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Article: Association of apolipoprotein E ε4 allele with bulbar-onset motor neuron disease

TitleAssociation of apolipoprotein E ε4 allele with bulbar-onset motor neuron disease
Authors
Issue Date1996
PublisherThe Lancet Publishing Group. The Journal's web site is located at http://www.elsevier.com/locate/lancet
Citation
Lancet, 1996, v. 347 n. 8995, p. 159-160 How to Cite?
AbstractBackground. Variants of the apolipoprotein E (APOE) gene influence the age of onset of Alzheimer's disease, APOE may influence the presentation of other neurological diseases. We investigated the relationship between the allelic variants of apolipoprotein E and clinical presentation in motor neuron disease, Methods. 123 patients with motor neuron disease and 121 controls were studied. Diagnosis, location of onset and date of onset were recorded prospectively, Genotyping was performed blind to clinical information. Findings. Possession of at least one ε4 allele was significantly more common in patients with bulbar onset motor neuron disease (14/33, 42%) than in limb onset patients (20/90, 22%) and controls (26/121, 21%) (χ2 = 4.93, p = 0.026 and χ2 = 5.91, p = 0.015, respectively). Interpretation. These results suggest that the apolipoprotein E ε4 allele may influence the pattern of motor neuron loss in motor neuron disease and that it may affect neuronal function in ways unrelated to the deposition of β-amyloid or accumulation of neurofibrillary tangles.
Persistent Identifierhttp://hdl.handle.net/10722/175757
ISSN
2023 Impact Factor: 98.4
2023 SCImago Journal Rankings: 12.113
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorAlChalabi, Aen_US
dc.contributor.authorEnayat, ZEen_US
dc.contributor.authorBakker, MCen_US
dc.contributor.authorSham, PCen_US
dc.contributor.authorBall, DMen_US
dc.contributor.authorShaw, CEen_US
dc.contributor.authorLloyd, CMen_US
dc.contributor.authorPowell, JFen_US
dc.contributor.authorLeigh, PNen_US
dc.date.accessioned2012-11-26T09:01:02Z-
dc.date.available2012-11-26T09:01:02Z-
dc.date.issued1996en_US
dc.identifier.citationLancet, 1996, v. 347 n. 8995, p. 159-160en_US
dc.identifier.issn0140-6736en_US
dc.identifier.urihttp://hdl.handle.net/10722/175757-
dc.description.abstractBackground. Variants of the apolipoprotein E (APOE) gene influence the age of onset of Alzheimer's disease, APOE may influence the presentation of other neurological diseases. We investigated the relationship between the allelic variants of apolipoprotein E and clinical presentation in motor neuron disease, Methods. 123 patients with motor neuron disease and 121 controls were studied. Diagnosis, location of onset and date of onset were recorded prospectively, Genotyping was performed blind to clinical information. Findings. Possession of at least one ε4 allele was significantly more common in patients with bulbar onset motor neuron disease (14/33, 42%) than in limb onset patients (20/90, 22%) and controls (26/121, 21%) (χ2 = 4.93, p = 0.026 and χ2 = 5.91, p = 0.015, respectively). Interpretation. These results suggest that the apolipoprotein E ε4 allele may influence the pattern of motor neuron loss in motor neuron disease and that it may affect neuronal function in ways unrelated to the deposition of β-amyloid or accumulation of neurofibrillary tangles.en_US
dc.languageengen_US
dc.publisherThe Lancet Publishing Group. The Journal's web site is located at http://www.elsevier.com/locate/lanceten_US
dc.relation.ispartofLanceten_US
dc.subject.meshAge Of Onseten_US
dc.subject.meshAllelesen_US
dc.subject.meshApolipoproteins E - Geneticsen_US
dc.subject.meshFemaleen_US
dc.subject.meshGenotypeen_US
dc.subject.meshHumansen_US
dc.subject.meshMaleen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshMotor Neuron Disease - Geneticsen_US
dc.subject.meshProspective Studiesen_US
dc.titleAssociation of apolipoprotein E ε4 allele with bulbar-onset motor neuron diseaseen_US
dc.typeArticleen_US
dc.identifier.emailSham, PC: pcsham@hku.hken_US
dc.identifier.authoritySham, PC=rp00459en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/S0140-6736(96)90343-8en_US
dc.identifier.pmid8544551-
dc.identifier.scopuseid_2-s2.0-0030025431en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0030025431&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume347en_US
dc.identifier.issue8995en_US
dc.identifier.spage159en_US
dc.identifier.epage160en_US
dc.identifier.isiWOS:A1996TQ24400012-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridAlChalabi, A=7003751621en_US
dc.identifier.scopusauthoridEnayat, ZE=6508324646en_US
dc.identifier.scopusauthoridBakker, MC=7101722373en_US
dc.identifier.scopusauthoridSham, PC=34573429300en_US
dc.identifier.scopusauthoridBall, DM=7202703810en_US
dc.identifier.scopusauthoridShaw, CE=35370282000en_US
dc.identifier.scopusauthoridLloyd, CM=7202193138en_US
dc.identifier.scopusauthoridPowell, JF=7403541196en_US
dc.identifier.scopusauthoridLeigh, PN=26643325600en_US
dc.identifier.issnl0140-6736-

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