Abstract
The central nervous system (CNS) is highly vascularized where neuronal cells are located in proximity to endothelial cells, astroglial limitans, and neuronal processes constituting integrated neurovascular units. In contrast to many other organs, the CNS has a blood-brain barrier (BBB), which becomes compromised due to infection, neuroinflammation, neurodegeneration, traumatic brain injury, and other reasons. BBB disruption is presumably involved in neuronal injury during epilepsy and psychiatric disorders. Therefore, many types of neuropsychological disorders are accompanied by an increase in BBB permeability leading to direct contact of circulating blood cells in the capillaries with neuronal cells in the CNS. The second most abundant type of blood cells are platelets, which come after erythrocytes and outnumber ~100-fold circulating leukocytes. When BBB becomes compromised, platelets swiftly respond to the vascular injury and become engaged in thrombosis and hemostasis. However, more recent studies demonstrated that platelets could also enter CNS parenchyma and directly interact with neuronal cells. Within CNS, platelets become activated by recognizing major brain gangliosides on the surface of astrocytes and neurons and releasing a milieu of pro-inflammatory mediators, neurotrophic factors, and neurotransmitters. Platelet-derived factors directly stimulate neuronal electric and synaptic activity and promote the formation of new synapses and axonal regrowth near the site of damage. Despite such active involvement in response to CNS damage, the role of platelets in neurological disorders was not extensively studied, which will be the focus of this review.
Highlights
Platelet biology recently gains a particular interest in neuroscience
We demonstrated that major brain gangliosides within neuronal lipid rafts in post-synaptic membranes induced platelets’ granule release (Sotnikov et al, 2013) suggesting a possible mechanism of Aβ secretion by platelets in the central nervous system (CNS)
We have previously shown that plateletderived 5-HT and plateletactivating factor (PAF) (Table 1) boosts the differentiation of pathogenic Th1 and Th17 cells during the early stages of multiple sclerosis (MS) and experimental autoimmune encephalitis (EAE) (Ponomarev, 2018), while at later stages of the disease, platelets become depleted in granule content but upregulate adhesion molecules such as CD62P to form aggregates with lymphocytes (Starossom et al, 2015)
Summary
BBB disruption is presumably involved in neuronal injury during epilepsy and psychiatric disorders. Many types of neuropsychological disorders are accompanied by an increase in BBB permeability leading to direct contact of circulating blood cells in the capillaries with neuronal cells in the CNS. More recent studies demonstrated that platelets could enter CNS parenchyma and directly interact with neuronal cells. Plateletderived factors directly stimulate neuronal electric and synaptic activity and promote the formation of new synapses and axonal regrowth near the site of damage. Despite such active involvement in response to CNS damage, the role of platelets in neurological disorders was not extensively studied, which will be the focus of this review
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