title: Genome-wide genotyping in amyotrophic lateral sclerosis and neurologically normal controls: first stage analysis and public release of data.
abstract: BACKGROUND
  The cause of sporadic ALS is currently unknown. Despite evidence for a role for genetics, no common genetic variants have been unequivocally linked to sporadic ALS. We sought to identify genetic variants associated with an increased or decreased risk for developing ALS in a cohort of American sporadic cases.
  
  
  METHODS
  We undertook a genome-wide association study using publicly available samples from 276 patients with sporadic ALS and 271 neurologically normal controls. 555 352 unique SNPs were assayed in each sample using the Illumina Infinium II HumanHap550 SNP chip.
  
  
  RESULTS
  More than 300 million genotypes were produced in 547 participants. These raw genotype data are freely available on the internet and represent the first publicly accessible SNP data for ALS cases. 34 SNPs with a p value less than 0.0001 (two degrees of freedom) were found, although none of these reached significance after Bonferroni correction.
  
  
  CONCLUSIONS
  We generated publicly available genotype data for sporadic ALS patients and controls. No single locus was definitively associated with increased risk of developing disease, although potentially associated candidate SNPs were identified.
authors.affiliation: Laboratory of Neurogenetics, National Institute on Aging, National Institute of Mental Health, National Institutes of Health, Bethesda, MD, USA.
authors.forename: Jennifer C
authors.initials: JC
authors.lastname: Schymick
authors.forename: Sonja W
authors.initials: SW
authors.lastname: Scholz
authors.forename: Hon-Chung
authors.initials: HC
authors.lastname: Fung
authors.forename: Angela
authors.initials: A
authors.lastname: Britton
authors.forename: Sampath
authors.initials: S
authors.lastname: Arepalli
authors.forename: J Raphael
authors.initials: JR
authors.lastname: Gibbs
authors.forename: Federica
authors.initials: F
authors.lastname: Lombardo
authors.forename: Mar
authors.initials: M
authors.lastname: Matarin
authors.forename: Dalia
authors.initials: D
authors.lastname: Kasperaviciute
authors.forename: Dena G
authors.initials: DG
authors.lastname: Hernandez
authors.forename: Cynthia
authors.initials: C
authors.lastname: Crews
authors.forename: Lucie
authors.initials: L
authors.lastname: Bruijn
authors.forename: Jeffrey
authors.initials: J
authors.lastname: Rothstein
authors.forename: Gabriele
authors.initials: G
authors.lastname: Mora
authors.forename: Gabriella
authors.initials: G
authors.lastname: Restagno
authors.forename: Adriano
authors.initials: A
authors.lastname: Chiò
authors.forename: Andrew
authors.initials: A
authors.lastname: Singleton
authors.forename: John
authors.initials: J
authors.lastname: Hardy
authors.forename: Bryan J
authors.initials: BJ
authors.lastname: Traynor
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000690:Amyotrophic Lateral Sclerosis / Q000235:genetics*; D004252:DNA Mutational Analysis / Q000379:methods*; D030541:Databases, Genetic / Q000592:standards / Q000639:trends; D005260:Female; D005819:Genetic Markers / Q000235:genetics; D020022:Genetic Predisposition to Disease / Q000235:genetics; D005820:Genetic Testing / Q000379:methods*; D015698:Genomic Library; D005838:Genotype; D006801:Humans; D008297:Male; D008875:Middle Aged; D008967:Molecular Biology / Q000379:methods* / Q000639:trends; D009154:Mutation / Q000235:genetics; D020641:Polymorphism, Single Nucleotide / Q000235:genetics; D017150:Public Sector / Q000592:standards*; D012016:Reference Values
chemical_list: D005819:Genetic Markers