Massive studies have focused on the understanding of the pathobiology of cellular and molecular changes and injury mechanisms after traumatic brain injury (TBI), but very few studies have specially discussed the role of synapses in the context of TBI. This paper specifically highlights the role and therapeutic potentials of synapses after TBI. First, we review and conclude how synapses interact with constant structural, metabolic, neuroendocrine, and inflammatory mechanisms after TBI. Second, we briefly describe several key synaptic proteins involved in neuroplasticity, which may be novel neuronal targets for specific intervention. Third, we address therapeutic interventions in association with synapses after TBI. Finally, we concisely discuss the study gaps in the synapses after TBI, in hopes that this would provide more insights for future studies. Synapses play an important role in TBI; while the understandings on the synaptic participation in the treatments and prognosis of TBI are lacking, more studies in this area are warranted.
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http://dx.doi.org/10.1155/2017/4296075 | DOI Listing |
J Biotechnol Biomed
November 2024
Department of Translational Research, College of Osteopathic Medicine of the Pacific, Western University of Health Sciences, Pomona CA 91766, USA.
Traumatic brain injury (TBI) is one of the growing public health problems and a leading cause of disabilities and mortality worldwide. After the mechanical impact to the head, patients of all ages suffer from cognitive and neurological deficits, as well as psychological disorders to different extents. In the last years, the use of electrical impulses and magnetic currents to achieve therapeutic effects have shown promising results and became potential treatments for TBI.
View Article and Find Full Text PDFFront Immunol
December 2024
Department of Neurology, Ulm University, Ulm, Germany.
Background: Traumatic brain injury (TBI) induces an acute reactive state of microglia, which contribute to secondary injury processes through phagocytic activity and release of cytokines. Several receptor tyrosine kinases (RTK) are activated in microglia upon TBI, and their blockade may reduce the acute inflammation and decrease the secondary loss of neurons; thus, RTKs are potential therapeutic targets. We have previously demonstrated that several members of the Fibroblast Growth Factor Receptor (FGFR) family are transiently phosporylated upon TBI; the availability for drug repurposing of FGFR inhibitors makes worthwhile the elucidation of the role of FGFR in the acute phases of the response to TBI and the effect of FGFR inhibition.
View Article and Find Full Text PDFSci Rep
November 2024
Center for Neuroscience, University of Pittsburgh, 4401 Penn Ave, Pittsburgh, PA, 15224, USA.
Reductions of neurogranin (Ng), a calcium-sensitive calmodulin-binding protein, result in significant impairment across various hippocampal-dependent learning and memory tasks. Conversely, increasing levels of Ng facilitates synaptic plasticity, increases synaptogenesis and boosts cognitive abilities. Controlled cortical impact (CCI), an experimental traumatic brain injury (TBI) model, results in significantly reduced hippocampal Ng protein expression up to 4 weeks post-injury, supporting a strategy to increase Ng to improve function.
View Article and Find Full Text PDFActa Neuropathol
October 2024
Department of Neuroscience, College of Medicine, Ohio State University, Columbus, OH, USA.
ACS Nano
October 2024
Institute of Integrative Medicine, Department of Integrated Traditional Chinese and Western Medicine, Xiangya Hospital, Central South University, Changsha 410008, P. R. China.
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