期刊
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
卷 1802, 期 1, 页码 62-65出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.bbadis.2009.06.008
关键词
Mitochondria; Huntington; Trafficking; Neurodegeneration
资金
- National Institutes of Health [NS036232, NS041669, AG019206, NS045016]
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS045016, R01NS036232, R01NS041669] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [R01AG031153, R01AG019206] Funding Source: NIH RePORTER
Impaired mitochondrial function has been well documented in Huntington's disease. Mutant huntingtin is found to affect mitochondria via various mechanisms including the dysregulation of gene transcription and impairment of mitochondrial function or trafficking. The lengthy and highly branched neuronal processes constitute complex neural networks in which there is a large demand for mitochondria-generated energy. Thus, the impaired mitochondrial trafficking in neuronal cells may play an important role in the selective neuropathology of Huntington's disease. Here we discuss the evidence for the effect of the Huntington's disease protein huntingtin on the intracellular trafficking of mitochondria and the involvement of this defective trafficking in the pathogenesis of Huntington's disease. (C) 2009 Elsevier B.V. All rights reserved.
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