ERP Generator Anomalies in Presymptomatic Carriers of the Alzheimer's Disease E280A PS-1 Mutation

ABSTRACT: Although subtle anatomical anomalies long precede the onset of clinical symptoms in Alzheimer’s disease, their impact on the reorganization of brain networks underlying cognitive functions has not been fully explored. A unique window into this reorganization is provided by presymptomatic c...

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Autores:
Lopera Restrepo, Francisco Javier
Bobes, María Antonieta
Fernández García, Yuriem
Quiroz, Yakeel Tatiana
Galán, Lídice
Trujillo, Nelson
Valdés Sosa, Mitchell
Valdés Sosa, Pedro
Vega, Mayrim
Tipo de recurso:
Article of investigation
Fecha de publicación:
2010
Institución:
Universidad de Antioquia
Repositorio:
Repositorio UdeA
Idioma:
eng
OAI Identifier:
oai:bibliotecadigital.udea.edu.co:10495/35035
Acceso en línea:
https://hdl.handle.net/10495/35035
Palabra clave:
Alzheimer Disease
Enfermedad de Alzheimer
Mutation
Mutación
Carrier State
Portador Sano
Evoked Potentials
Potenciales Evocados
Rights
openAccess
License
http://creativecommons.org/licenses/by/2.5/co/
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network_name_str Repositorio UdeA
repository_id_str
dc.title.spa.fl_str_mv ERP Generator Anomalies in Presymptomatic Carriers of the Alzheimer's Disease E280A PS-1 Mutation
title ERP Generator Anomalies in Presymptomatic Carriers of the Alzheimer's Disease E280A PS-1 Mutation
spellingShingle ERP Generator Anomalies in Presymptomatic Carriers of the Alzheimer's Disease E280A PS-1 Mutation
Alzheimer Disease
Enfermedad de Alzheimer
Mutation
Mutación
Carrier State
Portador Sano
Evoked Potentials
Potenciales Evocados
title_short ERP Generator Anomalies in Presymptomatic Carriers of the Alzheimer's Disease E280A PS-1 Mutation
title_full ERP Generator Anomalies in Presymptomatic Carriers of the Alzheimer's Disease E280A PS-1 Mutation
title_fullStr ERP Generator Anomalies in Presymptomatic Carriers of the Alzheimer's Disease E280A PS-1 Mutation
title_full_unstemmed ERP Generator Anomalies in Presymptomatic Carriers of the Alzheimer's Disease E280A PS-1 Mutation
title_sort ERP Generator Anomalies in Presymptomatic Carriers of the Alzheimer's Disease E280A PS-1 Mutation
dc.creator.fl_str_mv Lopera Restrepo, Francisco Javier
Bobes, María Antonieta
Fernández García, Yuriem
Quiroz, Yakeel Tatiana
Galán, Lídice
Trujillo, Nelson
Valdés Sosa, Mitchell
Valdés Sosa, Pedro
Vega, Mayrim
dc.contributor.author.none.fl_str_mv Lopera Restrepo, Francisco Javier
Bobes, María Antonieta
Fernández García, Yuriem
Quiroz, Yakeel Tatiana
Galán, Lídice
Trujillo, Nelson
Valdés Sosa, Mitchell
Valdés Sosa, Pedro
Vega, Mayrim
dc.contributor.researchgroup.spa.fl_str_mv Grupo de Neurociencias de Antioquia
dc.subject.decs.none.fl_str_mv Alzheimer Disease
Enfermedad de Alzheimer
Mutation
Mutación
Carrier State
Portador Sano
Evoked Potentials
Potenciales Evocados
topic Alzheimer Disease
Enfermedad de Alzheimer
Mutation
Mutación
Carrier State
Portador Sano
Evoked Potentials
Potenciales Evocados
description ABSTRACT: Although subtle anatomical anomalies long precede the onset of clinical symptoms in Alzheimer’s disease, their impact on the reorganization of brain networks underlying cognitive functions has not been fully explored. A unique window into this reorganization is provided by presymptomatic cases of familial Alzheimer’s disease (FAD). Here we studied neural circuitry related to semantic processing in presymptomatic FAD cases by estimating the intracranial sources of the N400 event-related potential (ERP). ERPs were obtained during a semantic-matching task from 24 presymptomatic carriers and 25 symptomatic carriers of the E280A presenilin-1 (PS-1) mutation, as well as 27 noncarriers (from the same families). As expected, the symptomatic-carrier group performed worse in the matching task and had lower N400 amplitudes than both asymptomatic groups, which did not differ from each other on these variables. However, N400 topography differed in mutation carrier groups with respect to the noncarriers. Intracranial source analysis evinced that the presymptomatic-carriers presented a decrease of N400 generator strength in right inferior-temporal and medial cingulate areas and increased generator strength in the left hippocampus and parahippocampus compared to the controls. This represents alterations in neural function without translation into behavioral impairments. Compared to controls, the symptomatic-carriers presented a similar anatomical shift in the distribution of N400 generators to that found in presymptomatic-carriers, albeit with a larger reduction in generator strength. The redistribution of N400 generators in presymptomatic-carriers indicates that early focal degeneration associated with the mutation induces neural reorganization, possibly contributing to a functional compensation that enables normal performance in the semantic task. Hum Brain Mapp 31:247–265, 2010.
