In Vivo Studies of Protein Misfolding and Neurodegeneration Induced by Metabolic Syndrome Relative to Chronic Cerebral Hypoperfusion: A Critical Review

Autores
Herrera, María I.; Luaces, Juan Pablo; Udovin, Lucas D.; Toro Urrego, Nicolas; Otero-losada, Matilde Estela; Capani, Francisco
Año de publicación
2020
Idioma
inglés
Tipo de recurso
parte de libro
Estado
versión publicada
Descripción
Metabolic syndrome (MetS) leads to microvascular dysfunction and chronic cerebral hypoperfusion (CCH) in an insidious way. Clinical evidence and several rodent models have contributed to determining the neurodegenerative effect of a sustained decrease in cerebral blood flow (CBF). Protein misfolding and aggrega- tion derived from CCH might account for the establishment of vascular cognitive impairment and dementia (VCID) and Alzheimer?s disease (AD). However, the complex and multifactorial etiology of cerebrovascular disease demands the combination of experimental models in scientific research. In this sense, the present work aims at summarizing the differential available rodent paradigms for studying the establishment of cognitive decline resulting from protein misfolding inducedby MetS in association with CCH. Revising experimental findings in the field will help further basic research on the pathophysiology of cerebrovascular disease and the future testing of protein-remodeling factors as neuroprotective agents for the prevention of cognitive impairment.
Fil: Herrera, María I.. No especifíca;
Fil: Luaces, Juan Pablo. Universidad Abierta Interamericana. Secretaría de Investigación. Centro de Altos Estudios En Ciencias Humanas y de la Salud - Sede Buenos Aires.; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Udovin, Lucas D.. No especifíca;
Fil: Toro Urrego, Nicolas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; Argentina
Fil: Otero-losada, Matilde Estela. Universidad Abierta Interamericana. Secretaría de Investigación. Centro de Altos Estudios En Ciencias Humanas y de la Salud - Sede Buenos Aires.; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Capani, Francisco. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Abierta Interamericana. Secretaría de Investigación. Centro de Altos Estudios En Ciencias Humanas y de la Salud - Sede Buenos Aires.; Argentina
Materia
metabolic syndrome (MetS)
chronic cerebral hypoperfusion (CCH)
protein misfolding
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/129456
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/129456
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling In Vivo Studies of Protein Misfolding and Neurodegeneration Induced by Metabolic Syndrome Relative to Chronic Cerebral Hypoperfusion: A Critical ReviewHerrera, María I.Luaces, Juan PabloUdovin, Lucas D.Toro Urrego, NicolasOtero-losada, Matilde EstelaCapani, Franciscometabolic syndrome (MetS)chronic cerebral hypoperfusion (CCH)protein misfoldinghttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Metabolic syndrome (MetS) leads to microvascular dysfunction and chronic cerebral hypoperfusion (CCH) in an insidious way. Clinical evidence and several rodent models have contributed to determining the neurodegenerative effect of a sustained decrease in cerebral blood flow (CBF). Protein misfolding and aggrega- tion derived from CCH might account for the establishment of vascular cognitive impairment and dementia (VCID) and Alzheimer?s disease (AD). However, the complex and multifactorial etiology of cerebrovascular disease demands the combination of experimental models in scientific research. In this sense, the present work aims at summarizing the differential available rodent paradigms for studying the establishment of cognitive decline resulting from protein misfolding inducedby MetS in association with CCH. Revising experimental