pubmed-article:8359498 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:8359498 | lifeskim:mentions | umls-concept:C0030567 | lld:lifeskim |
pubmed-article:8359498 | lifeskim:mentions | umls-concept:C0521451 | lld:lifeskim |
pubmed-article:8359498 | lifeskim:mentions | umls-concept:C0016693 | lld:lifeskim |
pubmed-article:8359498 | lifeskim:mentions | umls-concept:C0277785 | lld:lifeskim |
pubmed-article:8359498 | pubmed:issue | 2 | lld:pubmed |
pubmed-article:8359498 | pubmed:dateCreated | 1993-9-30 | lld:pubmed |
pubmed-article:8359498 | pubmed:abstractText | The precise relationship of the complex I deficiency in PD to the dopaminergic cell death and aetiology of this disorder is as yet unknown. However, evidence is accruing that this mitochondrial defect may play a central role in the cascade of events that terminates in nigral neuronal loss. Further work needs to be carried out to determine the molecular mechanisms that underlie the complex I deficiency as these may provide important indicators to the ultimate cause of PD. This may involve a genetic abnormality of complex I that may convey a susceptibility to developing PD. Alternatively, exogenous or endogenous toxic agents may target nigral complex I along pathways similar to those recognized for MPTP. A combination of a genetic predisposition in addition to an environmental precipitant has gained substantial support as an explanation for the cause of PD. | lld:pubmed |
pubmed-article:8359498 | pubmed:language | eng | lld:pubmed |
pubmed-article:8359498 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8359498 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:8359498 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8359498 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8359498 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:8359498 | pubmed:month | May | lld:pubmed |
pubmed-article:8359498 | pubmed:issn | 0300-5127 | lld:pubmed |
pubmed-article:8359498 | pubmed:author | pubmed-author:CleeterM WMW | lld:pubmed |
pubmed-article:8359498 | pubmed:author | pubmed-author:CooperJ MJM | lld:pubmed |
pubmed-article:8359498 | pubmed:author | pubmed-author:SchapiraA HAH | lld:pubmed |
pubmed-article:8359498 | pubmed:author | pubmed-author:HartleyAA | lld:pubmed |
pubmed-article:8359498 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:8359498 | pubmed:volume | 21 | lld:pubmed |
pubmed-article:8359498 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:8359498 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:8359498 | pubmed:pagination | 367-70 | lld:pubmed |
pubmed-article:8359498 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
pubmed-article:8359498 | pubmed:meshHeading | pubmed-meshheading:8359498-... | lld:pubmed |
pubmed-article:8359498 | pubmed:meshHeading | pubmed-meshheading:8359498-... | lld:pubmed |
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pubmed-article:8359498 | pubmed:meshHeading | pubmed-meshheading:8359498-... | lld:pubmed |
pubmed-article:8359498 | pubmed:meshHeading | pubmed-meshheading:8359498-... | lld:pubmed |
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pubmed-article:8359498 | pubmed:meshHeading | pubmed-meshheading:8359498-... | lld:pubmed |
pubmed-article:8359498 | pubmed:meshHeading | pubmed-meshheading:8359498-... | lld:pubmed |
pubmed-article:8359498 | pubmed:year | 1993 | lld:pubmed |
pubmed-article:8359498 | pubmed:articleTitle | Free radicals and mitochondrial dysfunction in Parkinson's disease. | lld:pubmed |
pubmed-article:8359498 | pubmed:affiliation | Department of Neuroscience, Royal Free Hospital School of Medicine, London, U.K. | lld:pubmed |
pubmed-article:8359498 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:8359498 | pubmed:publicationType | Review | lld:pubmed |
http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:8359498 | lld:pubmed |