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From the Department of Clinical Neurological Sciences (M.J. Greenway and Dr. Hardiman), Royal College of Surgeons in Ireland; Department of Neurology (Drs. Alexander and Hardiman, and B. Corr), Beaumont Hospital, Dublin; Department of Medical Genetics (Drs. Ennis, Traynor, and Green), Conway Institute of Biomolecular and Biomedical Research, University College Dublin, Our Lady’s Hospital for Sick Children, Ireland; Cecil B. Day Laboratory for Neuromuscular Research (Dr. Traynor), MassGeneral Institute for Neurodegenerative Disease, Boston, MA; and Irish Motor Neurone Disease Association (E. Frost), Dublin, Ireland.
Address correspondence and reprint requests to Dr. Matthew Greenway, Dept. of Molecular Genetics, National Centre for Medical Genetics, Our Lady’s Hospital for Sick Children, Crumlin, Dublin 12, Ireland; e-mail: mattgreenway{at}rcsi.ie or ohard{at}iol.ie
Sequence variations with biologic effect in ALS have been identified in the gene for vascular endothelial growth factor (VEGF). The gene for a related protein, angiogenin, lies on chromosome 14q11.2. Analysis of the angiogenin (ANG) gene in the authors’ population has demonstrated a significant allelic association with the rs11701 single nucleotide polymorphism (SNP) and identified a novel mutation in two individuals with sporadic ALS that potentially inhibits angiogenin function. These observations propose a candidate region for ALS on chromosome 14q11.2 and suggest that other genes with similar function to VEGF may be important in the pathogenesis of ALS.
Received March 2, 2004. Accepted in final form July 8, 2004.
*These authors contributed equally to this work.
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