Neuroprotection targeting protein misfolding on chronic cerebral hypoperfusion in the context of metabolic syndrome
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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Formato: | Artículo |
Lenguaje: | Inglés |
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Frontiers Media
2019
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Acceso en línea: | https://repositorio.uca.edu.ar/handle/123456789/6169 |
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I33-R139123456789-6169 |
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institution |
Universidad Católica Argentina |
institution_str |
I-33 |
repository_str |
R-139 |
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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 I. 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 I. Udovin, Lucas Daniel Toro-Urrego, Nicolás Kusnier, Carlos Federico Luaces, Juan P. Otero Losada, Matilde Capani, Francisco |
author_facet |
Herrera, María I. Udovin, Lucas Daniel Toro-Urrego, Nicolás Kusnier, Carlos Federico Luaces, Juan P. Otero Losada, Matilde Capani, Francisco |
author_sort |
Herrera, María I. |
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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bdutipo_str |
Repositorios |
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