Abstract
Recent studies have provided evidence toward the possible involvement of brain cholesterol homeostasis in late-onset Alzheimer's disease (LOAD). We analyzed an intronic T → C substitution (rs 754203) of the cholesterol 24S-hydroxylase (CYP46) gene, encoding an enzyme acting on brain cholesterol turnover, which has been recently associated with an increased risk of AD, dependent or not on Apolipoprotein E (ApoE) genotype. No significant association was found for the CYP46 polymorphism in LOAD compared to the controls, even after stratification for the presence/absence of the ApoE*4 allele. Our data do not support a role of the CYP46 polymorphism as a possible susceptibility factor for developing AD.
Original language | English |
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Journal | Neurobiology of Aging |
Volume | 27 |
Issue number | 5 |
DOIs | |
Publication status | Published - May 2006 |
Keywords
- Alzheimer's disease
- Apolipoprotein E
- Cholesterol 24S-hydroxylase
- Genetic factors
- Polymorphism
ASJC Scopus subject areas
- Clinical Neurology
- Biological Psychiatry
- Developmental Neuroscience
- Neurology
- Psychology(all)