Please use this identifier to cite or link to this item: https://repositorio.uca.edu.ar/handle/123456789/17277
Título : Neuroprotection from protein misfolding in cerebral hypoperfusion concurrent with metabolic syndrome: a translational perspective
Autor : Bordet, Sofía 
Luaces, Juan Pablo 
Herrera, María Inés 
Gonzalez, Liliana Mirta 
Kobiec, Tamara 
Pérez Lloret, Santiago 
Otero Losada, Matilde 
Capani, Francisco 
Palabras clave : SINDROME METABOLICODIABETESNEURODEGENERACIONENFERMEDAD DE ALZHEIMERDETERIORO COGNITIVODEMENCIA
Fecha de publicación : 2023
Editorial : Frontiers Media
Cita : Bordet, S. et al. Neuroprotection from protein misfolding in cerebral hypoperfusion concurrent with metabolic syndrome: a translational perspective [en línea]. Frontiers in Neuroscience. 2023, 17:1215041. doi: 10.3389/fnins.2023.1215041. Disponible en: https://repositorio.uca.edu.ar/handle/123456789/17277
Proyecto: Neuroprotección en asfixia perinatal desde un enfoque traslacional 
Resumen : Abstract: Based on clinical and experimental evidence, metabolic syndrome (MetS) and type 2 diabetes (T2D) are considered risk factors for chronic cerebral hypoperfusion (CCH) and neurodegeneration. Scientific evidence suggests that protein misfolding is a potential mechanism that explains how CCH can lead to either Alzheimer’s disease (AD) or vascular cognitive impairment and dementia (VCID). Over the last decade, there has been a significant increase in the number of experimental studies regarding this issue. Using several animal paradigms and different markers of CCH, scientists have discussed the extent to which MetSor T2D causes a decrease in cerebral blood flow (CBF). In addition, different models of CCH have explored how long-term reductions in oxygen and energy supply can trigger AD or VCID via protein misfolding and aggregation. Research that combines two or three animal models could broaden knowledge of the links between these pathological conditions. Recent experimental studies suggest novel neuroprotective properties of protein-remodeling factors. In this review, we present a summarized updated revision of preclinical findings, discussing clinical implications and proposing new experimental approaches from a translational perspective. We are confident that research studies, both clinical and experimental, may find new diagnostic and therapeutic tools to prevent neurodegeneration associated with MetS, diabetes, and any other chronic noncommunicable disease (NCD) associated with diet and lifestyle risk factors.
URI : https://repositorio.uca.edu.ar/handle/123456789/17277
ISSN : 1662-453X (online)
Disciplina: PSICOLOGIA
DOI: 10.3389/fnins.2023.1215041
Derechos: Acceso abierto
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