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Article: Behavioral and neurochemical characterization of transgenic mice carrying the human presenilin-1 gene with or without the leucine-to-proline mutation at codon 235

TitleBehavioral and neurochemical characterization of transgenic mice carrying the human presenilin-1 gene with or without the leucine-to-proline mutation at codon 235
Authors
Keywordsβ-Amyloid
Alzheimer's disease
Choline acetyltransferase
Object recognition memory
Presenilin-1
Somatostatin
Water maze
Issue Date2003
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/yexnr
Citation
Experimental Neurology, 2003, v. 183 n. 2, p. 673-681 How to Cite?
AbstractHuman presenilin-1 (PS1) mutations are associated with the incidence of familial Alzheimer's disease. The present study evaluated the behavioral and neurochemical effects of the L235P mutation (substitution of leucine by proline at codon 235) of the human PS1 gene, which has been linked to a form of early-onset Alzheimer's disease. Except for a significant increase in the production of β-amyloid-42, the mutant mice did not show any overt signs of Alzheimer-like neuropathology in the form of plaque formation, changes in choline acetyltransferase activity, or somatostatin content in the brain. Cognitive assays indicated that the mutation did not affect the acquisition or reversal of a spatial reference memory task in the water maze or performance on a spatial working memory task. In contrast, L235P PS1 transgenic mice exhibited a significant impairment in a test of spontaneous object recognition. This dissociation is suggestive of a preferential impairment of the extrahippocampal memory system and is consistent with what has been reported in another pathological mutation (substitution of leucine by valine at codon 286) of the PS1 gene. © 2003 Elsevier Science (USA). All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/81203
ISSN
2015 Impact Factor: 4.657
2015 SCImago Journal Rankings: 2.427
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorHuang, XGen_HK
dc.contributor.authorYee, BKen_HK
dc.contributor.authorNag, Sen_HK
dc.contributor.authorChan, STHen_HK
dc.contributor.authorTang, Fen_HK
dc.date.accessioned2010-09-06T08:15:00Z-
dc.date.available2010-09-06T08:15:00Z-
dc.date.issued2003en_HK
dc.identifier.citationExperimental Neurology, 2003, v. 183 n. 2, p. 673-681en_HK
dc.identifier.issn0014-4886en_HK
dc.identifier.urihttp://hdl.handle.net/10722/81203-
dc.description.abstractHuman presenilin-1 (PS1) mutations are associated with the incidence of familial Alzheimer's disease. The present study evaluated the behavioral and neurochemical effects of the L235P mutation (substitution of leucine by proline at codon 235) of the human PS1 gene, which has been linked to a form of early-onset Alzheimer's disease. Except for a significant increase in the production of β-amyloid-42, the mutant mice did not show any overt signs of Alzheimer-like neuropathology in the form of plaque formation, changes in choline acetyltransferase activity, or somatostatin content in the brain. Cognitive assays indicated that the mutation did not affect the acquisition or reversal of a spatial reference memory task in the water maze or performance on a spatial working memory task. In contrast, L235P PS1 transgenic mice exhibited a significant impairment in a test of spontaneous object recognition. This dissociation is suggestive of a preferential impairment of the extrahippocampal memory system and is consistent with what has been reported in another pathological mutation (substitution of leucine by valine at codon 286) of the PS1 gene. © 2003 Elsevier Science (USA). All rights reserved.en_HK
dc.languageengen_HK
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/yexnren_HK
dc.relation.ispartofExperimental Neurologyen_HK
dc.subjectβ-Amyloiden_HK
dc.subjectAlzheimer's diseaseen_HK
dc.subjectCholine acetyltransferaseen_HK
dc.subjectObject recognition memoryen_HK
dc.subjectPresenilin-1en_HK
dc.subjectSomatostatinen_HK
dc.subjectWater mazeen_HK
dc.titleBehavioral and neurochemical characterization of transgenic mice carrying the human presenilin-1 gene with or without the leucine-to-proline mutation at codon 235en_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0014-4886&volume=183&spage=673&epage=681&date=2003&atitle=Behavioral+and+neurochemical+characterization+of+transgenic+mice+carrying+the+human+presenilin-1+gene+with+or+without+the+leucine-to-proline+mutation+at+codon+235en_HK
dc.identifier.emailTang, F: ftang@hkucc.hku.hken_HK
dc.identifier.authorityTang, F=rp00327en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/S0014-4886(03)00242-5en_HK
dc.identifier.pmid14552909-
dc.identifier.scopuseid_2-s2.0-0141448940en_HK
dc.identifier.hkuros88487en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0141448940&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume183en_HK
dc.identifier.issue2en_HK
dc.identifier.spage673en_HK
dc.identifier.epage681en_HK
dc.identifier.isiWOS:000185724600045-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridHuang, XG=7410243326en_HK
dc.identifier.scopusauthoridYee, BK=7006955693en_HK
dc.identifier.scopusauthoridNag, S=7103093193en_HK
dc.identifier.scopusauthoridChan, STH=24368283200en_HK
dc.identifier.scopusauthoridTang, F=7201979770en_HK

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