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• W1984598610 abstract "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." @default.
• W1984598610 created "2016-06-24" @default.
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• W1984598610 date "2003-04-02" @default.
• W1984598610 modified "2023-09-29" @default.
• W1984598610 title "Presenilin 1 gene silencing by<i>S</i>-adenosylmethionine: a treatment for Alzheimer disease?" @default.
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• W1984598610 doi "https://doi.org/10.1016/s0014-5793(03)00277-1" @default.
• W1984598610 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/12706835" @default.
• W1984598610 hasPublicationYear "2003" @default.
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