findings in the field will help further basic research on the pathophysiology of cerebrovascular disease and the future testing of protein-remodeling factors as neuroprotective agents for the prevention of cognitive impairment.Fil: Herrera, María I.. No especifíca;Fil: Luaces, Juan Pablo. Universidad Abierta Interamericana. Secretaría de Investigación. Centro de Altos Estudios En Ciencias Humanas y de la Salud - Sede Buenos Aires.; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Udovin, Lucas D.. No especifíca;Fil: Toro Urrego, Nicolas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; ArgentinaFil: Otero-losada, Matilde Estela. Universidad Abierta Interamericana. Secretaría de Investigación. Centro de Altos Estudios En Ciencias Humanas y de la Salud - Sede Buenos Aires.; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Capani, Francisco. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Abierta Interamericana. Secretaría de Investigación. Centro de Altos Estudios En Ciencias Humanas y de la Salud - Sede Buenos Aires.; ArgentinaIntechOpenOtero-losada, Matilde EstelaCapani, FranciscoPerez Lloret, Santiago2020info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/bookParthttp://purl.org/coar/resource_type/c_3248info:ar-repo/semantics/parteDeLibroapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/129456Herrera, María I.; Luaces, Juan Pablo; Udovin, Lucas D.; Toro Urrego, Nicolas; Otero-losada, Matilde Estela; et al.; In Vivo Studies of Protein Misfolding and Neurodegeneration Induced by Metabolic Syndrome Relative to Chronic Cerebral Hypoperfusion: A Critical Review; IntechOpen; 2020; 1-15978-1-83880-440-4CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.intechopen.com/chapters/72902info:eu-repo/semantics/altIdentifier/doi/10.5772/intechopen.92603info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T10:06:35Zoai:ri.conicet.gov.ar:11336/129456instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-03 10:06:36.127CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv In Vivo Studies of Protein Misfolding and Neurodegeneration Induced by Metabolic Syndrome Relative to Chronic Cerebral Hypoperfusion: A Critical Review
title In Vivo Studies of Protein Misfolding and Neurodegeneration Induced by Metabolic Syndrome Relative to Chronic Cerebral Hypoperfusion: A Critical Review
spellingShingle In Vivo Studies of Protein Misfolding and Neurodegeneration Induced by Metabolic Syndrome Relative to Chronic Cerebral Hypoperfusion: A Critical Review
Herrera, María I.
metabolic syndrome (MetS)
chronic cerebral hypoperfusion (CCH)
protein misfolding
title_short In Vivo Studies of Protein Misfolding and Neurodegeneration Induced by Metabolic Syndrome Relative to Chronic Cerebral Hypoperfusion: A Critical Review
title_full In Vivo Studies of Protein Misfolding and Neurodegeneration Induced by Metabolic Syndrome Relative to Chronic Cerebral Hypoperfusion: A Critical Review
title_fullStr In Vivo Studies of Protein Misfolding and Neurodegeneration Induced by Metabolic Syndrome Relative to Chronic Cerebral Hypoperfusion: A Critical Review
title_full_unstemmed In Vivo Studies of Protein Misfolding and Neurodegeneration Induced by Metabolic Syndrome Relative to Chronic Cerebral Hypoperfusion: A Critical Review
title_sort In Vivo Studies of Protein Misfolding and Neurodegeneration Induced by Metabolic Syndrome Relative to Chronic Cerebral Hypoperfusion: A Critical Review
dc.creator.none.fl_str_mv Herrera, María I.
Luaces, Juan Pablo
Udovin, Lucas D.
Toro Urrego, Nicolas
Otero-losada, Matilde Estela
Capani, Francisco
author Herrera, María I.
author_facet Herrera, María I.
Luaces, Juan Pablo
Udovin, Lucas D.
Toro Urrego, Nicolas
Otero-losada, Matilde Estela
Capani, Francisco
author_role author
author2 Luaces, Juan Pablo
Udovin, Lucas D.
