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

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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 misfol...

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Autores principales: Herrera, María Inés, Udovin, Lucas Daniel, Toro-Urrego, Nicolás, Kusnier, Carlos Federico, Luaces, Juan P., Otero Losada, Matilde, Capani, Francisco
Formato: Artículo
Lenguaje:Inglés
Publicado: Frontiers Media 2019
Materias:
SINDROME METABOLICO
CEREBRO
PROTEINAS
ENFERMEDADES NEURODEGENERATIVAS
Acceso en línea:https://repositorio.uca.edu.ar/handle/123456789/6169
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Repositorio Institucional de la Universidad Católica Argentina (UCA) de Universidad Católica Argentina
id I33-R139-123456789-6169
record_format dspace
spelling I33-R139-123456789-61692024-03-26T10:27:23Z Neuroprotection targeting protein misfolding on chronic cerebral hypoperfusion in the context of metabolic syndrome Herrera, María Inés Udovin, Lucas Daniel Toro-Urrego, Nicolás Kusnier, Carlos Federico Luaces, Juan P. Otero Losada, Matilde Capani, Francisco SINDROME METABOLICO CEREBRO PROTEINAS ENFERMEDADES NEURODEGENERATIVAS 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. 2019-06-12T01:38:35Z 2019-06-12T01:38:35Z 2018 Artículo 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 1662-453X https://repositorio.uca.edu.ar/handle/123456789/6169 eng Acceso Abierto https://creativecommons.org/licenses/by-nc-sa/4.0/ application/pdf Frontiers Media Frontiers in Neuroscience, 12:339, 2018
institution Universidad Católica Argentina
institution_str I-33
repository_str R-139
collection Repositorio Institucional de la Universidad Católica Argentina (UCA)
language Inglés
topic SINDROME METABOLICO
CEREBRO
PROTEINAS
ENFERMEDADES NEURODEGENERATIVAS
spellingShingle SINDROME METABOLICO
CEREBRO
PROTEINAS
ENFERMEDADES NEURODEGENERATIVAS
Herrera, María Inés
Udovin, Lucas Daniel
Toro-Urrego, Nicolás
Kusnier, Carlos Federico
Luaces, Juan P.
Otero Losada, Matilde
Capani, Francisco
Neuroprotection targeting protein misfolding on chronic cerebral hypoperfusion in the context of metabolic syndrome
topic_facet SINDROME METABOLICO
CEREBRO
PROTEINAS
ENFERMEDADES NEURODEGENERATIVAS
description 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.
format Artículo
author Herrera, María Inés
Udovin, Lucas Daniel
Toro-Urrego, Nicolás
Kusnier, Carlos Federico
Luaces, Juan P.
Otero Losada, Matilde
Capani, Francisco
author_facet Herrera, María Inés
Udovin, Lucas Daniel
Toro-Urrego, Nicolás
Kusnier, Carlos Federico
Luaces, Juan P.
Otero Losada, Matilde
Capani, Francisco
author_sort Herrera, María Inés
title Neuroprotection targeting protein misfolding on chronic cerebral hypoperfusion in the context of metabolic syndrome
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
publisher Frontiers Media
publishDate 2019
url https://repositorio.uca.edu.ar/handle/123456789/6169
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