Neuroprotection targeting protein misfolding on chronic cerebral hypoperfusion in the context of metabolic syndrome

Autores
Herrera, María Inés; Udovin, Lucas Daniel; Toro-Urrego, Nicolás; Kusnier, Carlos Federico; Luaces, Juan P.; Otero Losada, Matilde; Capani, Francisco
Año de publicación
2018
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Fil: Herrera, María I. Universidad Católica Argentina. Facultad de Psicología y Psicopedagogía. Centro de Investigaciones en Psicología y Psicopedagogía; Argentina
Fil: Herrera, María I. Universidad de Buenos Aires. Instituto de Investigaciones Cardiológicas; Argentina
Fil: Udovin, Lucas Daniel. Universidad de Buenos Aires. Instituto de Investigaciones Cardiológicas; Argentina
Fil: Toro-Urrego, Nicolás. Universidad de Buenos Aires. Instituto de Investigaciones Cardiológicas; Argentina
Fil: Kusnier, Carlos. Universidad de Buenos Aires. Instituto de Investigaciones Cardiológicas; Argentina
Fil: Luaces, Juan P. Universidad de Buenos Aires. Instituto de Investigaciones Cardiológicas; Argentina
Fil: Otero Losada, Matilde. Universidad de Buenos Aires. Instituto de Investigaciones Cardiológicas; Argentina
Fil: Capani, Francisco. Universidad de Buenos Aires. Instituto de Investigaciones Cardiológicas; Argentina
Fil: Capani, Francisco. Universidad Católica Argentina. Facultad de Medicina; Argentina
Fil: Capani, Francisco. Universidad Autónoma de Chile; Chile
Abstract: Metabolic syndrome (MetS) is a cluster of risk factors that lead to microvasculardysfunction and chronic cerebral hypoperfusion (CCH). Long-standing reduction inoxygen and energy supply leads to brain hypoxia and protein misfolding, thereby linkingCCH to Alzheimer’s disease. Protein misfolding results in neurodegeneration as revealedby studying different experimental models of CCH. Regulating proteostasis networkthrough pathways like the unfolded protein response (UPR),the ubiquitin-proteasomesystem (UPS), chaperone-mediated autophagy (CMA), and macroautophagy emergesas a novel target for neuroprotection. Lipoxin A4 methyl ester, baclofen, URB597,N-stearoyl-L-tyrosine, and melatonin may pose potential neuroprotective agents forrebalancing the proteostasis network under CCH. Autophagyis one of the most studiedpathways of proteostatic cell response against the decrease in blood supply to the brainthough the role of the UPR-specific chaperones and the UPS system in CCH deservesfurther research. Pharmacotherapy targeting misfolded proteins at different stages in theproteostatic pathway might be promising in treating cognitive impairment following CCH.
Fuente
Frontiers in Neuroscience, 12:339, 2018
Materia
SINDROME METABOLICO
CEREBRO
PROTEINAS
ENFERMEDADES NEURODEGENERATIVAS
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/4.0/
Repositorio
Repositorio Institucional (UCA)
Institución
Pontificia Universidad Católica Argentina
OAI Identificador
oai:ucacris:123456789/6169
Acceder
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oai_identifier_str oai:ucacris:123456789/6169
network_acronym_str RIUCA
repository_id_str 2585
network_name_str Repositorio Institucional (UCA)
spelling Neuroprotection targeting protein misfolding on chronic cerebral hypoperfusion in the context of metabolic syndromeHerrera, María InésUdovin, Lucas DanielToro-Urrego, NicolásKusnier, Carlos FedericoLuaces, Juan P.Otero Losada, MatildeCapani, FranciscoSINDROME METABOLICOCEREBROPROTEINASENFERMEDADES NEURODEGENERATIVASFil: Herrera, María I. Universidad Católica Argentina. Facultad de Psicología y Psicopedagogía. Centro de Investigaciones en Psicología y Psicopedagogía; ArgentinaFil: Herrera, María I. Universidad de Buenos Aires. Instituto de Investigaciones Cardiológicas; ArgentinaFil: Udovin, Lucas Daniel. Universidad de Buenos Aires. Instituto de Investigaciones Cardiológicas; ArgentinaFil: Toro-Urrego, Nicolás. Universidad de Buenos Aires. Instituto de Investigaciones Cardiológicas; ArgentinaFil: Kusnier, Carlos. Universidad de Buenos Aires. Instituto de Investigaciones Cardiológicas; ArgentinaFil: Luaces, Juan P. Universidad de Buenos Aires. Instituto de Investigaciones Cardiológicas; ArgentinaFil: Otero