| pubmed-article:17803977 | pubmed:abstractText | Mounting evidence suggests that peroxisome proliferator-activated receptor-gamma (PPAR-gamma) is involved in the modulation of pathogenic events related to Alzheimer's disease (AD). Such events would include the cerebral deposition of amyloid-beta (Abeta) and the consequent local inflammatory response. PPAR-gamma has been shown to act on both fronts, reducing either the secretion of Abeta or the expression of pro-inflammatory cytokines. Recently, the relatively common Pro12Ala polymorphism in exon 2 of PPAR-gamma has been associated with higher risk for late onset AD. Here, we compare the effect of PPAR-gamma and its genetic variant on the secretion of Abeta. Our results indicate that, in neuronal cultured cells, the Pro12Ala substitution does not affect the anti-amyloidogenic capacity of PPAR-gamma. Additional factors, PPAR-gamma related, may therefore predispose aged subjects, carrying the Ala allele, to develop the neurodegenerative disease. | lld:pubmed |
