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dc.contributor.authorBordet, Sofía
dc.contributor.authorLuaces, Juan Pablo
dc.contributor.authorHerrera, Maria Ines
dc.contributor.authorGonzalez, Liliana Mirta
dc.contributor.authorKobiec, Tamara
dc.contributor.authorPerez-Lloret, Santiago
dc.contributor.authorOtero-Losada, Matilde
dc.contributor.authorCapani, Francisco
dc.date.accessioned2024-04-10T00:40:36Z
dc.date.available2024-04-10T00:40:36Z
dc.date.issued2023
dc.identifier10.3389/fnins.2023.1215041
dc.identifier.issn16624548
dc.identifier.urihttps://hdl.handle.net/20.500.12728/10494
dc.description.abstractBased 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 non-communicable disease (NCD) associated with diet and lifestyle risk factors. Copyright © 2023 Bordet, Luaces, Herrera, Gonzalez, Kobiec, Perez-Lloret, Otero-Losada and Capani.es_ES
dc.language.isoenes_ES
dc.publisherFrontiers Media SAes_ES
dc.subjectanimal modelses_ES
dc.subjectchronic cerebral hypoperfusiones_ES
dc.subjectmetabolic syndromees_ES
dc.subjectneurodegenerationes_ES
dc.subjectprotein misfoldinges_ES
dc.subjecttype 2 diabeteses_ES
dc.titleNeuroprotection from protein misfolding in cerebral hypoperfusion concurrent with metabolic syndrome. A translational perspectivees_ES
dc.typeArticlees_ES


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