Losada, Matilde. Universidad de Buenos Aires. Instituto de Investigaciones Cardiológicas; ArgentinaFil: Capani, Francisco. Universidad de Buenos Aires. Instituto de Investigaciones Cardiológicas; ArgentinaFil: Capani, Francisco. Universidad Católica Argentina. Facultad de Medicina; ArgentinaFil: Capani, Francisco. Universidad Autónoma de Chile; ChileAbstract: Metabolic syndrome (MetS) is a cluster of risk factors that lead to microvasculardysfunction and chronic cerebral hypoperfusion (CCH). Long-standing reduction inoxygen and energy supply leads to brain hypoxia and protein misfolding, thereby linkingCCH to Alzheimer’s disease. Protein misfolding results in neurodegeneration as revealedby studying different experimental models of CCH. Regulating proteostasis networkthrough pathways like the unfolded protein response (UPR),the ubiquitin-proteasomesystem (UPS), chaperone-mediated autophagy (CMA), and macroautophagy emergesas a novel target for neuroprotection. Lipoxin A4 methyl ester, baclofen, URB597,N-stearoyl-L-tyrosine, and melatonin may pose potential neuroprotective agents forrebalancing the proteostasis network under CCH. Autophagyis one of the most studiedpathways of proteostatic cell response against the decrease in blood supply to the brainthough the role of the UPR-specific chaperones and the UPS system in CCH deservesfurther research. Pharmacotherapy targeting misfolded proteins at different stages in theproteostatic pathway might be promising in treating cognitive impairment following CCH.Frontiers Media2018info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfhttps://repositorio.uca.edu.ar/handle/123456789/61691662-453XHerrera, M. I., Udovin, L. D., Toro-Urrego, N., Kusnier, C. F., Luaces, J. P., Otero-Losada, M. y Capani, F. (2018). Neuroprotection targeting protein misfolding on chronic cerebral hypoperfusion in the context of metabolic syndrome [en línea] Frontiers in Neuroscience, 12:339. doi: 10.3389/fnins.2018.00339 Disponible en: https://repositorio.uca.edu.ar/handle/123456789/6169Frontiers in Neuroscience, 12:339, 2018reponame:Repositorio Institucional (UCA)instname:Pontificia Universidad Católica Argentinaenginfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/4.0/2025-07-03T10:56:18Zoai:ucacris:123456789/6169instacron:UCAInstitucionalhttps://repositorio.uca.edu.ar/Universidad privadaNo correspondehttps://repositorio.uca.edu.ar/oaiclaudia_fernandez@uca.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:25852025-07-03 10:56:18.769Repositorio Institucional (UCA) - Pontificia Universidad Católica Argentinafalse
dc.title.none.fl_str_mv Neuroprotection targeting protein misfolding on chronic cerebral hypoperfusion in the context of metabolic syndrome
title Neuroprotection targeting protein misfolding on chronic cerebral hypoperfusion in the context of metabolic syndrome
spellingShingle Neuroprotection targeting protein misfolding on chronic cerebral hypoperfusion in the context of metabolic syndrome
Herrera, María Inés
SINDROME METABOLICO
CEREBRO
PROTEINAS
ENFERMEDADES NEURODEGENERATIVAS
title_short Neuroprotection targeting protein misfolding on chronic cerebral hypoperfusion in the context of metabolic syndrome
title_full Neuroprotection targeting protein misfolding on chronic cerebral hypoperfusion in the context of metabolic syndrome
title_fullStr Neuroprotection targeting protein misfolding on chronic cerebral hypoperfusion in the context of metabolic syndrome
title_full_unstemmed Neuroprotection targeting protein misfolding on chronic cerebral hypoperfusion in the context of metabolic syndrome
title_sort Neuroprotection targeting protein misfolding on chronic cerebral hypoperfusion in the context of metabolic syndrome
dc.creator.none.fl_str_mv Herrera, María Inés
Udovin, Lucas Daniel
Toro-Urrego, Nicolás
Kusnier, Carlos Federico
Luaces, Juan P.
Otero Losada, Matilde
Capani, Francisco
author Herrera, María Inés
author_facet Herrera, María Inés
Udovin, Lucas Daniel
Toro-Urrego, Nicolás
Kusnier, Carlos Federico
Luaces, Juan P.
Otero Losada, Matilde
Capani, Francisco
author_role author
author2 Udovin, Lucas Daniel
Toro-Urrego, Nicolás
Kusnier, Carlos Federico
Luaces, Juan P.
