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Titolo:
DOWN-REGULATION OF OXIDATIVE-PHOSPHORYLATION IN ALZHEIMER-DISEASE - LOSS OF CYTOCHROME-OXIDASE SUBUNIT MESSENGER-RNA IN THE HIPPOCAMPUS ANDENTORHINAL CORTEX
Autore:
CHANDRASEKARAN K; HATANPAA K; BRADY DR; STOLL J; RAPOPORT SI;
Indirizzi:
NIA,NEUROSCI LAB,NIH,BLDG 10,RM 6C 103 BETHESDA MD 20892 NIA,NEUROSCI LAB,NIH BETHESDA MD 20892
Titolo Testata:
Brain research
fascicolo: 1-2, volume: 796, anno: 1998,
pagine: 13 - 19
SICI:
0006-8993(1998)796:1-2<13:DOOIA->2.0.ZU;2-K
Fonte:
ISI
Lingua:
ENG
Soggetto:
MITOCHONDRIAL-DNA EXPRESSION; NEUROFIBRILLARY TANGLES; GENE-EXPRESSION; FUNCTIONAL ALTERATIONS; POSITRON TOMOGRAPHY; NEURONAL-ACTIVITY; MESSENGER-RNA; MONKEY BRAIN; C-OXIDASE; METABOLISM;
Keywords:
MITOCHONDRIA; NEUROFIBRILLARY TANGLES; NEURITIC PLAQUE; MITOCHONDRIAL DNA; SYNAPSE; NEURONAL ACTIVITY; OXIDATIVE DAMAGE; MUTATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
48
Recensione:
Indirizzi per estratti:
Citazione:
K. Chandrasekaran et al., "DOWN-REGULATION OF OXIDATIVE-PHOSPHORYLATION IN ALZHEIMER-DISEASE - LOSS OF CYTOCHROME-OXIDASE SUBUNIT MESSENGER-RNA IN THE HIPPOCAMPUS ANDENTORHINAL CORTEX", Brain research, 796(1-2), 1998, pp. 13-19

Abstract

Messenger RNA (mRNA) for cytochrome oxidase subunit II (COX II) was localized by in situ hybridization in the entorhinal cortex and hippocampal formation of postmortem brain tissue from normal human subjects and from patients with Alzheimer disease (AD). In the control entorhinal cortex, COX II mRNA was detected mainly in neuronal cell bodies of layers II and IV. In control hippocampal formation, highest levels werelocalized in neuronal cell bodies of the dentate gyrus and the CA3 and CA1 regions, neurons that are involved in the major input and outputpathways of the hippocampal formation. In AD brain, COX II mRNA was markedly reduced in the entorhinal cortex and the hippocampal formationcompared with control brain. In the AD hippocampal formation, reductions were in regions severely affected by AD pathology as well as in regions that were relatively spared. These results are consistent with the hypothesis that reduced mitochondrial energy metabolism reflects loss of neuronal connections in AD. (C) 1998 Elsevier Science B.V. All rights reserved.

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Documento generato il 31/03/20 alle ore 04:13:33