4.7 Article Proceedings Paper

Neuroprotective mechanisms of brain-derived neurotrophic factor against 3-nitropropionic acid toxicity: therapeutic implications for Huntington's disease

期刊

出版社

WILEY-BLACKWELL
DOI: 10.1111/j.1749-6632.2010.05628.x

关键词

Akt; cGMP; ERK1/2; mitochondria; nitric oxide; sonic hedgehog

资金

  1. National Science Council in Taiwan [NSC95-2314-B-010-093MY3, NSC97-2314-B-010-008MY3]
  2. Ministry of Education [95A-C-P30]
  3. Department of Health, Taipei City Government [97002-62-040]
  4. Cheng Hsin General Hospital [98F117CY20]

向作者/读者索取更多资源

3-Nitropropionic acid (3-NP) is an irreversible inhibitor of mitochondrial succinate dehydrogenase that has been used to explore the molecular mechanisms of cell death associated with mitochondrial dysfunction and neurodegeneration for Huntington's disease (HD). Brain-derived neurotrophic factor (BDNF) is a neurotrophin that may regulate neuronal survival and differentiation. Experimental evidence derived from both clinical as well as basic research suggests a close association between BDNF deficiency and HD pathogenesis. In this review, we focus on recent progress in the molecular mechanisms responsible for the BDNF-mediated neuroprotective effects against mitochondrial dysfunction induced by 3-NP. Delineation of BDNF-mediated neuroprotective actions against 3-NP toxicity may add in the development of therapeutic intervention for HD where mitochondrial dysfunction is known to play a crucial role in pathogenesis of this devastating disease.

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