| pubmed-article:7968373 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:7968373 | lifeskim:mentions | umls-concept:C0684336 | lld:lifeskim |
| pubmed-article:7968373 | lifeskim:mentions | umls-concept:C0002395 | lld:lifeskim |
| pubmed-article:7968373 | lifeskim:mentions | umls-concept:C0521451 | lld:lifeskim |
| pubmed-article:7968373 | lifeskim:mentions | umls-concept:C0010760 | lld:lifeskim |
| pubmed-article:7968373 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:7968373 | pubmed:issue | 1-4 | lld:pubmed |
| pubmed-article:7968373 | pubmed:dateCreated | 1994-12-7 | lld:pubmed |
| pubmed-article:7968373 | pubmed:abstractText | Brains from 5 patients with Alzheimer's disease (AD) showed a 50%-65% decrease in mRNA levels of the mitochondrial-encoded cytochrome oxidase (COX, a marker of oxidative metabolism) subunits I and III in the middle temporal association neocortex, but not in the primary motor cortex, as compared to 5 control brains. The amount of mitochondrial-encoded 12S rRNA was not altered, nor was the amount of nuclear-encoded lactate dehydrogenase B mRNA (a marker of glycolytic metabolism). These data suggest that the decrease in COX I and III subunits mRNA in affected brain regions may contribute to reduced brain oxidative metabolism in AD. | lld:pubmed |
| pubmed-article:7968373 | pubmed:language | eng | lld:pubmed |
| pubmed-article:7968373 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7968373 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:7968373 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:7968373 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:7968373 | pubmed:issn | 0169-328X | lld:pubmed |
| pubmed-article:7968373 | pubmed:author | pubmed-author:BradyD RDR | lld:pubmed |
| pubmed-article:7968373 | pubmed:author | pubmed-author:RapoportS ISI | lld:pubmed |
| pubmed-article:7968373 | pubmed:author | pubmed-author:StollJJ | lld:pubmed |
| pubmed-article:7968373 | pubmed:author | pubmed-author:MartinL JLJ | lld:pubmed |
| pubmed-article:7968373 | pubmed:author | pubmed-author:Chandrasekara... | lld:pubmed |
| pubmed-article:7968373 | pubmed:author | pubmed-author:GiordanoTT | lld:pubmed |
| pubmed-article:7968373 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:7968373 | pubmed:volume | 24 | lld:pubmed |
| pubmed-article:7968373 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:7968373 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:7968373 | pubmed:pagination | 336-40 | lld:pubmed |
| pubmed-article:7968373 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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| pubmed-article:7968373 | pubmed:year | 1994 | lld:pubmed |
| pubmed-article:7968373 | pubmed:articleTitle | Impairment in mitochondrial cytochrome oxidase gene expression in Alzheimer disease. | lld:pubmed |
| pubmed-article:7968373 | pubmed:affiliation | Laboratory of Neurosciences, National Institute on Aging, Bethesda, MD 20892. | lld:pubmed |
| pubmed-article:7968373 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:7968373 | pubmed:publicationType | Clinical Trial | lld:pubmed |
| pubmed-article:7968373 | pubmed:publicationType | Comparative Study | lld:pubmed |
| pubmed-article:7968373 | pubmed:publicationType | Controlled Clinical Trial | lld:pubmed |
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