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Vol. 41, No. 2, 1999
Issue release date: February 1999
Section title: Original Paper
Eur Neurol 1999;41:103–106
(DOI:10.1159/000008012)

The ACE Deletion Polymorphism Is Not Associated with Parkinson’s Disease

Mellick G.D. · Buchanan D.D. · McCann S.J. · Davis D.R. · Le Couteur D.G. · Chan D. · Johnson A.G.
aUniversity of Queensland, Department of Medicine, Princess Alexandra Hospital, Woolloongabba, bThe Canberra Clinical School of the University of Sydney, The Canberra Hospital, Garran, cPrince of Wales Hospital, Randwick, Australia

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Article / Publication Details

First-Page Preview
Abstract of Original Paper

Published online: 2/19/1999

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

ISSN: 0014-3022 (Print)
eISSN: 1421-9913 (Online)

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

Abstract

The deletion allele (D allele) polymorphism in the angiotensin converting enzyme (ACE) gene is associated with increased levels of the neuropeptide substance P in the basal ganglia and substantia nigra. A reduction of substance P levels in the brain occurs in Parkinson’s disease (PD) and has been implicated in the pathogenesis of the disease. We investigated the hypothesis that the D allele may be protective towards PD by examining the frequency of the ACE (I/D) polymorphism in 178 PD cases (male:female ratio = 1.4) and 192 controls (male:female ratio = 1.5). ACE (I/D) genotype was determined using polymerase chain reaction and 3% agarose gel electrophoresis. Unadjusted chi-square analysis revealed no significant difference between genotype frequencies (χ2 = 3.30, p > 0.10) or allele frequencies (χ2 = 2.52, p > 0.10) between patient and control groups, although PD patients were less likely to be homozygous (OR = 0.80, 95% CI = 0.49–1.29) or heterozygous (OR = 0.80, 95% CI = 0.59–1.06) for the D allele. A stepwise logistic regression analysis of the ACE deletion and risk factor data confirmed that there was no significant association between the ACE deletion (D allele) polymorphism and PD (OR = 0.62, 95% CI = 0.35–1.10, p = 0.10). This study does not support the hypothesis that the D allele of the ACE gene confers a protective effect with respect to PD.


  

Author Contacts

George Mellick, PhD
Department of Medicine, University of Queensland
Princess Alexandra Hospital, Woolloongabba, Qld. 4102 (Australia)
Tel. +61 7 3240 2903, Fax +61 7 3240 2900
E-Mail gmellick@medicine.pa.uq.edu.au

  

Article Information

Received: Received: April 28, 1998
Accepted: October 13, 1998
Number of Print Pages : 4
Number of Figures : 0, Number of Tables : 3, Number of References : 20

  

Publication Details

European Neurology
Founded 1897 as ‘Monatsschrift für Psychiatrie und Neurologie’

Vol. 41, No. 2, Year 1999 (Cover Date: Released February 1999)

Journal Editor: J. Bogousslavsky, Lausanne
ISSN: 0014–3022 (print), 1421–9913 (Online)

For additional information: http://www.karger.com/journals/ene


Article / Publication Details

First-Page Preview
Abstract of Original Paper

Published online: 2/19/1999

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

ISSN: 0014-3022 (Print)
eISSN: 1421-9913 (Online)

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


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