About this Research Topic
Over-release of glutamate can be observed a few seconds after a hypoxic injury episode before rapidly returning to control values. Moreover, neuronal death can occur several days following the hypoxic episode in question. Different types of signals may be involved in late neuronal cell death and they could be triggered at the synaptic level. Changes in postsynaptic densities have been described several months after brain injury and correlate with alterations in animal behavior. Among the new therapeutic strategies tested mainly experimentally, only hypothermia has shown clinical benefits to some extent. Up to now, there are no well-established treatments for brain repair. Hence, neuroprotection becomes imperative. The understanding of the pathophysiology of brain injury contributes to the identification of neuroprotective agents. In this sense, synapses might be one of the main targets to find neuroprotective candidates.
The audience is meant to be mainly experts in the field. This Research Topic focuses on neuroprotective strategies for the brain, their possible pathways, and the use of pharmacological analogs. Potential topics, mainly related to the synaptic role in brain injury, include:
• Biochemical and physiological aspects of neuroprotective agents focusing on synaptic modifications
• Pathophysiological aspects of brain hypoxia
• Pharmacological- and genetic-targeting strategies
• Beneficial effects of neuroprotective agents on neuroplasticity and behavior
• Clinical-related aspects of neuroprotective agents on associated damage and recovery following perinatal asphyxia
• An integrative in-silico approach for neuroprotective agents
Keywords: synapse-intracellular pathway, translational medicine, neurodegeneration, pharmacological strategies
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