Toro Urrego, Nicolas
Otero-losada, Matilde Estela
Capani, Francisco
author2_role author
author
author
author
author
dc.contributor.none.fl_str_mv Otero-losada, Matilde Estela
Capani, Francisco
Perez Lloret, Santiago
dc.subject.none.fl_str_mv metabolic syndrome (MetS)
chronic cerebral hypoperfusion (CCH)
protein misfolding
topic metabolic syndrome (MetS)
chronic cerebral hypoperfusion (CCH)
protein misfolding
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Metabolic syndrome (MetS) leads to microvascular dysfunction and chronic cerebral hypoperfusion (CCH) in an insidious way. Clinical evidence and several rodent models have contributed to determining the neurodegenerative effect of a sustained decrease in cerebral blood flow (CBF). Protein misfolding and aggrega- tion derived from CCH might account for the establishment of vascular cognitive impairment and dementia (VCID) and Alzheimer?s disease (AD). However, the complex and multifactorial etiology of cerebrovascular disease demands the combination of experimental models in scientific research. In this sense, the present work aims at summarizing the differential available rodent paradigms for studying the establishment of cognitive decline resulting from protein misfolding inducedby MetS in association with CCH. Revising experimental findings in the field will help further basic research on the pathophysiology of cerebrovascular disease and the future testing of protein-remodeling factors as neuroprotective agents for the prevention of cognitive impairment.
Fil: Herrera, María I.. No especifíca;
Fil: Luaces, Juan Pablo. Universidad Abierta Interamericana. Secretaría de Investigación. Centro de Altos Estudios En Ciencias Humanas y de la Salud - Sede Buenos Aires.; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Udovin, Lucas D.. No especifíca;
Fil: Toro Urrego, Nicolas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; Argentina
Fil: Otero-losada, Matilde Estela. Universidad Abierta Interamericana. Secretaría de Investigación. Centro de Altos Estudios En Ciencias Humanas y de la Salud - Sede Buenos Aires.; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Capani, Francisco. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Abierta Interamericana. Secretaría de Investigación. Centro de Altos Estudios En Ciencias Humanas y de la Salud - Sede Buenos Aires.; Argentina
description Metabolic syndrome (MetS) leads to microvascular dysfunction and chronic cerebral hypoperfusion (CCH) in an insidious way. Clinical evidence and several rodent models have contributed to determining the neurodegenerative effect of a sustained decrease in cerebral blood flow (CBF). Protein misfolding and aggrega- tion derived from CCH might account for the establishment of vascular cognitive impairment and dementia (VCID) and Alzheimer?s disease (AD). However, the complex and multifactorial etiology of cerebrovascular disease demands the combination of experimental models in scientific research. In this sense, the present work aims at summarizing the differential available rodent paradigms for studying the establishment of cognitive decline resulting from protein misfolding inducedby MetS in association with CCH. Revising experimental findings in the field will help further basic research on the pathophysiology of cerebrovascular disease and the future testing of protein-remodeling factors as neuroprotective agents for the prevention of cognitive impairment.
publishDate 2020
dc.date.none.fl_str_mv 2020
dc.type.none.fl_str_mv info:eu-repo/semantics/publishedVersion
info:eu-repo/semantics/bookPart
http://purl.org/coar/resource_type/c_3248
info:ar-repo/semantics/parteDeLibro
status_str publishedVersion
format bookPart
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/129456
Herrera, María I.; Luaces, Juan Pablo; Udovin, Lucas D.; Toro Urrego, Nicolas; Otero-losada, Matilde Estela; et al.; In Vivo Studies of Protein Misfolding and Neurodegeneration Induced by Metabolic Syndrome Relative to Chronic Cerebral Hypoperfusion: A Critical Review; IntechOpen; 2020; 1-15
978-1-83880-440-4
CONICET Digital
CONICET
url http://hdl.handle.net/11336/129456
identifier_str_mv Herrera, María I.; Luaces, Juan Pablo; Udovin, Lucas D.; Toro Urrego, Nicolas; Otero-losada, Matilde Estela; et al.; In Vivo Studies of Protein Misfolding and Neurodegeneration Induced by Metabolic Syndrome Relative to Chronic Cerebral Hypoperfusion: A Critical Review; IntechOpen; 2020; 1-15
978-1-83880-440-4
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://www.intechopen.com/chapters/72902
info:eu-repo/semantics/altIdentifier/doi/10.5772/intechopen.92603
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv IntechOpen
publisher.none.fl_str_mv IntechOpen
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
_version_ 1842269965784186880
score 13.13397

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