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Article: Alteration of nitric oxide synthase activity in young and aged apolipoprotein E-deficient mice

TitleAlteration of nitric oxide synthase activity in young and aged apolipoprotein E-deficient mice
Authors
Issue Date2003
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/neuaging
Citation
Neurobiology Of Aging, 2003, v. 24 n. 1, p. 187-190 How to Cite?
AbstractImpairments in cognitive performance have been observed in aged apolipoprotein E (apoE)-deficient mice, and apoE ε4 allele is a risk factor in Alzheimer's disease (AD). The absence of apoE correlates with diminished antioxidative capacity in animals, and elevated cerebral oxidative stress has been observed in AD individuals carrying the ε4 alleles. Nitric oxide (NO) is a neurosignaling molecule that has significant roles in cognition. NO has also been implicated in neurodegenerative diseases due to its oxidative properties. The current study examined the possible relationship between apoE and nitric oxide synthase (NOS) by comparing hippocampal and cortical NOS activities in wild-type and apoE-knockout mice. Our results showed that apoE deficiency had no effect on NOS activity in these animals; however, aged animals uniformly exhibited significantly higher NOS activity levels. These findings suggest that increased NOS activity may contribute to cognitive impairments in aged wild-type and apoE-knockout mice due to excess accumulation of oxidative damages in areas involved in learning and memory. © 2002 Elsevier Science Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/171915
ISSN
2015 Impact Factor: 5.153
2015 SCImago Journal Rankings: 2.613
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLaw, Aen_US
dc.contributor.authorGauthier, Sen_US
dc.contributor.authorQuirion, Ren_US
dc.date.accessioned2012-10-30T06:18:24Z-
dc.date.available2012-10-30T06:18:24Z-
dc.date.issued2003en_US
dc.identifier.citationNeurobiology Of Aging, 2003, v. 24 n. 1, p. 187-190en_US
dc.identifier.issn0197-4580en_US
dc.identifier.urihttp://hdl.handle.net/10722/171915-
dc.description.abstractImpairments in cognitive performance have been observed in aged apolipoprotein E (apoE)-deficient mice, and apoE ε4 allele is a risk factor in Alzheimer's disease (AD). The absence of apoE correlates with diminished antioxidative capacity in animals, and elevated cerebral oxidative stress has been observed in AD individuals carrying the ε4 alleles. Nitric oxide (NO) is a neurosignaling molecule that has significant roles in cognition. NO has also been implicated in neurodegenerative diseases due to its oxidative properties. The current study examined the possible relationship between apoE and nitric oxide synthase (NOS) by comparing hippocampal and cortical NOS activities in wild-type and apoE-knockout mice. Our results showed that apoE deficiency had no effect on NOS activity in these animals; however, aged animals uniformly exhibited significantly higher NOS activity levels. These findings suggest that increased NOS activity may contribute to cognitive impairments in aged wild-type and apoE-knockout mice due to excess accumulation of oxidative damages in areas involved in learning and memory. © 2002 Elsevier Science Inc. All rights reserved.en_US
dc.languageengen_US
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/neuagingen_US
dc.relation.ispartofNeurobiology of Agingen_US
dc.subject.meshAging - Metabolismen_US
dc.subject.meshAlzheimer Disease - Enzymology - Geneticsen_US
dc.subject.meshAnimalsen_US
dc.subject.meshApolipoproteins E - Deficiency - Genetics - Metabolismen_US
dc.subject.meshCerebral Cortex - Enzymologyen_US
dc.subject.meshHippocampus - Enzymologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Inbred C57bl - Metabolismen_US
dc.subject.meshMice, Knockouten_US
dc.subject.meshNitric Oxide Synthase - Analysis - Metabolismen_US
dc.subject.meshRisk Factorsen_US
dc.titleAlteration of nitric oxide synthase activity in young and aged apolipoprotein E-deficient miceen_US
dc.typeArticleen_US
dc.identifier.emailLaw, A:acklaw@hku.hken_US
dc.identifier.authorityLaw, A=rp00262en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/S0197-4580(02)00068-4en_US
dc.identifier.pmid12493565-
dc.identifier.scopuseid_2-s2.0-0037213685en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0037213685&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume24en_US
dc.identifier.issue1en_US
dc.identifier.spage187en_US
dc.identifier.epage190en_US
dc.identifier.isiWOS:000180458000019-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridLaw, A=26323772800en_US
dc.identifier.scopusauthoridGauthier, S=7102604782en_US
dc.identifier.scopusauthoridQuirion, R=7202416940en_US

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