Otero Losada, Matilde
Capani, Francisco
author2_role author
author
author
author
author
author
dc.subject.none.fl_str_mv SINDROME METABOLICO
CEREBRO
PROTEINAS
ENFERMEDADES NEURODEGENERATIVAS
topic SINDROME METABOLICO
CEREBRO
PROTEINAS
ENFERMEDADES NEURODEGENERATIVAS
dc.description.none.fl_txt_mv Fil: Herrera, María I. Universidad Católica Argentina. Facultad de Psicología y Psicopedagogía. Centro de Investigaciones en Psicología y Psicopedagogía; Argentina
Fil: Herrera, María I. Universidad de Buenos Aires. Instituto de Investigaciones Cardiológicas; Argentina
Fil: Udovin, Lucas Daniel. Universidad de Buenos Aires. Instituto de Investigaciones Cardiológicas; Argentina
Fil: Toro-Urrego, Nicolás. Universidad de Buenos Aires. Instituto de Investigaciones Cardiológicas; Argentina
Fil: Kusnier, Carlos. Universidad de Buenos Aires. Instituto de Investigaciones Cardiológicas; Argentina
Fil: Luaces, Juan P. Universidad de Buenos Aires. Instituto de Investigaciones Cardiológicas; Argentina
Fil: Otero Losada, Matilde. Universidad de Buenos Aires. Instituto de Investigaciones Cardiológicas; Argentina
Fil: Capani, Francisco. Universidad de Buenos Aires. Instituto de Investigaciones Cardiológicas; Argentina
Fil: Capani, Francisco. Universidad Católica Argentina. Facultad de Medicina; Argentina
Fil: Capani, Francisco. Universidad Autónoma de Chile; Chile
Abstract: Metabolic syndrome (MetS) is a cluster of risk factors that lead to microvasculardysfunction and chronic cerebral hypoperfusion (CCH). Long-standing reduction inoxygen and energy supply leads to brain hypoxia and protein misfolding, thereby linkingCCH to Alzheimer’s disease. Protein misfolding results in neurodegeneration as revealedby studying different experimental models of CCH. Regulating proteostasis networkthrough pathways like the unfolded protein response (UPR),the ubiquitin-proteasomesystem (UPS), chaperone-mediated autophagy (CMA), and macroautophagy emergesas a novel target for neuroprotection. Lipoxin A4 methyl ester, baclofen, URB597,N-stearoyl-L-tyrosine, and melatonin may pose potential neuroprotective agents forrebalancing the proteostasis network under CCH. Autophagyis one of the most studiedpathways of proteostatic cell response against the decrease in blood supply to the brainthough the role of the UPR-specific chaperones and the UPS system in CCH deservesfurther research. Pharmacotherapy targeting misfolded proteins at different stages in theproteostatic pathway might be promising in treating cognitive impairment following CCH.
description Fil: Herrera, María I. Universidad Católica Argentina. Facultad de Psicología y Psicopedagogía. Centro de Investigaciones en Psicología y Psicopedagogía; Argentina
publishDate 2018
dc.date.none.fl_str_mv 2018
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv https://repositorio.uca.edu.ar/handle/123456789/6169
1662-453X
Herrera, M. I., Udovin, L. D., Toro-Urrego, N., Kusnier, C. F., Luaces, J. P., Otero-Losada, M. y Capani, F. (2018). Neuroprotection targeting protein misfolding on chronic cerebral hypoperfusion in the context of metabolic syndrome [en línea] Frontiers in Neuroscience, 12:339. doi: 10.3389/fnins.2018.00339 Disponible en: https://repositorio.uca.edu.ar/handle/123456789/6169
url https://repositorio.uca.edu.ar/handle/123456789/6169
identifier_str_mv 1662-453X
Herrera, M. I., Udovin, L. D., Toro-Urrego, N., Kusnier, C. F., Luaces, J. P., Otero-Losada, M. y Capani, F. (2018). Neuroprotection targeting protein misfolding on chronic cerebral hypoperfusion in the context of metabolic syndrome [en línea] Frontiers in Neuroscience, 12:339. doi: 10.3389/fnins.2018.00339 Disponible en: https://repositorio.uca.edu.ar/handle/123456789/6169
dc.language.none.fl_str_mv eng
language eng
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/4.0/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/4.0/
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Frontiers Media
publisher.none.fl_str_mv Frontiers Media
dc.source.none.fl_str_mv Frontiers in Neuroscience, 12:339, 2018
reponame:Repositorio Institucional (UCA)
instname:Pontificia Universidad Católica Argentina
reponame_str Repositorio Institucional (UCA)
collection Repositorio Institucional (UCA)
instname_str Pontificia Universidad Católica Argentina
repository.name.fl_str_mv Repositorio Institucional (UCA) - Pontificia Universidad Católica Argentina
repository.mail.fl_str_mv claudia_fernandez@uca.edu.ar
_version_ 1836638341501550592
score 13.13397

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