Biomarkers Assessing Endothelial Dysfunction in Alzheimer’s Disease
Alzheimer’s disease (AD) is the most common degenerative disorder in the elderly in developed countries. Currently, growing evidence is pointing at endothelial dysfunction as a key player in the cognitive decline course of AD. As a main component of the blood–brain barrier (BBB), the dysfunction of...
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| Format: | Article |
| Language: | English |
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MDPI AG
2023-03-01
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| Series: | Cells |
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| Online Access: | https://www.mdpi.com/2073-4409/12/6/962 |
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| author | Antía Custodia Marta Aramburu-Núñez Mariña Rodríguez-Arrizabalaga Juan Manuel Pías-Peleteiro Laura Vázquez-Vázquez Javier Camino-Castiñeiras José Manuel Aldrey José Castillo Alberto Ouro Tomás Sobrino Daniel Romaus-Sanjurjo |
| author_facet | Antía Custodia Marta Aramburu-Núñez Mariña Rodríguez-Arrizabalaga Juan Manuel Pías-Peleteiro Laura Vázquez-Vázquez Javier Camino-Castiñeiras José Manuel Aldrey José Castillo Alberto Ouro Tomás Sobrino Daniel Romaus-Sanjurjo |
| author_sort | Antía Custodia |
| collection | DOAJ |
| description | Alzheimer’s disease (AD) is the most common degenerative disorder in the elderly in developed countries. Currently, growing evidence is pointing at endothelial dysfunction as a key player in the cognitive decline course of AD. As a main component of the blood–brain barrier (BBB), the dysfunction of endothelial cells driven by vascular risk factors associated with AD allows the passage of toxic substances to the cerebral parenchyma, producing chronic hypoperfusion that eventually causes an inflammatory and neurotoxic response. In this process, the levels of several biomarkers are disrupted, such as an increase in adhesion molecules that allow the passage of leukocytes to the cerebral parenchyma, increasing the permeability of the BBB; moreover, other vascular players, including endothelin-1, also mediate artery inflammation. As a consequence of the disruption of the BBB, a progressive neuroinflammatory response is produced that, added to the astrogliosis, eventually triggers neuronal degeneration (possibly responsible for cognitive deterioration). Recently, new molecules have been proposed as early biomarkers for endothelial dysfunction that can constitute new therapeutic targets as well as early diagnostic and prognostic markers for AD. |
| first_indexed | 2024-03-11T06:48:12Z |
| format | Article |
| id | doaj.art-fbeb72730f184b6b81536d805c6075db |
| institution | Directory Open Access Journal |
| issn | 2073-4409 |
| language | English |
| last_indexed | 2024-03-11T06:48:12Z |
| publishDate | 2023-03-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Cells |
| spelling | doaj.art-fbeb72730f184b6b81536d805c6075db2023-11-17T10:14:20ZengMDPI AGCells2073-44092023-03-0112696210.3390/cells12060962Biomarkers Assessing Endothelial Dysfunction in Alzheimer’s DiseaseAntía Custodia0Marta Aramburu-Núñez1Mariña Rodríguez-Arrizabalaga2Juan Manuel Pías-Peleteiro3Laura Vázquez-Vázquez4Javier Camino-Castiñeiras5José Manuel Aldrey6José Castillo7Alberto Ouro8Tomás Sobrino9Daniel Romaus-Sanjurjo10NeuroAging Group (NEURAL), Clinical Neurosciences Research Laboratory (LINC), Health Research Institute of Santiago de Compostela (IDIS), 15706 Santiago de Compostela, SpainNeuroAging Group (NEURAL), Clinical Neurosciences Research Laboratory (LINC), Health Research Institute of Santiago de Compostela (IDIS), 15706 Santiago de Compostela, SpainNeuroAging Group (NEURAL), Clinical Neurosciences Research Laboratory (LINC), Health Research Institute of Santiago de Compostela (IDIS), 15706 Santiago de Compostela, SpainNeuroAging Group (NEURAL), Clinical