Neuroprotection from protein misfolding in cerebral hypoperfusion concurrent with metabolic syndrome: a translational perspective

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 CC...

Descripción completa

Guardado en:
Detalles Bibliográficos
Autores principales: Bordet, Sofía, Luaces, Juan Pablo, Herrera, María Inés, Gonzalez, Liliana Mirta, Kobiec, Tamara, Pérez Lloret, Santiago, Otero Losada, Matilde, Capani, Francisco
Formato: Artículo
Lenguaje:Inglés
Publicado: Frontiers Media 2023
Materias:
SINDROME METABOLICO
DIABETES
NEURODEGENERACION
ENFERMEDAD DE ALZHEIMER
DETERIORO COGNITIVO
DEMENCIA
Acceso en línea:https://repositorio.uca.edu.ar/handle/123456789/17277
Aporte de:
Repositorio Institucional de la Universidad Católica Argentina (UCA) de Universidad Católica Argentina
id I33-R139-123456789-17277
record_format dspace
spelling I33-R139-123456789-172772024-02-08T19:08:14Z Neuroprotection from protein misfolding in cerebral hypoperfusion concurrent with metabolic syndrome: a translational perspective Bordet, Sofía Luaces, Juan Pablo Herrera, María Inés Gonzalez, Liliana Mirta Kobiec, Tamara Pérez Lloret, Santiago Otero Losada, Matilde Capani, Francisco SINDROME METABOLICO DIABETES NEURODEGENERACION ENFERMEDAD DE ALZHEIMER DETERIORO COGNITIVO DEMENCIA 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. 2023-10-12T11:22:39Z 2023-10-12T11:22:46Z 2023-10-12T11:22:39Z 2023-10-12T11:22:46Z 2023 Artículo 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 1662-453X (online) https://repositorio.uca.edu.ar/handle/123456789/17277 10.3389/fnins.2023.1215041 eng Neuroprotección en asfixia perinatal desde un enfoque traslacional Acceso abierto http://creativecommons.org/licenses/by-nc-sa/4.0/ application/pdf Frontiers Media Frontiers in Neuroscience. Vol.17:1215041, 2023
institution Universidad Católica Argentina
institution_str I-33
repository_str R-139
collection Repositorio Institucional de la Universidad Católica Argentina (UCA)
language Inglés
topic SINDROME METABOLICO
DIABETES
NEURODEGENERACION
ENFERMEDAD DE ALZHEIMER
DETERIORO COGNITIVO
DEMENCIA
spellingShingle SINDROME METABOLICO
DIABETES
NEURODEGENERACION
ENFERMEDAD DE ALZHEIMER
DETERIORO COGNITIVO
DEMENCIA
Bordet, Sofía
Luaces, Juan Pablo
Herrera, María Inés
Gonzalez, Liliana Mirta
Kobiec, Tamara
Pérez Lloret, Santiago
Otero Losada, Matilde
Capani, Francisco
Neuroprotection from protein misfolding in cerebral hypoperfusion concurrent with metabolic syndrome: a translational perspective
topic_facet SINDROME METABOLICO
DIABETES
NEURODEGENERACION
ENFERMEDAD DE ALZHEIMER
DETERIORO COGNITIVO
DEMENCIA
description 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.
format Artículo
author Bordet, Sofía
Luaces, Juan Pablo
Herrera, María Inés
Gonzalez, Liliana Mirta
Kobiec, Tamara
Pérez Lloret, Santiago
Otero Losada, Matilde
Capani, Francisco
author_facet Bordet, Sofía
Luaces, Juan Pablo
Herrera, María Inés
Gonzalez, Liliana Mirta
Kobiec, Tamara
Pérez Lloret, Santiago
Otero Losada, Matilde
Capani, Francisco
author_sort Bordet, Sofía
title Neuroprotection from protein misfolding in cerebral hypoperfusion concurrent with metabolic syndrome: a translational perspective
title_short Neuroprotection from protein misfolding in cerebral hypoperfusion concurrent with metabolic syndrome: a translational perspective
title_full Neuroprotection from protein misfolding in cerebral hypoperfusion concurrent with metabolic syndrome: a translational perspective
title_fullStr Neuroprotection from protein misfolding in cerebral hypoperfusion concurrent with metabolic syndrome: a translational perspective
title_full_unstemmed Neuroprotection from protein misfolding in cerebral hypoperfusion concurrent with metabolic syndrome: a translational perspective
title_sort neuroprotection from protein misfolding in cerebral hypoperfusion concurrent with metabolic syndrome: a translational perspective
publisher Frontiers Media
publishDate 2023
url https://repositorio.uca.edu.ar/handle/123456789/17277
work_keys_str_mv AT bordetsofia neuroprotectionfromproteinmisfoldingincerebralhypoperfusionconcurrentwithmetabolicsyndromeatranslationalperspective
AT luacesjuanpablo neuroprotectionfromproteinmisfoldingincerebralhypoperfusionconcurrentwithmetabolicsyndromeatranslationalperspective
AT herreramariaines neuroprotectionfromproteinmisfoldingincerebralhypoperfusionconcurrentwithmetabolicsyndromeatranslationalperspective
AT gonzalezlilianamirta neuroprotectionfromproteinmisfoldingincerebralhypoperfusionconcurrentwithmetabolicsyndromeatranslationalperspective
AT kobiectamara neuroprotectionfromproteinmisfoldingincerebralhypoperfusionconcurrentwithmetabolicsyndromeatranslationalperspective
AT perezlloretsantiago neuroprotectionfromproteinmisfoldingincerebralhypoperfusionconcurrentwithmetabolicsyndromeatranslationalperspective
AT oterolosadamatilde neuroprotectionfromproteinmisfoldingincerebralhypoperfusionconcurrentwithmetabolicsyndromeatranslationalperspective
AT capanifrancisco neuroprotectionfromproteinmisfoldingincerebralhypoperfusionconcurrentwithmetabolicsyndromeatranslationalperspective
_version_ 1807949319175667712

Ejemplares similares