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Endothelial Progenitor Cells and Vascular Alterations in Alzheimer's Disease
Antía Custodia1, Alberto Ouro1, Daniel Romaus-Sanjurjo1
1NeuroAging Group (NEURAL), Clinical Neurosciences Research Laboratory (LINC), Health Research Institute of Santiago de Compostela (IDIS), Santiago de Compostela, Spain.
Insights
Alzheimer's disease (AD) involves brain vascular damage, potentially initiating beta-amyloid accumulation. Endothelial progenitor cells (EPCs) may serve as biomarkers or therapeutic targets for AD.
Area of Science:
- Neuroscience
- Vascular Biology
- Dementia Research
Background:
- Alzheimer's disease (AD) is the leading cause of dementia globally.
- Early AD diagnosis is challenging due to disease complexity and unknown causes.
- The two-hit vascular hypothesis suggests cerebral vasculature damage initiates AD pathology.
Purpose of the Study:
- To review the role of endothelial dysfunction in AD onset and progression.
- To explore endothelial progenitor cells (EPCs) as potential AD biomarkers.
- To investigate EPCs as a therapeutic target for Alzheimer's disease.
Main Methods:
- Literature review focusing on vascular alterations in AD.
- Analysis of the role of endothelial progenitor cells (EPCs) in endothelial repair.
- Examination of the connection between vascular health and AD pathogenesis.
Main Results:
- Vascular and angiogenic alterations are prevalent in Alzheimer's disease.
- Endothelial progenitor cells (EPCs) are crucial for repairing damaged vasculature.
- Dysfunction in EPCs may contribute to AD development.
Conclusions:
- Endothelial dysfunction is implicated in the initiation and progression of Alzheimer's disease.
- Endothelial progenitor cells (EPCs) show promise as diagnostic biomarkers for AD.
- Targeting EPCs represents a potential therapeutic strategy for Alzheimer's disease.
Abstract:
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.
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