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Article: Say NO to Alzheimer's disease: The putative links between nitric oxide and dementia of the Alzheimer's type

TitleSay NO to Alzheimer's disease: The putative links between nitric oxide and dementia of the Alzheimer's type
Authors
Issue Date2001
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/brainresrev
Citation
Brain Research Reviews, 2001, v. 35 n. 1, p. 73-96 How to Cite?
AbstractAlzheimer's disease (AD) is the most common form of dementia, with progressive cognitive deficits being the primary symptom. AD is neuropathologically characterized by amyloid and neurofibrillary tangle depositions, basal forebrain cholinergic deficit, and extensive neuronal loss and synaptic changes in the cortex and hippocampus. Mutations of amyloid precursor protein or presenilin genes or apolipoprotein E gene polymorphism appear to affect amyloid formation, which in turn causes neuronal death via a number of possible mechanisms, including Ca2+ homeostasis disruption, oxidative stress, excitotoxicity, energy depletion, neuro-inflammation and apoptosis. Nitric oxide (NO) is an enzymatic product of nitric oxide synthase, which exists in three isoforms. In addition to its vasoactive and immunological properties, NO has significant neurophysiological functions. However, NO can also be neurotoxic primarily due to its free radical properties, and it has been implicated in neurodegenerative diseases. Interestingly, there is increasing evidence that NO may have a role in the aforementioned AD pathogenetic mechanisms, and putative links between NO and AD are beginning to be recognized. This review focuses on these issues highlighting the possible relevance of NO in AD, either as a neuroprotective or neurotoxic agent. © 2001 Elsevier Science B.V.
Persistent Identifierhttp://hdl.handle.net/10722/171904
ISSN
2013 Impact Factor: 5.93
2014 SCImago Journal Rankings: 2.982
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLaw, Aen_US
dc.contributor.authorGauthier, Sen_US
dc.contributor.authorQuirion, Ren_US
dc.date.accessioned2012-10-30T06:18:20Z-
dc.date.available2012-10-30T06:18:20Z-
dc.date.issued2001en_US
dc.identifier.citationBrain Research Reviews, 2001, v. 35 n. 1, p. 73-96en_US
dc.identifier.issn0165-0173en_US
dc.identifier.urihttp://hdl.handle.net/10722/171904-
dc.description.abstractAlzheimer's disease (AD) is the most common form of dementia, with progressive cognitive deficits being the primary symptom. AD is neuropathologically characterized by amyloid and neurofibrillary tangle depositions, basal forebrain cholinergic deficit, and extensive neuronal loss and synaptic changes in the cortex and hippocampus. Mutations of amyloid precursor protein or presenilin genes or apolipoprotein E gene polymorphism appear to affect amyloid formation, which in turn causes neuronal death via a number of possible mechanisms, including Ca2+ homeostasis disruption, oxidative stress, excitotoxicity, energy depletion, neuro-inflammation and apoptosis. Nitric oxide (NO) is an enzymatic product of nitric oxide synthase, which exists in three isoforms. In addition to its vasoactive and immunological properties, NO has significant neurophysiological functions. However, NO can also be neurotoxic primarily due to its free radical properties, and it has been implicated in neurodegenerative diseases. Interestingly, there is increasing evidence that NO may have a role in the aforementioned AD pathogenetic mechanisms, and putative links between NO and AD are beginning to be recognized. This review focuses on these issues highlighting the possible relevance of NO in AD, either as a neuroprotective or neurotoxic agent. © 2001 Elsevier Science B.V.en_US
dc.languageengen_US
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/brainresreven_US
dc.relation.ispartofBrain Research Reviewsen_US
dc.subject.meshAlzheimer Disease - Etiology - Genetics - Pathology - Physiopathologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBrain - Pathologyen_US
dc.subject.meshHumansen_US
dc.subject.meshNitric Oxide - Physiologyen_US
dc.subject.meshNitric Oxide Synthase - Physiologyen_US
dc.titleSay NO to Alzheimer's disease: The putative links between nitric oxide and dementia of the Alzheimer's typeen_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/S0165-0173(00)00051-5en_US
dc.identifier.pmid11245887-
dc.identifier.scopuseid_2-s2.0-0035105932en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0035105932&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume35en_US
dc.identifier.issue1en_US
dc.identifier.spage73en_US
dc.identifier.epage96en_US
dc.identifier.isiWOS:000167645200005-
dc.publisher.placeNetherlandsen_US
dc.identifier.scopusauthoridLaw, A=26323772800en_US
dc.identifier.scopusauthoridGauthier, S=7102604782en_US
dc.identifier.scopusauthoridQuirion, R=7202416940en_US

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