Parkinson's disease (PD) occurs in both familial and sporadic forms, and both 
monogenic and complex genetic factors have been identified. Early onset PD 
(EOPD) is particularly associated with autosomal recessive (AR) mutations, and 
three genes, PARK2, PARK7 and PINK1, have been found to carry mutations leading 
to AR disease. Since mutations in these genes account for less than 10% of EOPD 
patients, we hypothesized that further recessive genetic factors are involved in 
this disorder, which may appear in extended runs of homozygosity.We carried out 
genome wide SNP genotyping to look for extended runs of homozygosity (ROHs) in 
1,445 EOPD cases and 6,987 controls. Logistic regression analyses showed an 
increased level of genomic homozygosity in EOPD cases compared to controls. 
These differences are larger for ROH of 9 Mb and above, where there is a more 
than three-fold increase in the proportion of cases carrying a ROH. These 
differences are not explained by occult recessive mutations at existing loci. 
Controlling for genome wide homozygosity in logistic regression analyses 
increased the differences between cases and controls, indicating that in EOPD 
cases ROHs do not simply relate to genome wide measures of inbreeding. 
Homozygosity at a locus on chromosome19p13.3 was identified as being more common 
in EOPD cases as compared to controls. Sequencing analysis of genes and 
predicted transcripts within this locus failed to identify a novel mutation 
causing EOPD in our cohort.There is an increased rate of genome wide 
homozygosity in EOPD, as measured by an increase in ROHs. These ROHs are a 
signature of inbreeding and do not necessarily harbour disease-causing genetic 
variants. Although there might be other regions of interest apart from 
chromosome 19p13.3, we lack the power to detect them with this analysis.