| pubmed-article:19853657 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19853657 | lifeskim:mentions | umls-concept:C0026237 | lld:lifeskim |
| pubmed-article:19853657 | lifeskim:mentions | umls-concept:C0027746 | lld:lifeskim |
| pubmed-article:19853657 | lifeskim:mentions | umls-concept:C0302350 | lld:lifeskim |
| pubmed-article:19853657 | lifeskim:mentions | umls-concept:C1521840 | lld:lifeskim |
| pubmed-article:19853657 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:19853657 | pubmed:dateCreated | 2009-12-8 | lld:pubmed |
| pubmed-article:19853657 | pubmed:abstractText | Mitochondrial dysfunction has long been associated with neurodegenerative disease. Therefore, mitochondrial protective agents represent a unique direction for the development of drug candidates that can modify the pathogenesis of neurodegeneration. This review discusses evidence showing that mitochondrial dysfunction has a central role in the pathogenesis of Alzheimer's, Parkinson's and Huntington's diseases and amyotrophic lateral sclerosis. We also debate the potential therapeutic efficacy of metabolic antioxidants, mitochondria-directed antioxidants and Szeto-Schiller (SS) peptides. Since these compounds preferentially target mitochondria, a major source of oxidative damage, they are promising therapeutic candidates for neurodegenerative diseases. Furthermore, we will briefly discuss the novel action of the antihistamine drug Dimebon on mitochondria. | lld:pubmed |
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