Mark R. Cookson
Cell Biology and Gene Expression Unit, Laboratory of Neurogenetics, National Institute on Aging, Bethesda, Maryland, U.S.A.
In 1997, Hasegawa and Kowa reported a family from the Sagamihara area of Japan with autosomal dominant inheritance of Parkinson's disease (PD)-like symptoms (1). In 2002, after excluding known loci (2), the same group reported linkage to the long arm of chromosome 12 and named the locus PARK8 (3). By 2004, two groups simultaneously published the identification of the gene responsible, LRRK2 (for leucine-rich repeat kinase 2), for the PARK8 locus in four additional families from different parts of the world (4,5). Within a year of that discovery, the LRRK2 gene was shown to be the most common genetic cause of PD to date (6). This short chronology says a great deal about the accelerating pace of discovery in the genetics of PD, which, as others have pointed out (7), was once considered the archetype of a nongenetic disease. But, as is discussed in this chapter, these discoveries have blurred the boundaries between PD and atypical parkinsonian disorders and raise interesting questions about the etiopathogenesis of these diseases.
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