Traumatic brain injury (TBI) is an increasing health problem. It is a complex, progressive disease that consists of many factors affecting memory. Studies have shown that increased blood-brain barrier (BBB) permeability initiates pathological changes in neuro-vascular network but the role of cerebrovascular dysfunction and its mediated mechanisms associated with memory reduction during TBI are still not well understood. Changes in BBB, inflammation, extravasation of blood plasma components, activation of neuroglia lead to neurodegeneration. Extravasated proteins such as amyloid-beta, fibrinogen, and cellular prion protein may form degradation resistant complexes that can lead to neuronal dysfunction and degeneration. They also have the ability to activate astrocytes, and thus, can be involved in memory impairment. Understanding the triggering mechanisms and the places they originate in vasculature or in extravascular tissue may help to identify potential therapeutic targets to ameliorate memory reduction during TBI. The goal of this review is to discuss conceptual mechanisms that lead to short-term memory reduction during non-severe TBI considering distinction between vascular and non-vascular effects on neurons. Some aspects of these mechanisms need to be confirmed further. Therefore, we hope that the discussion presented bellow may lead to experiments that may clarify the triggering mechanisms of memory reduction after head trauma.
Keywords: astrocytes; cerebral vessel; fibrinogen; neuronal degeneration; short-term memory.
© 2019 Federation of European Neuroscience Societies and John Wiley & Sons Ltd.