Serum Insulin-Like Growth Factor I Deficiency Associates to Alzheimer's Disease Co-Morbidities

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We are thankful to M. Garcia for technical support. This work was funded by a grant from Ciberned, by and Inter-CIBER project (PIE14/00061), and from SAF2016-76462-C2-1-P (MINECO). J.A. ZegarraValdivia acknowledges the financial support from the National Council of Science, Technology and Technologi...

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Detalles Bibliográficos
Autores: Zegarra-Valdivia, JA, Santi, A, de Sevilla, MEF, Nunez, A, Aleman, IT
Formato: artículo
Fecha de Publicación:2019
Institución:Consejo Nacional de Ciencia Tecnología e Innovación
Repositorio:CONCYTEC-Institucional
Lenguaje:inglés
OAI Identifier:oai:repositorio.concytec.gob.pe:20.500.12390/1142
Enlace del recurso:https://hdl.handle.net/20.500.12390/1142
https://doi.org/10.3233/JAD-190241
Nivel de acceso:acceso abierto
Materia:insulin-like growth factor 1
Alzheimer’s disease
animal models of disease
co-morbidities
https://purl.org/pe-repo/ocde/ford#3.02.00
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network_acronym_str CONC
network_name_str CONCYTEC-Institucional
repository_id_str 4689
dc.title.none.fl_str_mv Serum Insulin-Like Growth Factor I Deficiency Associates to Alzheimer's Disease Co-Morbidities
title Serum Insulin-Like Growth Factor I Deficiency Associates to Alzheimer's Disease Co-Morbidities
spellingShingle Serum Insulin-Like Growth Factor I Deficiency Associates to Alzheimer's Disease Co-Morbidities
Zegarra-Valdivia, JA
insulin-like growth factor 1
Alzheimer’s disease
animal models of disease
co-morbidities
https://purl.org/pe-repo/ocde/ford#3.02.00
title_short Serum Insulin-Like Growth Factor I Deficiency Associates to Alzheimer's Disease Co-Morbidities
title_full Serum Insulin-Like Growth Factor I Deficiency Associates to Alzheimer's Disease Co-Morbidities
title_fullStr Serum Insulin-Like Growth Factor I Deficiency Associates to Alzheimer's Disease Co-Morbidities
title_full_unstemmed Serum Insulin-Like Growth Factor I Deficiency Associates to Alzheimer's Disease Co-Morbidities
title_sort Serum Insulin-Like Growth Factor I Deficiency Associates to Alzheimer's Disease Co-Morbidities
author Zegarra-Valdivia, JA
author_facet Zegarra-Valdivia, JA
Santi, A
de Sevilla, MEF
Nunez, A
Aleman, IT
author_role author
author2 Santi, A
de Sevilla, MEF
Nunez, A
Aleman, IT
author2_role author
author
author
author
dc.contributor.author.fl_str_mv Zegarra-Valdivia, JA
Santi, A
de Sevilla, MEF
Nunez, A
Aleman, IT
dc.subject.none.fl_str_mv insulin-like growth factor 1
topic insulin-like growth factor 1
Alzheimer’s disease
animal models of disease
co-morbidities
https://purl.org/pe-repo/ocde/ford#3.02.00
dc.subject.es_PE.fl_str_mv Alzheimer’s disease
animal models of disease
co-morbidities
dc.subject.ocde.none.fl_str_mv https://purl.org/pe-repo/ocde/ford#3.02.00
description We are thankful to M. Garcia for technical support. This work was funded by a grant from Ciberned, by and Inter-CIBER project (PIE14/00061), and from SAF2016-76462-C2-1-P (MINECO). J.A. ZegarraValdivia acknowledges the financial support from the National Council of Science, Technology and Technological Innovation (CONCYTEC, Peru) through ´the National Fund for Scientific and Technological Development (FONDECYT, Peru). ´Authors’ disclosures available online (https://www.j-alz.com/manuscript-disclosures/19-0241).
