Brain Endothelial Dysfunction a Key Target in Neurodegenerative Diseases

Dear Colleagues,

It is well established that several risk factors, such as genetic, diet, aging, or previous cerebrovascular diseases, are associated with the possibility of developing neurodegenerative diseases, such as Alzheimer's or Parkinson's disease. However, since there is currently no target to stop or slow this neurodegeneration, it is tempting to hypothesize that other known or unknown factors are playing pivotal roles in the onset of these neurodegenerative conditions. Indeed, many cellular mechanisms underlying neurodegeneration start “quietly” a long time before clinical symptoms are detected. Although the exact cause of synaptic dysfunction and neurodegeneration in the early stages is largely unknown, in recent years, the involvement of brain endothelial dysfunction in the initial pathophysiological processes of neurodegenerative diseases has been defined. During neurodegeneration, cerebral arterioles suffer a progressive alteration leading to an increased permeability of the blood–brain barrier. This increases the rate in the passage of potential toxic and pro-inflammatory components to cerebral parenchyma, causing microglia activation and neurotoxicity.

However, the cellular mechanism underlying these cerebrovascular damages is not fully understood. Therefore, detection of early biomarkers that lead to the identification of cerebral endothelial dysfunction may constitute new diagnostic and therapeutic targets for neurodegenerative diseases at early stages.

In this Special Issue, we invite potential authors to contribute with original and/or review articles that provide a new perspective on this topic.

Dr. Alberto Ouro
Dr. Daniel Romaus-Sanjurjo
Guest Editors

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