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Effect of aging on brain energy-metabolism
The aging process involves morphological and functional changes in cerebral vasculature and deterioration of mitochondrial number and function. Furthermore, slow oscillations of cerebral blood flow and oxidative metabolism occur in animals under different pathological conditions such as ischemia. Th...
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Published in: | Comparative biochemistry and physiology. Part A, Molecular & integrative physiology Molecular & integrative physiology, 2002-05, Vol.132 (1), p.117-120 |
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creator | Zarchin, Nili Meilin, Sigal Rifkind, Joseph Mayevsky, Avraham |
description | The aging process involves morphological and functional changes in cerebral vasculature and deterioration of mitochondrial number and function. Furthermore, slow oscillations of cerebral blood flow and oxidative metabolism occur in animals under different pathological conditions such as ischemia. The aim of this study was to evaluate the effect of aging on energy-metabolism of the rat brain during anoxia and normoxia and to further investigate the occurrence of oscillations under normoxia in the aging brain. Simultaneous hemodynamical (CBF), biochemical (NADH/NAD ratio) and electrical activity from the cerebral cortex were measured by means of a multiparametric assembly (MPA) system. Exposure of adult rats to anoxia (100% N
2) resulted in a 36±2% elevation of NADH. Furthermore, exposure of the aged group to anoxia caused NADH elevation as low as 9.6±4% (
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doi_str_mv | 10.1016/S1095-6433(01)00537-2 |
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2) resulted in a 36±2% elevation of NADH. Furthermore, exposure of the aged group to anoxia caused NADH elevation as low as 9.6±4% (
P<0.05). The changes in the NADH levels were followed by an increase in CBF. In addition, during the normoxic periods, hemodynamic oscillations were recorded in the old animals. This study suggests that the structural and functional changes that occur in vessels in the aging brain cause disability of cerebromicrovessels to optimally deliver nutrients and oxygen to the brain, affecting the mitochondrial ability to respond to anoxia. Furthermore, this study supports the approach that the hemodynamic oscillations are related to the development of a pathological state and are not a normal cerebral function.</description><identifier>ISSN: 1095-6433</identifier><identifier>EISSN: 1531-4332</identifier><identifier>DOI: 10.1016/S1095-6433(01)00537-2</identifier><identifier>PMID: 12062199</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Aging - metabolism ; Aging brain ; Animals ; Anoxia ; Brain - blood supply ; Brain - metabolism ; Cerebral blood flow ; Cerebrovascular Circulation ; Energy Metabolism ; Hypoxia - metabolism ; Metabolic oscillations ; Mitochondria - metabolism ; Mitochondrial NADH ; Multiparameter monitoring ; NAD - metabolism ; Oxygen - metabolism ; Rats ; Time Factors</subject><ispartof>Comparative biochemistry and physiology. Part A, Molecular & integrative physiology, 2002-05, Vol.132 (1), p.117-120</ispartof><rights>2002 Elsevier Science Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c361t-7f6106123efbb1c1b4bfca5d3bb7ae0e9f4769cff79617fc96d7d697faa2a0543</citedby><cites>FETCH-LOGICAL-c361t-7f6106123efbb1c1b4bfca5d3bb7ae0e9f4769cff79617fc96d7d697faa2a0543</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12062199$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zarchin, Nili</creatorcontrib><creatorcontrib>Meilin, Sigal</creatorcontrib><creatorcontrib>Rifkind, Joseph</creatorcontrib><creatorcontrib>Mayevsky, Avraham</creatorcontrib><title>Effect of aging on brain energy-metabolism</title><title>Comparative biochemistry and physiology. Part A, Molecular & integrative physiology</title><addtitle>Comp Biochem Physiol A Mol Integr Physiol</addtitle><description>The aging process involves morphological and functional changes in cerebral vasculature and deterioration of mitochondrial number and function. Furthermore, slow oscillations of cerebral blood flow and oxidative metabolism occur in animals under different pathological conditions such as ischemia. The aim of this study was to evaluate the effect of aging on energy-metabolism of the rat brain during anoxia and normoxia and to further investigate the occurrence of oscillations under normoxia in the aging brain. Simultaneous hemodynamical (CBF), biochemical (NADH/NAD ratio) and electrical activity from the cerebral cortex were measured by means of a multiparametric assembly (MPA) system. Exposure of adult rats to anoxia (100% N
