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Deletion of the gene encoding ABCA1, responsible for lipidating ApoE in the CNS, resulted in an increase in Aβ deposition (Wahrle et al., 2005) Conversely, overexpression of ABCA1 resulted in a decrease in Aβ deposition (Wahrle et al., 2008) in amyloid mouse models, suggesting that increasing ApoE lipidation can reduce Aβ pathology

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