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

Abstract

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.