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Table of Contents
Vol. 23, No. 4, 2007
Issue release date: March 2007
Section title: Original Research Article
Dement Geriatr Cogn Disord 2007;23:215–218
(DOI:10.1159/000099471)

Interaction between Poly(ADP-Ribose) Polymerase 1 and Interleukin 1A Genes Is Associated with Alzheimer’s Disease Risk

Infante J.a · Llorca J.b · Mateo I.a · Rodríguez-Rodríguez E.a · Sánchez-Quintana C.a · Sánchez-Juan P.a · Fernández-Viadero C.c · Peña N.c · Berciano J.a · Combarros O.a
aNeurology Service, Marqués de Valdecilla University Hospital, University of Cantabria, bDivision of Preventive Medicine, University of Cantabria School of Medicine, and cRTE Santander, Consejería de Sanidad, Santander, Spain

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Article / Publication Details

First-Page Preview
Abstract of Original Research Article

Received: September 01, 2006
Accepted: October 25, 2006
Published online: February 09, 2007
Issue release date: March 2007

Number of Print Pages: 4
Number of Figures: 0
Number of Tables: 3

ISSN: 1420-8008 (Print)
eISSN: 1421-9824 (Online)

For additional information: http://www.karger.com/DEM

Abstract

Excessive release of proinflammatory cytokines by activated microglia surrounding senile plaques might contribute to the neurodegeneration associated with Alzheimer’s disease (AD). Poly(ADP-ribose) polymerase 1 (PARP-1) is a nuclear protein recently implicated in the initial inflammatory response by modulating expression of inflammation-related genes, like interleukin 1 (IL-1). As PARP-1 overactivity has been shown in the AD brain, we tested the hypothesis that the PARP-1 –410 and –1672 polymorphisms would predispose people to AD due to overexpression of the PARP-1 gene, independently or in concert with the proinflammatory IL-1A –889 polymorphism. So, we performed a case-control study in 263 Spanish AD patients and 293 healthy controls. PARP-1 –410 and PARP-1 –1672 haplotypes were associated with an increased risk for AD (global haplotype association p value = 0.019), and, in addition, PARP-1 haplotypes increased the risk of AD by interaction with the IL-1A –889 allele 2.

© 2007 S. Karger AG, Basel


Article / Publication Details

First-Page Preview
Abstract of Original Research Article

Received: September 01, 2006
Accepted: October 25, 2006
Published online: February 09, 2007
Issue release date: March 2007

Number of Print Pages: 4
Number of Figures: 0
Number of Tables: 3

ISSN: 1420-8008 (Print)
eISSN: 1421-9824 (Online)

For additional information: http://www.karger.com/DEM


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