Abstract
A bidirectional crosstalk between peripheral players of immunity and the central nervous system (CNS) exists. Hence, blood–brain barrier (BBB) breakdown is emerging as a participant mechanism of dysregulated peripheral–CNS interplay, promoting diseases. Here, we examine the implication of BBB damage in neurodegeneration, linking it to peripheral brain-directed autoantibodies and gut–brain axis mechanisms. As BBB breakdown is a factor contributing to, or even anticipating, neuronal dysfunction(s), we here identify contemporary pharmacological strategies that could be exploited to repair the BBB in disease conditions. Developing neurovascular, add on, therapeutic strategies may lead to a more efficacious pre-clinical to clinical transition with the goal of curbing the progression of neurodegeneration.
Highlights
Inhibition of PDGFR signalingVascular endothelial growth factor Cardiovascular Nitric oxide donor Analgesic, anti-inflammatory, antineoplastic
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Blood–brain barrier (BBB) breakdown is emerging as a participant mechanism of dysregulated peripheral–central nervous system (CNS) interplay, promoting diseases
Summary
Vascular endothelial growth factor Cardiovascular Nitric oxide donor Analgesic, anti-inflammatory, antineoplastic. Decreased JMJD3 gene expression, suppression of MMP-2, MMP-3, and MMP-9 gene activation Binding to FRP2 receptor, inhibition of phospholipase-2
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