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Co-aggregation With Apolipoprotein E Modulates The Function Of Amyloid-β In Alzheimer’s Disease

Zengjie Xia, Emily Prescott, Tom Leah, Helen Dakin, Eleni Dimou, Eric Zuo, Yu P. Zhang, Jeff Y.L. Lam, John S. H. Danial, Hong Jiang, Heather Mortiboys, Peter Thornton, Damian C. Crowther, David M. Holtzman, Rohan T. Ranasinghe, David Klenerman, Suman De

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AbstractIsoforms of Apolipoprotein E (ApoE) determine our risk of developing late-onset Alzheimer’s Disease (AD), but the mechanism underlying this link is poorly understood. In particular, the relevance of direct interactions between ApoE and Amyloid-β (Aβ) remains controversial. Here, single-molecule imaging shows that in the early stages of aggregation, all isoforms of ApoE associate with Aβ in large co-aggregates, but then fall away as fibrillation happens. Similar large co-aggregates exist in the brains of AD patients, accounting for around 50% of the mass of aggregated Aβ detected in the frontal cortices of homozygotes with the higher-risk APOE4 gene. The cellular uptake and toxicity of these large co-aggregates are isoform-dependent, suggesting a mechanistic role for ApoE-Aβ interactions in AD.