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Human Molecular Genetics 2007 16(R2):R233-R242; doi:10.1093/hmg/ddm215
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© The Author 2007. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Genetics of sporadic amyotrophic lateral sclerosis

J.C. Schymick1,3, K. Talbot3,4 and B.J. Traynor2,5,*

1 Laboratory of Neurogenetics, NIA and 2 Neurogenetics Branch, NINDS, NIH, Bethesda, MD 20892, USA , 3 Department of Physiology, Anatomy and Genetics, University of Oxford, Henry Wellcome Building of Gene Function, South Parks Road, Oxford OX1 3QX, UK, 4 Department of Clinical Neurology, University of Oxford, John Radcliffe Hospital, Oxford OX3 9DU, UK and 5 Neurology Department, Johns Hopkins Hospital, 600 N. Wolfe Street, Meyer 6-109, Baltimore, MD 21287, USA

* To whom correspondence should be addressed. Tel: +1 3014517606; Fax: +1 3014517295; Email: traynorb{at}mail.nih.gov

Received July 26, 2007; Accepted July 27, 2007

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized clinically by rapidly progressive paralysis leading ultimately to death from respiratory failure. There is substantial evidence suggesting that ALS is a heritable disease, and a number of genes have been identified as being causative in familial ALS. In contrast, the genetics of the much commoner sporadic form of the disease is poorly understood and no single gene has been definitively shown to increase the risk of developing ALS. In this review, we discuss the genetic evidence for each candidate gene that has been putatively associated with increased risk of sporadic ALS. We also review whole genome association studies of ALS and discuss the potential of this methodology for identifying genes relevant to motor neuron degeneration.


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