Neurochemical and Neurogenetic Correlates of Parkinson's Disease

• Published in: Journal of neurochemistry Vol. 71; no. 3; pp. 893 - 902
• Main Authors: Mizuno, Yoshikuni, Hattori, Nobutaka, Matsumine, Hiroto
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Science Ltd 01.09.1998; Blackwell
• Subjects: Biological and medical sciences; Brain - metabolism; Brain - physiopathology; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases; Etiology and pathogenesis; Familial Parkinson's disease; Genes, Dominant - genetics; Genes, Recessive - genetics; Genetic Predisposition to Disease; Humans; Medical sciences; Mitochondria; MPTP; Neurology; Neurotoxin; Oxidative stress; Parkinson Disease - genetics; Parkinson Disease - metabolism; Parkinson's disease; Pedigree; Human; Oxidative stress; Nervous system diseases; Pathogenesis; Parkinson disease; Review; Cerebral disorder; Mitochondria; Etiology; Central nervous system disease; Predisposition; Genetics; Degenerative disease; Extrapyramidal syndrome
• ISSN: 0022-3042; 1471-4159
• DOI: 10.1046/j.1471-4159.1998.71030893.x

: We discuss neurochemical and neurogenetic correlates of Parkinson's disease (PD) based on the recent progress in the study of its etiology and pathogenesis. Nigral degeneration with the presence of Lewy bodies in the remaining neurons is the pathologic hallmark of PD, and the resultant loss of striatal dopamine is responsible for most of the clinical manifestations. Although the primary cause is still unknown, mitochondrial respiratory failure and oxidative stress appear to be two major contributors to the nigral cell death. Many endogenous and exogenous compounds with structural similarity to MPTP have been postulated as potential neurotoxins inducing nigral cell death in PD, but there is little evidence of accumulation of such compounds in the nigra. Genetic influence has increasingly been recognized as an important risk factor for PD. In this respect, genetic linkage analysis and molecular cloning of the disease genes in familial parkinsonism are of utmost importance today. Recently, the disease gene for one of the autosomal dominant forms of familial PD was identified, and we cloned the gene for an autosomal recessive type of familial parkinsonism that had been mapped to the long arm of chromosome 6 by our group. Information obtained on familial parkinsonism will contribute to the studies on sporadic PD as well.