publishDate 2010
dc.date.issued.none.fl_str_mv 2010
dc.date.accessioned.none.fl_str_mv 2023-05-16T22:15:05Z
dc.date.available.none.fl_str_mv 2023-05-16T22:15:05Z
dc.type.spa.fl_str_mv Artículo de investigación
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dc.identifier.citation.spa.fl_str_mv Bobes MA, García YF, Lopera F, Quiroz YT, Galán L, Vega M, Trujillo N, Valdes-Sosa M, Valdes-Sosa P. ERP generator anomalies in presymptomatic carriers of the Alzheimer's disease E280A PS-1 mutation. Hum Brain Mapp. 2010 Feb;31(2):247-65. doi: 10.1002/hbm.20861.
dc.identifier.issn.none.fl_str_mv 1065-9471
dc.identifier.uri.none.fl_str_mv https://hdl.handle.net/10495/35035
dc.identifier.doi.none.fl_str_mv 10.1002/hbm.20861
dc.identifier.eissn.none.fl_str_mv 1097-0193
identifier_str_mv Bobes MA, García YF, Lopera F, Quiroz YT, Galán L, Vega M, Trujillo N, Valdes-Sosa M, Valdes-Sosa P. ERP generator anomalies in presymptomatic carriers of the Alzheimer's disease E280A PS-1 mutation. Hum Brain Mapp. 2010 Feb;31(2):247-65. doi: 10.1002/hbm.20861.
1065-9471
10.1002/hbm.20861
1097-0193
url https://hdl.handle.net/10495/35035
dc.language.iso.spa.fl_str_mv eng
language eng
dc.relation.ispartofjournalabbrev.spa.fl_str_mv Hum. Brain Mapp.
dc.relation.citationendpage.spa.fl_str_mv 265
dc.relation.citationissue.spa.fl_str_mv 2
dc.relation.citationstartpage.spa.fl_str_mv 247
dc.relation.citationvolume.spa.fl_str_mv 31
dc.relation.ispartofjournal.spa.fl_str_mv Human Brain Mapping
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dc.publisher.place.spa.fl_str_mv Nueva York, Estados Unidos
institution Universidad de Antioquia
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spelling Lopera Restrepo, Francisco JavierBobes, María AntonietaFernández García, YuriemQuiroz, Yakeel TatianaGalán, LídiceTrujillo, NelsonValdés Sosa, MitchellValdés Sosa, PedroVega, MayrimGrupo de Neurociencias de Antioquia2023-05-16T22:15:05Z2023-05-16T22:15:05Z2010Bobes MA, García YF, Lopera F, Quiroz YT, Galán L, Vega M, Trujillo N, Valdes-Sosa M, Valdes-Sosa P. ERP generator anomalies in presymptomatic carriers of the Alzheimer's disease E280A PS-1 mutation. Hum Brain Mapp. 2010 Feb;31(2):247-65. doi: 10.1002/hbm.20861.1065-9471https://hdl.handle.net/10495/3503510.1002/hbm.208611097-0193ABSTRACT: Although subtle anatomical anomalies long precede the onset of clinical symptoms in Alzheimer’s disease, their impact on the reorganization of brain networks underlying cognitive functions has not been fully explored. A unique window into this reorganization is provided by presymptomatic cases of familial Alzheimer’s disease (FAD). Here we studied neural circuitry related to semantic processing in presymptomatic FAD cases by estimating the intracranial sources of the N400 event-related potential (ERP). ERPs were obtained during a semantic-matching task from 24 presymptomatic carriers and 25 symptomatic carriers of the E280A presenilin-1 (PS-1) mutation, as well as 27 noncarriers (from the same families). As expected, the symptomatic-carrier group performed worse in the matching task and had lower N400 amplitudes than both asymptomatic groups, which did not differ from each other on these variables. However, N400 topography differed in mutation carrier groups with respect to the noncarriers. Intracranial source analysis evinced that the presymptomatic-carriers presented a decrease of N400 generator strength in right inferior-temporal and medial cingulate areas and increased generator strength in the left hippocampus and parahippocampus compared to the controls. This represents alterations in neural function without translation into behavioral impairments. Compared to controls, the symptomatic-carriers presented a similar anatomical shift in the distribution of N400 generators to that found in presymptomatic-carriers, albeit with a larger reduction in generator strength. The redistribution of N400 generators in presymptomatic-carriers indicates that early focal degeneration associated with the mutation induces neural reorganization, possibly contributing to a functional compensation that enables normal performance in the semantic task. Hum Brain Mapp 31:247–265, 2010.COL001074419application/pdfengWileyNueva York, Estados Unidoshttp://creativecommons.org/licenses/by/2.5/co/https://creativecommons.org/licenses/by/4.0/info:eu-repo/semantics/openAccesshttp://purl.org/coar/access_right/c_abf2ERP Generator Anomalies in Presymptomatic Carriers of the Alzheimer's Disease E280A PS-1 MutationArtículo de investigaciónhttp://purl.org/coar/resource_type/c_2df8fbb1https://purl.org/redcol/resource_type/ARThttp://purl.org/coar/version/c_970fb48d4fbd8a85info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionAlzheimer DiseaseEnfermedad de AlzheimerMutationMutaciónCarrier StatePortador SanoEvoked PotentialsPotenciales EvocadosHum. 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