Parkinson's disease (PD) is the second most common neurodegenerative disorder after Alzheimer's disease (AD). Most patients with PD have sporadic disease with a complex etiology arising from the interaction of three events: an individual's inherited genetic susceptibility, subsequent environmental exposures, and aging. To date, genetic linkage and positional cloning studies in familial PD have identified eight causative genes: α-synuclein, parkin, Omi/. HtrA2, UCHL1 (ubiquitin C-terminal hydroxylase L1), DJ-1, PINK-1 (PTEN-induced kinase 1), LRRK2 (leucine-rich repeat kinase 2), and Nurr1 (nuclear receptor-related 1), and at least four other loci have been implicated. There are two approaches involved in genetic PD association studies. One is based on random genome screening to detect genetic linkages using nonparametric methods. Such analyses have linked PD with genes on chromosomes 2, 4q21-23, 5, 13, X, and 17q, 8p, 5q, 6, 9q. The other approach is the candidate-gene approach, which is based on the understanding of the pathology of PD. A number of association studies suggest that functional polymorphisms in genes of dopamine metabolism and transport, iron homeostasis, inflammation, mitochondrial abnormalities, and exogenous or endogenous toxin metabolism might play a role in individual predisposition to developing idiopathic PD. The genetic association studies on PD indicate that gene-gene and gene-environment interactions play significant roles in the pathogenesis of PD and also reflect the different genetic constitution in different ethnic backgrounds. In addition, genetic variations influencing the process of aging might also contribute to PD risk and course. © 2007 Elsevier B.V. All rights reserved.