Endothelial Dysfunction, Inflammation and Cognition

Dear Colleagues,

The endothelium is an abundant organ, constituted of a monolayer of cells, which covers the inner surface of all blood vessels. It is involved in various physiological functions: the control of vasomotor tone, vascular permeability, cellular growth, and the maintenance of blood fluidity as well as the recruitment of immune cells. Moreover, depending on the location, the endothelium presents specificities in terms of structure and function, and, like all organs, it senses and responds to various physical and chemical stimuli.

The endothelium regulates its functions via the synthesis and secretion of numerous factors. Nitric oxide (NO) is the best-characterized factor, which is involved in many functions. Indeed, endothelial dysfunction (ED) is usually defined as a reduction in NO synthesis or NO inactivation.

Ten years ago, our laboratory discovered that the adult cardiovascular system contains as much brain-derived neurotrophic factor (BDNF) as the brain and that the endothelium was the main source of it. This neurotrophin plays a critical role in many brain functions, with a central role in both synaptic plasticity and communication by binding to its specific receptor: tropomyosin-related kinase receptor type B (TrkB). Our group also showed that cerebral ED is characterized by a marked decrease in the cerebral levels of BDNF, and a link between ED, BDNF, and cognition has emerged.

Endothelial cells participate actively in both innate and adaptive immune responses, and endothelial cells are particularly sensitive to pro- and anti-inflammatory mediators. Many clinical and animal studies have reported associations between low cerebral BDNF levels and high levels of inflammatory markers, as well as the development of behavioral symptoms of cognitive defects. Moreover, ED has been reported in different disorders, such as Alzheimer’s disease and rheumatoid arthritis; patients with these disorders suffer from cognitive defects or are at risk of cognitive comorbidities. Inflammation, ED, and cognition therefore appear to be closely related.

The main purposes of this Special Issue are as follows:

1. To explore the interplay between inflammation and endothelial dysfunction and its impact on cognition.
2. To clarify the contribution of NO and BDNF in this interplay, given that little is known about endothelial BDNF in terms of role and metabolism.
3. To evaluate the effects of non-pharmaceutical and pharmaceutical therapies on this interplay.

Original research papers, reviews, commentaries, and opinion papers are all welcome.

Dr. Christelle Basset
Dr. Anne S. Prigent-Tessier
Guest Editors

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• inflammation
• endothelial dysfunction
• cognition
• nitric oxide (NO)
• BDNF
• physical exercise