Infused Rat Model of Alzheimer’s Disease
by: Chenxia Sheng, et al.
Published: (2020-01-01)