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Homocysteine levels in patients with Alzheimer's disease are influenced by the glutathione s-transferase omega-1 (GSTO1) gene

Conference contribution
Authors Annica Johansson
Kaj Blennow
Lennart Minthon
Henrik Zetterberg
Elisabet Londos
Siegbert Warkentin
Björn Regland
Published in Haematologica Reports
Volume 2005
Issue 1(3):June
ISSN 1824-9337
Publication year 2005
Published at Institute of Clinical Neurosciences
Institute of Clinical Neurosciences, Section of Experimental Neuroscience
Institute of Clinical Neurosciences, Section of Psychiatry
Language en
Links www.pagepress.org/journals/index.ph...
Subject categories Clinical Medicine, Psychiatry

Abstract

Background: A substantial body of literature confirms an association between elevated blood levels of homocysteine and cognitive dysfunction, including Alzheimer’s disease (AD). Oxidative stress is a risk factor for AD. Elevated homocysteine levels might partially reflect redox status; its remethylation to methionine is coordinated by the redox-sensitive enzyme methionine synthase. Glutathione S-transferase omega-1 (GSTO1) is protective against oxidative stress, and the polymorphism Ala140Asp modifies the age-of-onset of AD. Aim: To investigate whether the GSTO1 Ala140Asp polymorphism is related to homocysteine levels in AD patients. Methods: Plasma homocysteine levels and the GSTO1 polymorphism Ala140Asp were analysed in 244 consecutive patients with clinically diagnosed AD. Results: Homocysteine levels differed significantly between the three genotypes (p=0.002) analysis of variance, Durbin-Watson D Statistic. The levels were 11.8±3.6 µmol/L in patients with the Ala/Ala genotype (n=118), 13.5±5.0 µmol/L in the Ala/Asp group (n=105), and 14.1±6.0 µmol/L in patients with the Asp/Asp genotype (n=21). Carriers of at least one Asp allele showed significantly higher plasma homocysteine levels compared to non-carriers (p=0.002) two-sample t-test. Conclusion: The association between homocysteine levels and this GSTO1 polymorphism supports the suggestion that increased homocysteine in AD patients may be a consequence of oxidative stress.

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