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dc.contributor.authorWimalasena, Kandatege
dc.date.accessioned2016-05-13T18:09:18Z
dc.date.available2016-05-13T18:09:18Z
dc.date.issued2016-03-16
dc.identifier.citationWimalasena K. The inherent high vulnerability of dopaminergic neurons toward mitochondrial toxins may contribute to the etiology of Parkinson's disease . Neural Regen Res 2016;11:246-7en_US
dc.identifier.issn1673-5374
dc.identifier.otherWOS:000373221900024
dc.identifier.urihttp://dx.doi.org/10.4103/1673-5374.177730
dc.identifier.urihttp://hdl.handle.net/10057/12043
dc.descriptionClick on the DOI link to access the article (may not be free).en_US
dc.description.abstractAlthough the exact mechanism(s) of the degeneration of dopaminergic neurons in Parkinson's disease (PD) is not well understood, mitochondrial dysfunction is proposed to play a central role. This proposal is strongly strengthened by the findings that compromised mitochondrial functions and/or exposure to mitochondrial toxins such as rotenone, paraquat, or MPTP causes degeneration of the midbrain dopaminergic system and manifest symptoms similar to Parkinson's disease in primates and rodents (Goldman, 2014). In fact, the specific dopaminergic toxin MPTP is one of the most commonly used models in the mechanistic studies of environmental factors associated with the etiology of PD, particularly due to the availability of direct and unequivocal clinical and biochemical evidence from human and primate subjects.en_US
dc.language.isoen_USen_US
dc.publisherMedknowen_US
dc.relation.ispartofseriesNeural Regen Research;v.11:no.2
dc.subjectOrganic cationsen_US
dc.subjectTransporteren_US
dc.subjectMechanismen_US
dc.subjectToxicityen_US
dc.subject1-methyl-4-phenylpyridiumen_US
dc.titleThe inherent high vulnerability of dopaminergic neurons toward mitochondrial toxins may contribute to the etiology of Parkinsons diseaseen_US
dc.typeArticleen_US
dc.rights.holder© Neural Regeneration Research | Published by Wolters Kluwer - Medknowen_US


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