No evidence that extended tracts of homozygosity are associated with Alzheimer's disease.
Sims R., Dwyer S., Harold D., Gerrish A., Hollingworth P., Chapman J., Jones N., Abraham R., Ivanov D., Pahwa JS., Moskvina V., Dowzell K., Thomas C., Stretton A., Lovestone S., Powell J., Proitsi P., Lupton MK., Brayne C., Rubinsztein DC., Gill M., Lawlor B., Lynch A., Morgan K., Brown KS., Passmore PA., Craig D., McGuiness B., Todd S., Johnston JA., Holmes C., Mann D., Smith AD., Love S., Kehoe PG., Hardy J., Mead S., Fox N., Rossor M., Collinge J., Livingston G., Bass NJ., Gurling H., McQuillin A., Jones L., Holmans PA., O'Donovan M., Owen MJ., Williams J.
We sought to investigate the contribution of extended runs of homozygosity in a genome-wide association dataset of 1,955 Alzheimer's disease cases and 955 elderly screened controls genotyped for 529,205 autosomal single nucleotide polymorphisms. Tracts of homozygosity may mark regions inherited from a common ancestor and could reflect disease loci if observed more frequently in cases than controls. We found no excess of homozygous tracts in Alzheimer's disease cases compared to controls and no individual run of homozygosity showed association to Alzheimer's disease.