期刊
EMBO JOURNAL
卷 31, 期 14, 页码 3038-3062出版社
WILEY
DOI: 10.1038/emboj.2012.170
关键词
mitochondria; parkin; Parkinson; PINK1; synuclein
资金
- Deutsche Forschungsgemeinschaft [SFB 596]
- German Ministry for Education and Research (NGFN plus 'Functional Genomics of Parkinson's Disease')
- Helmholtz Alliance 'Mental Health in an Ageing Society'
- Center for Integrated Protein Science Munich (CIPSM)
- LMU Excellence Program
Neurons are critically dependent on mitochondrial integrity based on specific morphological, biochemical, and physiological features. They are characterized by high rates of metabolic activity and need to respond promptly to activity-dependent fluctuations in bioenergetic demand. The dimensions and polarity of neurons require efficient transport of mitochondria to hot spots of energy consumption, such as presynaptic and postsynaptic sites. Moreover, the postmitotic state of neurons in combination with their exposure to intrinsic and extrinsic neuronal stress factors call for a high fidelity of mitochondrial quality control systems. Consequently, it is not surprising that mitochondrial alterations can promote neuronal dysfunction and degeneration. In particular, mitochondrial dysfunction has long been implicated in the etiopathogenesis of Parkinson's disease (PD), based on the observation that mitochondrial toxins can cause parkinsonism in humans and animal models. Substantial progress towards understanding the role of mitochondria in the disease process has been made by the identification and characterization of genes causing familial variants of PD. Studies on the function and dysfunction of these genes revealed that various aspects of mitochondrial biology appear to be affected in PD, comprising mitochondrial biogenesis, bioenergetics, dynamics, transport, and quality control. The EMBO Journal (2012) 31, 3038-3062. doi: 10.1038/emboj.2012.170; Published online 26 June 2012
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