publishDate 2019
dc.date.accessioned.none.fl_str_mv 2024-05-30T23:13:38Z
dc.date.available.none.fl_str_mv 2024-05-30T23:13:38Z
dc.date.issued.fl_str_mv 2019
dc.type.none.fl_str_mv info:eu-repo/semantics/article
format article
dc.identifier.uri.none.fl_str_mv https://hdl.handle.net/20.500.12390/1142
dc.identifier.doi.none.fl_str_mv https://doi.org/10.3233/JAD-190241
dc.identifier.isi.none.fl_str_mv 472086100008
url https://hdl.handle.net/20.500.12390/1142
https://doi.org/10.3233/JAD-190241
identifier_str_mv 472086100008
dc.language.iso.none.fl_str_mv eng
language eng
dc.relation.ispartof.none.fl_str_mv Journal of Alzheimer's Disease
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.publisher.none.fl_str_mv IOS Press, Inc.
publisher.none.fl_str_mv IOS Press, Inc.
dc.source.none.fl_str_mv reponame:CONCYTEC-Institucional
instname:Consejo Nacional de Ciencia Tecnología e Innovación
instacron:CONCYTEC
instname_str Consejo Nacional de Ciencia Tecnología e Innovación
instacron_str CONCYTEC
institution CONCYTEC
reponame_str CONCYTEC-Institucional
collection CONCYTEC-Institucional
repository.name.fl_str_mv Repositorio Institucional CONCYTEC
repository.mail.fl_str_mv repositorio@concytec.gob.pe
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spelling Publicationrp02671500rp03230600rp03229600rp01848500rp01083500Zegarra-Valdivia, JASanti, Ade Sevilla, MEFNunez, AAleman, IT2024-05-30T23:13:38Z2024-05-30T23:13:38Z2019https://hdl.handle.net/20.500.12390/1142https://doi.org/10.3233/JAD-190241472086100008We are thankful to M. Garcia for technical support. This work was funded by a grant from Ciberned, by and Inter-CIBER project (PIE14/00061), and from SAF2016-76462-C2-1-P (MINECO). J.A. ZegarraValdivia acknowledges the financial support from the National Council of Science, Technology and Technological Innovation (CONCYTEC, Peru) through ´the National Fund for Scientific and Technological Development (FONDECYT, Peru). ´Authors’ disclosures available online (https://www.j-alz.com/manuscript-disclosures/19-0241).Increasing evidence supports the notion that Alzheimer's disease (AD), a condition that presents heterogeneous pathological disturbances, is also associated to perturbed metabolic function affecting insulin and insulin-like growth factor I (IGF-I). While impaired insulin activity leading to insulin resistance has been associated to AD, whether altered IGF-I function affects the disease is not entirely clear. Despite the limitations of mouse models to mimic AD pathology, we took advantage that serum IGF-I deficient mice (LID mice) present many functional perturbations present in AD, most prominently cognitive loss, which is reversed by treatment with systemic IGF-I. We analyzed whether these mice display other pathological traits that are usual co-morbidities of AD. We found that LID mice not only display cognitive disturbances, but also show altered mood and sociability, increased susceptibility to epileptiform activity, and a disturbed sleep/wake cycle. Collectively, these data suggest that reduced IGF-I activity contributes to heterogeneous deficits commonly associated to AD. We suggest that impaired IGF-I activity needs to be taken into consideration when modeling this condition.Consejo Nacional de Ciencia, Tecnología e Innovación Tecnológica - ConcytecengIOS Press, Inc.Journal of Alzheimer's Diseaseinfo:eu-repo/semantics/openAccessinsulin-like growth factor 1Alzheimer’s disease-1animal models of disease-1co-morbidities-1https://purl.org/pe-repo/ocde/ford#3.02.00-1Serum Insulin-Like Growth Factor I Deficiency Associates to Alzheimer's Disease Co-Morbiditiesinfo:eu-repo/semantics/articlereponame:CONCYTEC-Institucionalinstname:Consejo