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Cholesterol and Alzheimer’s Disease

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Abeta Peptide and Alzheimer’s Disease

Abstract

Recent studies indicate that cholesterol plays an important part in the regulation of amyloid-β peptide (Aβ) production, with high cholesterol levels being linked to increased Aβ generation and deposition. The mechanisms underlying the role(s) of cholesterol are not fully understood at present, but from the evidence currently available, it appears that there are many different ways in which abnormalities in cholesterol metabolism can affect the development of Alzheimer’s disease (AD). Polymorphisms in genes involved in cholesterol catabolism and transport have been associated with an increased level of Aβ and are therefore potential risk factors for the disease. The best known of these genes is the apolipoprotein E gene (apoE), which encodes a protein involved in cholesterol transport. The existence of a particular allele of apoE, ε4, is the major genetic risk factor known for late-onset AD. Other genes implicated include cholesterol 24-hydroxylase (Cyp46), the LDL receptor related protein (LRP), the cholesterol transporters ABCA1 and ABCA2, acyl-CoA:cholesterol acetyl transferase (ACAT), and the LDL receptor (LDLR).

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Cordy, J.M., Wolozin, B. (2007). Cholesterol and Alzheimer’s Disease. In: Barrow, C.J., Small, D.H. (eds) Abeta Peptide and Alzheimer’s Disease. Springer, London. https://doi.org/10.1007/978-1-84628-440-3_9

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