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Extra resources for Advances in Research on Neurodegeneration: Volume 7
2-27. Am J Hum Genet 60: 588-596 Matsumine H, Yamamura Y, Hattori N, Kobayashi T, Kitada T, Yoritaka A, Mizuno Y (1998) A microdeletion of D6S305 in a family of autosomal recessive juvenile parkinsonism (PARK2). Genomics 49: 143-146 Mezey E, Dehejia A, Harta G, Papp MI, Polymeropoulos MH, Brownstein MJ (1998) Alpha synuclein in neurodegenerative disorders: murderer or accomplice? Nature Med 4: 755-757 Mori H, Kondo J, Ihara Y (1987) Ubiquitin is a component of paired helical filaments in Alzheimer's disease.
Shimizu et al. two independent mutant alleles in two different exons which are not detected by the current PCR amplification assay. Most of the exon deletion mutations were located in a region between intron 2 and intron 5, indicating this region may be mutation hot spots (Fig. 2D). , 1994). , 1996). , 1999). Furthermore, subcellular fractionation of brain tissues revealed that Parkin protein is mostly in the Golgi apparatus and cytosol and not in the nucleus. Thus, Parkin protein in PD patients is apparently involved in the Lewy body formation and proteasome pathway.
Only a few months after the demonstration of linkage, the same group discovered a missense mutation within one candidate gene of the linked region, a-synuclein, in the Con tursi-kindred and in three Greek kindreds with dominantly inherited early-onset parkinsonism. This mutation Table 1. Genetically defined forms of Parkinson's disease and parkinsonism Locus inheritance onset pathology map position gene PARK1 dominant 40s 4q21 a-synuclein PARK2 recessive 20s 6q25 parkin PARK3 dominant 60s 2p13 ?