ApoE-ε4 is the strongest genetic risk factor for late-onset Alzheimer’s disease, linked to increased amyloid-β deposition, however, the molecular mechanism underpinning the pathological role of apoE4 is still unclear. Here, the authors use advanced microscopy techniques to reveal that apoE4 is less effective in inhibiting Aβ42 fibril elongation and exhibits reduced affinity for the growing fibril ends, suggesting a mechanism for impaired microglial clearance and increased amyloid deposition in ApoE-ε4 carriers.
- Sourav Dasadhikari
- Shamasree Ghosh
- Kanchan Garai
