Abstract
APOE genotype, aging and midlife hypercholesterolemia are well-established risk factors for late-onset Alzheimer’s disease (AD). ApoE and cholesterol are involved in the pathogenesis of AD since they influence amyloid-β accumulation and Tau pathology. APOE ε4 carriers were found to present lower levels of amyloid-β1–42, higher tau and phosphorylated tau and a higher degree of brain atrophy at any disease stage. Presence of ApoE4 shifts the onset of the disease towards a younger age and makes progression faster. Hypercholesterolemia together with other major cardiovascular risk factors were found to be involved in the pathogenesis of AD, but reduced plasma cholesterol levels were described in demented patients. Significant correlations were found between cholesterol precursors lathosterol, lanosterol and 24S-hydroxycholesterol (a putative marker of brain cholesterol turnover) in plasma and brain atrophy as quantified by MRI. It is likely that neurodegeneration affects both brain and whole-body cholesterol metabolism in AD.
Published Version
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