Neurosciences Research Laboratory (LINC), Health Research Institute of Santiago de Compostela (IDIS), 15706 Santiago de Compostela, SpainNeuroAging Group (NEURAL), Clinical Neurosciences Research Laboratory (LINC), Health Research Institute of Santiago de Compostela (IDIS), 15706 Santiago de Compostela, SpainNeuroAging Group (NEURAL), Clinical Neurosciences Research Laboratory (LINC), Health Research Institute of Santiago de Compostela (IDIS), 15706 Santiago de Compostela, SpainNeuroAging Group (NEURAL), Clinical Neurosciences Research Laboratory (LINC), Health Research Institute of Santiago de Compostela (IDIS), 15706 Santiago de Compostela, SpainNeuroimaging and Biotechnology Laboratory (NOBEL), Clinical Neurosciences Research Laboratory (LINC), Health Research Institute of Santiago de Compostela (IDIS), 15706 Santiago de Compostela, SpainNeuroAging Group (NEURAL), Clinical Neurosciences Research Laboratory (LINC), Health Research Institute of Santiago de Compostela (IDIS), 15706 Santiago de Compostela, SpainNeuroAging Group (NEURAL), Clinical Neurosciences Research Laboratory (LINC), Health Research Institute of Santiago de Compostela (IDIS), 15706 Santiago de Compostela, SpainNeuroAging Group (NEURAL), Clinical Neurosciences Research Laboratory (LINC), Health Research Institute of Santiago de Compostela (IDIS), 15706 Santiago de Compostela, SpainAlzheimer’s disease (AD) is the most common degenerative disorder in the elderly in developed countries. Currently, growing evidence is pointing at endothelial dysfunction as a key player in the cognitive decline course of AD. As a main component of the blood–brain barrier (BBB), the dysfunction of endothelial cells driven by vascular risk factors associated with AD allows the passage of toxic substances to the cerebral parenchyma, producing chronic hypoperfusion that eventually causes an inflammatory and neurotoxic response. In this process, the levels of several biomarkers are disrupted, such as an increase in adhesion molecules that allow the passage of leukocytes to the cerebral parenchyma, increasing the permeability of the BBB; moreover, other vascular players, including endothelin-1, also mediate artery inflammation. As a consequence of the disruption of the BBB, a progressive neuroinflammatory response is produced that, added to the astrogliosis, eventually triggers neuronal degeneration (possibly responsible for cognitive deterioration). Recently, new molecules have been proposed as early biomarkers for endothelial dysfunction that can constitute new therapeutic targets as well as early diagnostic and prognostic markers for AD.https://www.mdpi.com/2073-4409/12/6/962albuminAlzheimer’s diseasecell adhesion moleculesendothelial dysfunctionendothelin-1EPCs |
| spellingShingle | Antía Custodia Marta Aramburu-Núñez Mariña Rodríguez-Arrizabalaga Juan Manuel Pías-Peleteiro Laura Vázquez-Vázquez Javier Camino-Castiñeiras José Manuel Aldrey José Castillo Alberto Ouro Tomás Sobrino Daniel Romaus-Sanjurjo Biomarkers Assessing Endothelial Dysfunction in Alzheimer’s Disease Cells albumin Alzheimer’s disease cell adhesion molecules endothelial dysfunction endothelin-1 EPCs |
| title | Biomarkers Assessing Endothelial Dysfunction in Alzheimer’s Disease |
| title_full | Biomarkers Assessing Endothelial Dysfunction in Alzheimer’s Disease |
| title_fullStr | Biomarkers Assessing Endothelial Dysfunction in Alzheimer’s Disease |
| title_full_unstemmed | Biomarkers Assessing Endothelial Dysfunction in Alzheimer’s Disease |
| title_short | Biomarkers Assessing Endothelial Dysfunction in Alzheimer’s Disease |
| title_sort | biomarkers assessing endothelial dysfunction in alzheimer s disease |
| topic | albumin Alzheimer’s disease cell adhesion molecules endothelial dysfunction endothelin-1 EPCs |
| url | https://www.mdpi.com/2073-4409/12/6/962 |
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