Nacional de Ciencia Tecnología e Innovacióninstacron:CONCYTEC#PLACEHOLDER_PARENT_METADATA_VALUE##PLACEHOLDER_PARENT_METADATA_VALUE##PLACEHOLDER_PARENT_METADATA_VALUE##PLACEHOLDER_PARENT_METADATA_VALUE##PLACEHOLDER_PARENT_METADATA_VALUE#20.500.12390/1142oai:repositorio.concytec.gob.pe:20.500.12390/11422024-05-30 15:23:45.68http://purl.org/coar/access_right/c_14cbinfo:eu-repo/semantics/closedAccessmetadata only accesshttps://repositorio.concytec.gob.peRepositorio Institucional CONCYTECrepositorio@concytec.gob.pe#PLACEHOLDER_PARENT_METADATA_VALUE##PLACEHOLDER_PARENT_METADATA_VALUE##PLACEHOLDER_PARENT_METADATA_VALUE##PLACEHOLDER_PARENT_METADATA_VALUE##PLACEHOLDER_PARENT_METADATA_VALUE#<Publication xmlns="https://www.openaire.eu/cerif-profile/1.1/" id="89c568ef-5baf-409b-8160-84377475d87e"> <Type xmlns="https://www.openaire.eu/cerif-profile/vocab/COAR_Publication_Types">http://purl.org/coar/resource_type/c_1843</Type> <Language>eng</Language> <Title>Serum Insulin-Like Growth Factor I Deficiency Associates to Alzheimer&apos;s Disease Co-Morbidities</Title> <PublishedIn> <Publication> <Title>Journal of Alzheimer&apos;s Disease</Title> </Publication> </PublishedIn> <PublicationDate>2019</PublicationDate> <DOI>https://doi.org/10.3233/JAD-190241</DOI> <ISI-Number>472086100008</ISI-Number> <Authors> <Author> <DisplayName>Zegarra-Valdivia, JA</DisplayName> <Person id="rp02671" /> <Affiliation> <OrgUnit> </OrgUnit> </Affiliation> </Author> <Author> <DisplayName>Santi, A</DisplayName> <Person id="rp03230" /> <Affiliation> <OrgUnit> </OrgUnit> </Affiliation> </Author> <Author> <DisplayName>de Sevilla, MEF</DisplayName> <Person id="rp03229" /> <Affiliation> <OrgUnit> </OrgUnit> </Affiliation> </Author> <Author> <DisplayName>Nunez, A</DisplayName> <Person id="rp01848" /> <Affiliation> <OrgUnit> </OrgUnit> </Affiliation> </Author> <Author> <DisplayName>Aleman, IT</DisplayName> <Person id="rp01083" /> <Affiliation> <OrgUnit> </OrgUnit> </Affiliation> </Author> </Authors> <Editors> </Editors> <Publishers> <Publisher> <DisplayName>IOS Press, Inc.</DisplayName> <OrgUnit /> </Publisher> </Publishers> <Keyword>insulin-like growth factor 1</Keyword> <Keyword>Alzheimer’s disease</Keyword> <Keyword>animal models of disease</Keyword> <Keyword>co-morbidities</Keyword> <Abstract>Increasing evidence supports the notion that Alzheimer&apos;s disease (AD), a condition that presents heterogeneous pathological disturbances, is also associated to perturbed metabolic function affecting insulin and insulin-like growth factor I (IGF-I). While impaired insulin activity leading to insulin resistance has been associated to AD, whether altered IGF-I function affects the disease is not entirely clear. Despite the limitations of mouse models to mimic AD pathology, we took advantage that serum IGF-I deficient mice (LID mice) present many functional perturbations present in AD, most prominently cognitive loss, which is reversed by treatment with systemic IGF-I. We analyzed whether these mice display other pathological traits that are usual co-morbidities of AD. We found that LID mice not only display cognitive disturbances, but also show altered mood and sociability, increased susceptibility to epileptiform activity, and a disturbed sleep/wake cycle. Collectively, these data suggest that reduced IGF-I activity contributes to heterogeneous deficits commonly associated to AD. We suggest that impaired IGF-I activity needs to be taken into consideration when modeling this condition.</Abstract> <Access xmlns="http://purl.org/coar/access_right" > </Access> </Publication> -1
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