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



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Autor:
Herrera, María I.
Udovin, Lucas Daniel
Toro-Urrego, Nicolás
Kusnier, Carlos
Luaces, Juan P.
Otero Losada, Matilde
Capani, Francisco

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


Frontiers Media

Palabras clave:
SINDROME METABOLICO
CEREBRO
PROTEINAS
ENFERMEDADES NEURODEGENERATIVAS

Frontiers in Neuroscience, 12:339, 2018

ISSN 1662-453X

Disponibilidad: Acceso abierto

Cita: 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://www.frontiersin.org/articles/10.3389/fnins.2018.00339/full Registro disponible en: http://bibliotecadigital.uca.edu.ar/greenstone/cgi-bin/library.cgi?a=d&c=investigacion&d=neuroprotection-targeting-protein-misfolding [Fecha de consulta: ….]

Descripción: 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.

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
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