期刊
BIOCHIMICA ET BIOPHYSICA ACTA-BIOENERGETICS
卷 1777, 期 7-8, 页码 777-782出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.bbabio.2008.05.443
关键词
complex I; brain mitochondria; metabolic control analysis; neurodegeneration; Parkinson's disease
Mitochondrial electron transport chain (ETC) deficiencies are thought to underlie defects in energy metabolism and have been implicated in the neurodegenerative process. In particular, reductions in complex I activities in Parkinson's disease are thought to cause bioenergetic dysfunction with subsequent degeneration of doparninergic neurons. In terms of bioenergetics and assessing ETC-related problems in the brain, the presence of heterogeneous mitochondria has complicated matters as isolated non-synaptic mitochondria have different energy thresholds and flux control coefficients compared to isolated mitochondria of synaptic origin. The molecular mechanisms that underlie complex I deficiencies in the parkinsonian brain are unknown and are the source of intensive research. This review explores the relationship between complex I activity and energy metabolism in the brain as well as the nature of the complex I defect. (c) 2008 Elsevier B.V. All rights reserved.
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