In vitro effect of PPAR-γ2 Pro12Ala polymorphism on the deposition of Alzheimer's amyloid-β peptides

Cristina d'Abramo, Jean Marc Zingg, Antonio Pizzuti, Francesca Argellati, Maria A. Pronzato, Roberta Ricciarelli

Research output: Contribution to journalArticlepeer-review

1 Scopus citations

Abstract

Mounting evidence suggests that peroxisome proliferator-activated receptor-γ (PPAR-γ) is involved in the modulation of pathogenic events related to Alzheimer's disease (AD). Such events would include the cerebral deposition of amyloid-β (Aβ) and the consequent local inflammatory response. PPAR-γ has been shown to act on both fronts, reducing either the secretion of Aβ or the expression of pro-inflammatory cytokines. Recently, the relatively common Pro12Ala polymorphism in exon 2 of PPAR-γ has been associated with higher risk for late onset AD. Here, we compare the effect of PPAR-γ and its genetic variant on the secretion of Aβ. Our results indicate that, in neuronal cultured cells, the Pro12Ala substitution does not affect the anti-amyloidogenic capacity of PPAR-γ. Additional factors, PPAR-γ related, may therefore predispose aged subjects, carrying the Ala allele, to develop the neurodegenerative disease.

Original languageEnglish (US)
Pages (from-to)1-5
Number of pages5
JournalBrain research
Volume1173
Issue number1
DOIs
StatePublished - Oct 10 2007
Externally publishedYes

Keywords

  • Alzheimer's disease
  • Amyloid-beta
  • Peroxisome proliferator-activated receptor gamma (PPAR-γ)

ASJC Scopus subject areas

  • Neuroscience(all)
  • Molecular Biology
  • Clinical Neurology
  • Developmental Biology

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