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Título : Neuroprotection targeting protein misfolding on chronic cerebral hypoperfusion in the context of metabolic syndrome
Autor : Herrera, María I. 
Udovin, Lucas Daniel 
Toro-Urrego, Nicolás 
Kusnier, Carlos Federico 
Luaces, Juan P. 
Otero Losada, Matilde 
Capani, Francisco 
Fecha de publicación : 2018
Editorial : Frontiers Media
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:
Resumen : 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.
ISSN : 1662-453X
Disciplina: PSICOLOGIA
Derechos: Acceso Abierto
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