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• W1979940972 abstract "<b>Background: </b><i>SMN1</i> gene deletions cause spinal muscular atrophy, and <i>SMN2</i> gene deletions have been associated with sporadic lower motor neuron diseases. <b>Objectives: </b> To study the frequency of abnormal <i>SMN1</i> gene copy numbers and to determine whether <i>SMN2</i> gene modulates the risk of amyotrophic lateral sclerosis (ALS) or the duration of evolution. <b>Method: </b> The authors studied <i>SMN1</i> and <i>SMN2</i> genes in 600 patients with sporadic ALS and 621 controls using a quantitative PCR method. <b>Results: </b> The authors found an association of ALS with an abnormal copy number (one or three copies) of <i>SMN1</i> gene (<i>p</i> < 0.0001) with an OR of 2.8 (1.8 to 4.4, 95% CI). There was no association with <i>SMN2</i> copy numbers and no effect of <i>SMN2</i> copies on the duration of evolution in ALS independently of <i>SMN1</i> copy number. <b>Conclusion: </b> Abnormal <i>SMN1</i> gene copy numbers are a genetic risk factor in sporadic amyotrophic lateral sclerosis. There was no modulator effect of the <i>SMN2</i> gene." @default.
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• W1979940972 date "2006-08-23" @default.
• W1979940972 modified "2023-09-27" @default.
• W1979940972 title "SMN1 gene, but not SMN2, is a risk factor for sporadic ALS" @default.
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• W1979940972 doi "https://doi.org/10.1212/01.wnl.0000233830.85206.1e" @default.
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