The Insertion/Deletion Polymorphism of the Angiotensin Converting Enzyme (ACE) in Parkinson’s Disease
Spiridon Papapetropoulos*, 1, 2, Kostantinos Glynos3, Zongmin Zhou3, Stylianos E Orfanos3, Georgia Mitsi4, Andreas Papapetropoulos5
Identifiers and Pagination:Year: 2008
First Page: 66
Last Page: 70
Publisher ID: TONEUJ-2-66
Article History:Received Date: 16/4/2008
Revision Received Date: 17/9/2008
Acceptance Date: 19/9/2008
Electronic publication date: 31/10/2008
Collection year: 2008
open-access license: This is an open access article licensed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.
Parkinson’s disease (PDI is a neurodegenerative disorder of unknown etiology. Both genetic and environmental factors are thought to be implicated to some extent. The ACE gene insertion/deletion (I/D) polymorphism has been associated with common neurodegenerative disorders that share similar clinical and neuropathological features with PD (Alzheimer’s disease). In this study we set out to examine the role of the ACE gene insertion/deletion (I/D) polymorphism in Parkinson’s disease (PD).
We conducted a case-control association study among 77 PD patients and 50 non-PD controls from Greece.
The genotype frequencies for II, ID, and DD were 39, 48, and 13%, respectively, in the PD group and 32, 50, and 18% in the control group. Although the DD frequency was higher in the case group statistical significance was not reached.
We conclude that although disease modifying effects cannot be excluded, the ACE insertion/deletion polymorphism is unlikely to be an important determinant of susceptibility to PD in this population.