Presenilin 1 gene silencing by S-adenosylmethionine: A treatment for Alzheimer disease?

Sigfrido Scarpa, Andrea Fuso, Fabrizio D'Anselmi, Rosaria A. Cavallaro

Research output: Contribution to journalArticlepeer-review


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.

Original languageEnglish
Pages (from-to)145-148
Number of pages4
JournalFEBS Letters
Issue number1-3
Publication statusPublished - Apr 24 2003


  • β-Amyloid
  • Alzheimer disease
  • DNA methylation
  • Homocysteine
  • Presenilin 1
  • S-Adenosylmethionine

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology


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