APP processing and b-amyloid deposition in sporadic Creutzfeldt-Jakob patients is dependent on Dab1.

Alzheimer"s disease and prion pathologies (e.g., Creutzfeldt-Jakob disease (CJD)) display profound neural lesions associated with aberrant protein processing and extracellular amyloid deposits. Dab1 has been implicated in the regulation of Amyloid Precursor Protein (APP), but a direct link betw...

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Detalles Bibliográficos
Autores: Gavín Marín, Rosalina, Ferrer, Isidro (Ferrer Abizanda), Río Fernández, José Antonio del
Tipo de recurso: artículo
Estado:Versión aceptada para publicación
Fecha de publicación:2010
País:España
Institución:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)
Repositorio:Recercat. Dipósit de la Recerca de Catalunya
OAI Identifier:oai:recercat.cat:2445/34862
Acceso en línea:https://hdl.handle.net/2445/34862
Access Level:acceso abierto
Palabra clave:Malaltia d'Alzheimer
Malalties per prions
Malalties del sistema nerviós central
Alzheimer's disease
Prion diseases
Central nervous system diseases
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spelling APP processing and b-amyloid deposition in sporadic Creutzfeldt-Jakob patients is dependent on Dab1.Gavín Marín, RosalinaFerrer, Isidro (Ferrer Abizanda)Río Fernández, José Antonio delMalaltia d'AlzheimerMalalties per prionsMalalties del sistema nerviós centralAlzheimer's diseasePrion diseasesCentral nervous system diseasesAlzheimer"s disease and prion pathologies (e.g., Creutzfeldt-Jakob disease (CJD)) display profound neural lesions associated with aberrant protein processing and extracellular amyloid deposits. Dab1 has been implicated in the regulation of Amyloid Precursor Protein (APP), but a direct link between human prion diseases and Dab1/APP interactions has not been published. Here we examined this putative relationship in seventeen cases of sporadic CJD (sCJD) post mortem. Biochemical analyses of brain tissue revealed two groups, which also correlated with PrPsc types 1 and 2. One group, with PrPsc type 1 showed increased Dab1 phosphorylation, and lower CTF production with an absence of A deposition. The second sCJD group, which carried PrPsc type 2, showed lower levels of Dab1 phosphorylation and CTF production, and A deposition. Thus, the present observations suggest a correlation between Dab1-phosphorylation, A deposition and PrPsc type in sCJD.Elsevier2013201320102013info:eu-repo/semantics/articleinfo:eu-repo/semantics/acceptedVersion20 p.application/pdfapplication/pdfhttps://hdl.handle.net/2445/34862Articles publicats en revistes (Biologia Cel·lular, Fisiologia i Immunologia)reponame:Recercat. Dipósit de la Recerca de Catalunyainstname:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)InglésVersió postprint del document publicat a: http://dx.doi.org/10.1016/j.nbd.2009.10.010Neurobiology of Disease, 2010, vol. 37, p. 324-329http://dx.doi.org/10.1016/j.nbd.2009.10.010(c) Elsevier, 2010info:eu-repo/semantics/openAccessoai:recercat.cat:2445/348622026-05-29T05:05:01Z
dc.title.none.fl_str_mv APP processing and b-amyloid deposition in sporadic Creutzfeldt-Jakob patients is dependent on Dab1.
title APP processing and b-amyloid deposition in sporadic Creutzfeldt-Jakob patients is dependent on Dab1.
spellingShingle APP processing and b-amyloid deposition in sporadic Creutzfeldt-Jakob patients is dependent on Dab1.
Gavín Marín, Rosalina
Malaltia d'Alzheimer
Malalties per prions
Malalties del sistema nerviós central
Alzheimer's disease
Prion diseases
Central nervous system diseases
title_short APP processing and b-amyloid deposition in sporadic Creutzfeldt-Jakob patients is dependent on Dab1.
title_full APP processing and b-amyloid deposition in sporadic Creutzfeldt-Jakob patients is dependent on Dab1.
title_fullStr APP processing and b-amyloid deposition in sporadic Creutzfeldt-Jakob patients is dependent on Dab1.
title_full_unstemmed APP processing and b-amyloid deposition in sporadic Creutzfeldt-Jakob patients is dependent on Dab1.
title_sort APP processing and b-amyloid deposition in sporadic Creutzfeldt-Jakob patients is dependent on Dab1.
dc.creator.none.fl_str_mv Gavín Marín, Rosalina
Ferrer, Isidro (Ferrer Abizanda)
Río Fernández, José Antonio del
author Gavín Marín, Rosalina
author_facet Gavín Marín, Rosalina
Ferrer, Isidro (Ferrer Abizanda)
Río Fernández, José Antonio del
author_role author
author2 Ferrer, Isidro (Ferrer Abizanda)
Río Fernández, José Antonio del
author2_role author
author
dc.subject.none.fl_str_mv Malaltia d'Alzheimer
Malalties per prions
Malalties del sistema nerviós central
Alzheimer's disease
Prion diseases
Central nervous system diseases
topic Malaltia d'Alzheimer
Malalties per prions
Malalties del sistema nerviós central
Alzheimer's disease
Prion diseases
Central nervous system diseases
description Alzheimer"s disease and prion pathologies (e.g., Creutzfeldt-Jakob disease (CJD)) display profound neural lesions associated with aberrant protein processing and extracellular amyloid deposits. Dab1 has been implicated in the regulation of Amyloid Precursor Protein (APP), but a direct link between human prion diseases and Dab1/APP interactions has not been published. Here we examined this putative relationship in seventeen cases of sporadic CJD (sCJD) post mortem. Biochemical analyses of brain tissue revealed two groups, which also correlated with PrPsc types 1 and 2. One group, with PrPsc type 1 showed increased Dab1 phosphorylation, and lower CTF production with an absence of A deposition. The second sCJD group, which carried PrPsc type 2, showed lower levels of Dab1 phosphorylation and CTF production, and A deposition. Thus, the present observations suggest a correlation between Dab1-phosphorylation, A deposition and PrPsc type in sCJD.
publishDate 2010
dc.date.none.fl_str_mv 2010
2013
2013
2013
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/acceptedVersion
format article
status_str acceptedVersion
dc.identifier.none.fl_str_mv https://hdl.handle.net/2445/34862
url https://hdl.handle.net/2445/34862
dc.language.none.fl_str_mv Inglés
language_invalid_str_mv Inglés
dc.relation.none.fl_str_mv Versió postprint del document publicat a: http://dx.doi.org/10.1016/j.nbd.2009.10.010
Neurobiology of Disease, 2010, vol. 37, p. 324-329
http://dx.doi.org/10.1016/j.nbd.2009.10.010
dc.rights.none.fl_str_mv (c) Elsevier, 2010
info:eu-repo/semantics/openAccess
rights_invalid_str_mv (c) Elsevier, 2010
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv 20 p.
application/pdf
application/pdf
dc.publisher.none.fl_str_mv Elsevier
publisher.none.fl_str_mv Elsevier
dc.source.none.fl_str_mv Articles publicats en revistes (Biologia Cel·lular, Fisiologia i Immunologia)
reponame:Recercat. Dipósit de la Recerca de Catalunya
instname:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)
instname_str Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)
reponame_str Recercat. Dipósit de la Recerca de Catalunya
collection Recercat. Dipósit de la Recerca de Catalunya
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repository.mail.fl_str_mv
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