2) resulted in a 36±2% elevation of NADH. Furthermore, exposure of the aged group to anoxia caused NADH elevation as low as 9.6±4% (
P<0.05). The changes in the NADH levels were followed by an increase in CBF. In addition, during the normoxic periods, hemodynamic oscillations were recorded in the old animals. This study suggests that the structural and functional changes that occur in vessels in the aging brain cause disability of cerebromicrovessels to optimally deliver nutrients and oxygen to the brain, affecting the mitochondrial ability to respond to anoxia. Furthermore, this study supports the approach that the hemodynamic oscillations are related to the development of a pathological state and are not a normal cerebral function.</description><subject>Aging - metabolism</subject><subject>Aging brain</subject><subject>Animals</subject><subject>Anoxia</subject><subject>Brain - blood supply</subject><subject>Brain - metabolism</subject><subject>Cerebral blood flow</subject><subject>Cerebrovascular Circulation</subject><subject>Energy Metabolism</subject><subject>Hypoxia - metabolism</subject><subject>Metabolic oscillations</subject><subject>Mitochondria - metabolism</subject><subject>Mitochondrial NADH</subject><subject>Multiparameter monitoring</subject><subject>NAD - metabolism</subject><subject>Oxygen - metabolism</subject><subject>Rats</subject><subject>Time Factors</subject><issn>1095-6433</issn><issn>1531-4332</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><recordid>eNqFkEtLAzEQgIMotlZ_grInUWE1s9lNmpNIqQ8oeFDPIclOSmQfNdkV-u_dPsSjc5lh-GaG-Qg5B3oLFPjdG1BZpDxn7IrCNaUFE2l2QMZQMEiHbnY41L_IiJzE-EmHyCE_JiPIKM9AyjG5mTuHtktal-ilb5ZJ2yQmaN8k2GBYrtMaO23aysf6lBw5XUU82-cJ-Xicv8-e08Xr08vsYZFaxqFLheNAOWQMnTFgweTGWV2UzBihkaJ0ueDSOickB-Gs5KUouRRO60zTImcTcrnbuwrtV4-xU7WPFqtKN9j2UQmYAkynG7DYgTa0MQZ0ahV8rcNaAVUbSWorSW0MKApqK0llw9zF_kBvaiz_pvZWBuB-B-Dw5rfHoKL12FgsfRhkqbL1_5z4AZE-dZo</recordid><startdate>20020501</startdate><enddate>20020501</enddate><creator>Zarchin, Nili</creator><creator>Meilin, Sigal</creator><creator>Rifkind, Joseph</creator><creator>Mayevsky, Avraham</creator><general>Elsevier Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20020501</creationdate><title>Effect of aging on brain energy-metabolism</title><author>Zarchin, Nili ; Meilin, Sigal ; Rifkind, Joseph ; Mayevsky, Avraham</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c361t-7f6106123efbb1c1b4bfca5d3bb7ae0e9f4769cff79617fc96d7d697faa2a0543</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Aging - metabolism</topic><topic>Aging brain</topic><topic>Animals</topic><topic>Anoxia</topic><topic>Brain - blood supply</topic><topic>Brain - metabolism</topic><topic>Cerebral blood flow</topic><topic>Cerebrovascular Circulation</topic><topic>Energy Metabolism</topic><topic>Hypoxia - metabolism</topic><topic>Metabolic oscillations</topic><topic>Mitochondria - metabolism</topic><topic>Mitochondrial NADH</topic><topic>Multiparameter monitoring</topic><topic>NAD - metabolism</topic><topic>Oxygen - metabolism</topic><topic>Rats</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zarchin, Nili</creatorcontrib><creatorcontrib>Meilin, Sigal</creatorcontrib><creatorcontrib>Rifkind, Joseph</creatorcontrib><creatorcontrib>Mayevsky, Avraham</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Comparative biochemistry and physiology. 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2) resulted in a 36±2% elevation of NADH. Furthermore, exposure of the aged group to anoxia caused NADH elevation as low as 9.6±4% (
P<0.05). The changes in the NADH levels were followed by an increase in CBF. In addition, during the normoxic periods, hemodynamic oscillations were recorded in the old animals. This study suggests that the structural and functional changes that occur in vessels in the aging brain cause disability of cerebromicrovessels to optimally deliver nutrients and oxygen to the brain, affecting the mitochondrial ability to respond to anoxia. Furthermore, this study supports the approach that the hemodynamic oscillations are related to the development of a pathological state and are not a normal cerebral function.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>12062199</pmid><doi>10.1016/S1095-6433(01)00537-2</doi><tpages>4</tpages></addata></record> |
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subjects | Aging - metabolism Aging brain Animals Anoxia Brain - blood supply Brain - metabolism Cerebral blood flow Cerebrovascular Circulation Energy Metabolism Hypoxia - metabolism Metabolic oscillations Mitochondria - metabolism Mitochondrial NADH Multiparameter monitoring NAD - metabolism Oxygen - metabolism Rats Time Factors |
title | Effect of aging on brain energy-metabolism |
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