Journal
NEUROBIOLOGY OF AGING
Volume 33, Issue 2, Pages 418-420Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.neurobiolaging.2010.03.007
Keywords
Amyotrophic lateral sclerosis; Excitotoxicity; GluR2; Motor neuron
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Funding
- University of Leuven
- American ALS Association
- Belgian Science Policy Office (BELSPO) [P6/43]
- Jagiellonian University (Krakow, Poland) [nK/ZDS/001076]
- NIH, National Institute on Aging [Z01-AG000949-02]
- Packard Center for ALS Research
- E. von Behring Chair for Neuromuscular and Neurodegenerative Disorders
- Flanders Government
- ALS Therapy Alliance
- Angel Fund
- Pierre L. de Bourgknecht ALS Research Foundation
- Al-Athel ALS Research Foundation
- ALS Family Charitable Foundation
- National Institute for Neurological Disorders and Stroke
- Medical Research Council [G0000934]
- Wellcome Trust [068545/Z/02]
- MRC [G0600974, G0500289, G0900688, G0000934] Funding Source: UKRI
- Medical Research Council [G0900688, G0500289B, G0000934, G0600974, G0500289] Funding Source: researchfish
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Excitotoxicity is thought to play a pathogenic role in amyotrophic lateral sclerosis (ALS). Excitotoxic motor neuron death is mediated through the Ca(2+)-permeable alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA)-type of glutamate receptors and Ca(2+) permeability is determined by the GluR2 subunit. We investigated whether polymorphisms or mutations in the GluR2 gene (GRIA2) predispose patients to ALS. Upon sequencing 24 patients and 24 controls no nonsynonymous coding variants were observed but 24 polymorphisms were identified, 9 of which were novel. In a screening set of 310 Belgian ALS cases and 794 healthy controls and a replication set of 3157 cases and 5397 controls from 6 additional populations no association with susceptibility, age at onset, or disease duration was observed. We conclude that polymorphisms in the GluR2 gene (GRIA2) are not a major contributory factor in the pathogenesis of ALS. (C) 2012 Elsevier Inc. All rights reserved.
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