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Titolo:
MITOCHONDRIAL DYSFUNCTION IN PARKINSONS-DISEASE
Autore:
MIZUNO Y; YOSHINO H; IKEBE S; HATTORI N; KOBAYASHI T; SHIMODAMATSUBAYASHI S; MATSUMINE H; KONDO T;
Indirizzi:
JUNTENDO UNIV,SCH MED,DEPT NEUROL,BUNKYO KU,2-1-1 HONGO TOKYO 113 JAPAN
Titolo Testata:
Annals of neurology
fascicolo: 3, volume: 44, anno: 1998, supplemento:, 1
pagine: 99 - 109
SICI:
0364-5134(1998)44:3<99:MDIP>2.0.ZU;2-C
Fonte:
ISI
Lingua:
ENG
Soggetto:
MANGANESE SUPEROXIDE-DISMUTASE; NADH-UBIQUINONE OXIDOREDUCTASE; ALPHA-KETOGLUTARATE DEHYDROGENASE; HUMAN DIHYDROLIPOAMIDE SUCCINYLTRANSFERASE; CHAIN ENZYME-ACTIVITIES; COMPLEX I DEFICIENCY; RESPIRATORY-CHAIN; SUBSTANTIA-NIGRA; DOPAMINERGIC NEUROTOXIN; SKELETAL-MUSCLE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
107
Recensione:
Indirizzi per estratti:
Citazione:
Y. Mizuno et al., "MITOCHONDRIAL DYSFUNCTION IN PARKINSONS-DISEASE", Annals of neurology, 44(3), 1998, pp. 99-109

Abstract

This review discusses the etiology and pathogenesis of Parkinson's disease (PD). Mitochondrial respiratory failure and oxidative stress appear to be two major contributors to nigral neuronal death in PD. Complex I deficiency has been reported by several groups and appears to be one of the basic abnormalities responsible for mitochondrial failure. The principal question is whether or not complex I deficiency is primary or secondary. The second question is whether or not complex I deficiency is localized in the nigrostriatal system or is systemically present. It is our impression that complex I deficiency is not the primarycause but that its deficiency appears to be systemic. The primary cause may be the combination of genetic background and potential nigral neurotoxins. Exposure of nigral neurons to a high risk for oxidative damage because of its high dopamine content may be the reason for more pronounced nigral complex I deficiency compared to systemic organs. Oxidative stress and mitochondrial failure produce a vicious cycle in nigral neurons. To explore the genetic risk factors of sporadic PD, studies on familial PD and parkinsonism are important. Recently, an autosomal dominant form of familial PD was found to be caused by point mutations of the alpha-synuclein gene, and an autosomal recessive familial parkinsonism was mapped to the long arm of chromosome 6 near the Mn-SODgene locus. Information obtained in these familiar cases will contribute to the research on sporadic PD.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 01/04/20 alle ore 16:39:25