Molecular Links Between Endothelial Dysfunction and Neurodegeneration in Alzheimer's Disease
Abstract
Alzheimer's disease (AD) is characterized by a progressive decline of cognitive functions and represents the most common form of dementia and a major cause of morbidity and mortality in the modern, westernized societies. There is accumulating evidence to support the hypothesis that a primary cerebral vascular dysfunction initiates a cascade of events that lead to neuronal injury in Alzheimer's dementia. The endothelium, in specific, constitutes a part of the blood brain barrier, the dysfunction of which is thought to play an important role to disturbed amyloid-β homeostasis and infiltration of the brain parenchyma with circulating toxic molecules in the disease. Furthermore, the endothelium itself is under certain conditions capable of producing neurotoxic and inflammatory factors, whereas common growth factors regulate the development and maintenance of both neurons and blood vessels. Reliance of both endothelial and neuronal cells on mitochondrial integrity and common molecular pathways for apoptosis also imply that there is a link between vascular pathology and neurodegeneration. The present article intends to review available evidence on molecular players implicated in the above mechanisms with the potential to develop biomarkers or novel therapeutic targets.
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AD is commonly accompanied by BBB dysfunction.
“Also, it is commonly accompanied by BBB dysfunction (Erickson and Banks, 2013; Lyros et al., 2014).”
From The impact of microglial activation on blood-brain barrier in brain diseases (2014) · cites this paper as Lyros et al., 2014
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When a Metabolite Becomes a Neurotoxin: Homocysteine and Brain Diseases
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- Authors
- Lyros, E., Bakogiannis, C., Liu, Y., & Fassbender, K.
- Affiliations
- Saarland University (DE)
- Corresponding author
- Fassbender, Klaus
- Venue
- Current Alzheimer Research
- Publisher
- Bentham Science Publishers Ltd.
- Published
- 2014-01-31
- Volume
- 11
- Issue
- 1
- Pages
- 18-26
- ISSN
- 1567-2050 (ISSN-L)
- OpenAlex
- W2165470282
- Cited by
- 70
- References
- 0
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 7 · 2023: 4 · 2022: 4 · 2021: 7 · 2020: 6 · 2019: 3 · 2018: 6 · 2017: 7 · 2016: 5 · 2015: 15 · 2014: 2 · 2013: 1
- FWCI
- 5.04
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Current Alzheimer Research (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Neurology › Barrier Structure and Function Studies
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- Alzheimer's disease, endothelial dysfunction, neurodegeneration, blood-brain barrier, cerebrovascular dysfunction, neuroinflammation, neurovascular unit, mitochondrial integrity, apoptosis, growth factors, biomarkers, therapeutic target
- MeSH terms
- Alzheimer Disease, Animals, Blood-Brain Barrier, Brain, Cerebrovascular Circulation, Endothelium, Vascular, Humans, Nerve Degeneration
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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