Reduction in Levels of 24S-Hydroxycholesterol by Statin Treatment in Patients With Alzheimer Disease

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Abstract
ALZHEIMER DISEASE (AD) is the most common late-life dementing illness.1 A central event in the development of AD is thought to be abnormal processing of the cell membrane–associated amyloid precursor protein followed by deposition of toxic β-amyloid protein in the form of amyloid plaques in the extracellular space of the neocortex.2 It has been demonstrated that amyloid plaques contain apolipoprotein E (apo E), a lipid transporter. It has also been shown that there is a higher frequency of the apo E allele named ϵ4 in patients with AD than in the general population (allele frequency of 40% vs 15%).3 However, the mechanism of this association is still poorly understood at the molecular level. Another emerging lipid candidate for AD risk is the level of 24S-hydroxycholesterol in plasma.4