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Presenilin 1 gene silencing by S ‐adenosylmethionine: a treatment for Alzheimer disease?
Author(s) -
Scarpa Sigfrido,
Fuso Andrea,
D'Anselmi Fabrizio,
Cavallaro Rosaria A
Publication year - 2003
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(03)00277-1
Subject(s) - gene silencing , presenilin , methylation , promoter , gene , cpg site , dna methylation , amyloid precursor protein , biology , microbiology and biotechnology , gene expression , alzheimer's disease , genetics , disease , medicine
Presenilin 1 (PS1) is a key factor for β‐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.