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Nrf2-encoding NFE2L2 haplotypes influence disease progression but not risk in Alzheimer's disease and age-related cataract.

Journal article
Authors Malin von Otter
Sara Landgren
Staffan Nilsson
Madeleine Zetterberg
Dragana Celojevic
Petra Bergström
Lennart Minthon
Nenad Bogdanovic
Niels Andreasen
Deborah Gustafson
Ingmar Skoog
Anders Wallin
Gunnar Tasa
Kaj Blennow
Michael Nilsson
Ola Hammarsten
Henrik Zetterberg
Published in Mechanisms of ageing and development
Volume 131
Issue 2
Pages 105-110
ISSN 1872-6216
Publication year 2010
Published at Institute of Neuroscience and Physiology, Department of Clinical Neuroscience and Rehabilitation
Institute of Biomedicine, Department of Clinical Chemistry and Transfusion Medicine
Department of Mathematical Sciences, Mathematical Statistics
Institute of Biomedicine
Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry
Institute of Neuroscience and Physiology, Department of Pharmacology
Pages 105-110
Language en
Links dx.doi.org/10.1016/j.mad.2009.12.00...
Subject categories Physiology, Chemistry, Psychiatry

Abstract

Alzheimer's disease (AD) and age-related cataract, disorders characterized by protein aggregation causing late-onset disease, both involve oxidative stress. We hypothesize that common variants of NFE2L2 and KEAP1, the genes encoding the main regulators of the Nrf2 system, an important defence system against oxidative stress, may influence risk of AD and/or age-related cataract. This case-control study combines an AD material (725 cases and 845 controls), and a cataract material (489 cases and 182 controls). Genetic variation in NFE2L2 and KEAP1 was tagged by eight and three tag single nucleotide polymorphisms (SNPs), respectively. Single SNPs and haplotypes were analyzed for associations with disease risk, age parameters, MMSE and AD cerebrospinal fluid biomarkers. NFE2L2 and KEAP1 were not associated with risk of AD or cataract. However, one haplotype allele of NFE2L2 was associated with 2 years earlier age at AD onset (p(c)=0.013) and 4 years earlier age at surgery for posterior subcapsular cataract (p(c)=0.019). Another haplotype of NFE2L2 was associated with 4 years later age at surgery for cortical cataract (p(c)=0.009). Our findings do not support NFE2L2 or KEAP1 as susceptibility genes for AD or cataract. However, common variants of the NFE2L2 gene may affect disease progression, potentially altering clinically recognized disease onset.

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