TY - JOUR
T1 - Endothelial Progenitor Cells and Vascular Alterations in Alzheimer’s Disease
AU - Custodia, Antía
AU - Ouro, Alberto
AU - Romaus-Sanjurjo, Daniel
AU - Pías-Peleteiro, Juan Manuel
AU - de Vries, Helga E.
AU - Castillo, José
AU - Sobrino, Tomás
N1 - Funding Information: This study was partially supported by grants from the Xunta de Galicia (TS: IN607A2018/3, TS: IN607D 2020/09, AC: IN606A-2021/015, and DR-S: IN606B-2021/010), and Science Ministry of Spain (TS: RTI2018-102165-B-I00 and TS: RTC2019-007373-1). Furthermore, this study was also supported by grants from the INTERREG Atlantic Area (TS: EAPA_791/2018_ NEUROATLANTIC project), INTER-REG V A España Portugal (POCTEP) (TS: 0624_2IQBIONEURO_6_E), and the European Regional Development Fund (ERDF). Moreover, this work was financed by grants from Horizon 2020 #686009-PANA Project (TS and HV). Finally, TS (CPII17/00027) was recipient of a research contract from the Miguel Servet Program from the Instituto de Salud Carlos III. The funders had no role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript. Funding Information: This study was partially supported by grants from the Xunta de Galicia (TS: IN607A2018/3, TS: IN607D 2020/09, AC: IN606A-2021/015, and DR-S: IN606B-2021/010), and Science Ministry of Spain (TS: RTI2018-102165-B-I00 and TS: RTC2019-007373-1). Furthermore, this study was also supported by grants from the INTERREG Atlantic Area (TS: EAPA_791/2018_ NEUROATLANTIC project), INTER-REG V A Espa?a Portugal (POCTEP) (TS: 0624_2IQBIONEURO_6_E), and the European Regional Development Fund (ERDF). Moreover, this work was financed by grants from Horizon 2020 #686009-PANA Project (TS and HV). Finally, TS (CPII17/00027) was recipient of a research contract from the Miguel Servet Program from the Instituto de Salud Carlos III. The funders had no role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript. Publisher Copyright: Copyright © 2022 Custodia, Ouro, Romaus-Sanjurjo, Pías-Peleteiro, de Vries, Castillo and Sobrino.
PY - 2022/1/26
Y1 - 2022/1/26
N2 - Alzheimer’s disease (AD) is a neurodegenerative disease representing the most common type of dementia worldwide. The early diagnosis of AD is very difficult to achieve due to its complexity and the practically unknown etiology. Therefore, this is one of the greatest challenges in the field in order to develop an accurate therapy. Within the different etiological hypotheses proposed for AD, we will focus on the two-hit vascular hypothesis and vascular alterations occurring in the disease. According to this hypothesis, the accumulation of β-amyloid protein in the brain starts as a consequence of damage in the cerebral vasculature. Given that there are several vascular and angiogenic alterations in AD, and that endothelial progenitor cells (EPCs) play a key role in endothelial repair processes, the study of EPCs in AD may be relevant to the disease etiology and perhaps a biomarker and/or therapeutic target. This review focuses on the involvement of endothelial dysfunction in the onset and progression of AD with special emphasis on EPCs as a biomarker and potential therapeutic target.
AB - Alzheimer’s disease (AD) is a neurodegenerative disease representing the most common type of dementia worldwide. The early diagnosis of AD is very difficult to achieve due to its complexity and the practically unknown etiology. Therefore, this is one of the greatest challenges in the field in order to develop an accurate therapy. Within the different etiological hypotheses proposed for AD, we will focus on the two-hit vascular hypothesis and vascular alterations occurring in the disease. According to this hypothesis, the accumulation of β-amyloid protein in the brain starts as a consequence of damage in the cerebral vasculature. Given that there are several vascular and angiogenic alterations in AD, and that endothelial progenitor cells (EPCs) play a key role in endothelial repair processes, the study of EPCs in AD may be relevant to the disease etiology and perhaps a biomarker and/or therapeutic target. This review focuses on the involvement of endothelial dysfunction in the onset and progression of AD with special emphasis on EPCs as a biomarker and potential therapeutic target.
KW - Alzheimer’s disease
KW - biomarkers
KW - blood brain barrier dysfunction
KW - endothelial progenitor cells
KW - endothelial repair
KW - neurotoxicity
KW - two-hit vascular hypothesis
KW - vascular alteration
UR - http://www.scopus.com/inward/record.url?scp=85124552534&partnerID=8YFLogxK
U2 - https://doi.org/10.3389/fnagi.2021.811210
DO - https://doi.org/10.3389/fnagi.2021.811210
M3 - Review article
C2 - 35153724
SN - 1663-4365
VL - 13
JO - Frontiers in aging neuroscience
JF - Frontiers in aging neuroscience
M1 - 811210
ER -