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Extra resources for Advances in Research on Neurodegeneration: Volume 7
C. elegans possesses caspase (Ced-3) and Bcl-2-like proteins (Ced-9 and Egl-1), and the basic mechanism of apoptotic cell death appears to be well conserved during evolution. 42 Y. , 1985; Cleary and Sklar, 1985). , 1990). , 1993). Heterodimerization between anti-apoptotic and pro-apoptotic members of this family is considered to inhibit the biological activity of their partners. In addition to the regulation of apoptosis by heterodimerization of anti~apoptotic and pro-apoptotic members of the Bel-2 family, some of these proteins have been suggested to regulate apoptosis independently of each other (Knudson and Korsmeyer, 1997).
Sch. Med, B. Elibol at the Dept. Neurol. Faculty Med. Hacettepe Univ, AJ. Brookes at the Dept. Med. , Biomed. Center. This work was supported in part by the grants from the Ministry of Education, Science, Sports and Culture, Japan Society of Promotion of Science , and the National Parkinson Foundation. PARKIN as a pathogenic gene for autosomal recessive juvenile parkinsonism 29 References Asakawa S, Abe I, Kudoh Y, Kishi N, Wang Y, Kubota R, Kudoh J, Kawasaki K, Minoshima S, Shimizu N (1997) Human BAC library: construction and screening.
N. jp Autosomal-dominantly inherited forms of Parkinson's disease T. Gasser Neurologische Klinik und Poliklinik, Klinikum GroBhadern, Ludwig-Maximilians-Universitat, Munich, Federal Republic of Germany Summary. Today, a genetic contribution to the etiology of Parkinson's disease (PD) is generally accepted, based on the demonstration of a familial aggregation of the disease, as demonstrated by several case-control and twinstudies. However, most cases of PD appear to be sporadic, and in the majority of those with a positive family history, no clear mendelian mode of inheritance can be established.