期刊
FEBS LETTERS
卷 541, 期 1-3, 页码 145-148出版社
WILEY
DOI: 10.1016/S0014-5793(03)00277-1
关键词
Alzheimer disease; beta-amyloid; DNA methylation; presenilin 1; homocysteine; S-adenosylmethionine
Presenilin 1 (PS1) is a key factor for beta-amyloid (Ab) formation in Alzheimer disease (AD). Homocysteine accumulation, frequently observed in AD patients, may be a sign of a metabolic alteration in the S-adenosylmethionine (SAM) cycle, which generates the overexpression of genes controlled by methylation of their promoters, when the cytosine in CpG moieties becomes unmethylated. The methylation of a gene involved in the processing of amyloid precursor protein may prevent Ab formation by silencing the gene. Here we report that SAM administration, in human neuroblastoma SK-N-SH cell cultures, downregulates PS1 gene expression and Ab production. (C) 2003 Published by Elsevier Science B.V. on behalf of the Federation of European Biochemical Societies.
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