Molecular Links Between Endothelial Dysfunction and Neurodegeneration in Alzheimer's Disease
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.
Keywords: Alzheimer's disease, dementia, endothelium, vascular, β-amyloid.
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