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Parkinson's disease: What remains of the “missing heritability”?

In recent years, the feasibility of performing large, genome-wide association studies (GWASs) has provided a powerful tool to identify susceptibility loci in complex diseases. GWASs utilize microarrays of several hundred thousand single-nucleotide polymorphisms (SNPs) to capture a significant amount of an individual’s genetic variation. The underlying rationale for GWASs is the ‘‘common disease, common variant’’ hypothesis, attributing the genetic risk for complex diseases largely to genetic variants present in more than 1% to 5% of the population. Thousands of such variants have been identified in various disorders, providing valuable insights into the genetic architecture of disease and generating hypotheses for further research. However, these variants have typically explained only a small proportion of heritability and familial clustering, leaving researchers faced with a problem of ‘‘missing heritability.’’ In the case of PD, global GWAS efforts are now reaching sample sizes where it might be fruitful to close in on this problem and, perhaps, redefine it more precisely.