Neuroscience
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A new method for analyzing brain complex dynamics and states is presented. This method constructs functional brain graphs and is comprised of two pylons: (a) Operational architectonics (OA) concept of brain and mind functioning. (b) Network neuroscience. In particular, the algorithm utilizes OA framework for a non-parametric segmentation of EEG signals, which leads to the identification of change points, namely abrupt jumps in EEG amplitude, called Rapid Transition Processes (RTPs). ⋯ The classification results, based on a Naïve Bayes classifier, show that the overall accuracies were found to be above chance level in all tested cases. This method was also compared with other state-of-the-art computational approaches commonly used for functional network generation, exhibiting competitive performance. The method can be useful to neuroscientists wishing to enhance their repository of brain research algorithms.
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Deficits in the neuronal connection that succumbs to the impairment of sensory and motor neurons are the hallmarks of spinal cord injury (SCI). Secondary pathogenesis, which initiates after the primary mechanical insult to the spinal cord, depicts a pivotal role in producing inflammation, lesion formation and ultimately causes fibrotic scar formation in the chronic period. This fibrotic scar formed acts as a major hindrance in facilitating axonal regeneration and is one of the root causes of motor impairment. ⋯ Subsequently, this scar formed inhibits the propagation of action potential from one neuron to adjacent neurons. Ethamsylate, an anti-hemorrhagic drug, has the potential to maintain early hemostasis as well as restore capillary resistance. Therefore, we hypothesized that ethamsylate, by virtue of its anti-hemorrhagic activity, reduces hemorrhagic ischemia-induced neuronal apoptosis, maintains the blood spinal cord barrier integrity, and decreases secondary damage severity, thereby reduce the extent of fibrotic scar formation, and demonstrates a neuroprotective role in SCI.
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Inflammation contributes to amyloid beta (Aβ) aggregation and neuron loss in Alzheimer's disease (AD). Meanwhile, tumor necrosis factor-α (TNF-α) inhibitors present strong effect on suppressing inflammation. Thus, this study aimed to investigated the effect and molecular mechanism of etanercept (ETN) (a commonly used TNF-α inhibitor) on neuron injury and neuroinflammation in AD. ⋯ Besides, ETN treatment reduced neuron injury (reflected by Hematoxylin-Eosin (HE) and terminal-deoxynucleoitidyl transferase mediated nick end labeling (TUNEL) assays) and levels of pro-inflammatory cytokines (including TNF-α, interleukin-1β, Interleukin-6 and CCL2) in AD mice. Moreover, ETN repressed the activation of c-Jun N-terminal kinase (JNK) and nuclear factor-κB (NF-κB) pathways in AD both in vitro and in vivo. In conclusion, ETN exerts neuroprotective function via inactivating JNK and NF-κB pathways in AD, indicating the potential of ETN for improving AD management.
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Recent studies using genomic and functional approaches in the fruit fly Drosophila melanogaster have revealed the effects of viral infection on nervous system homeostasis. An established connection between viral infection and brain function is critical due to its significant contribution to several areas of biomedical research, particularly the molecular pathogenesis of neurotropic viruses, the neurobiology of viral disease, and understanding the genetic basis and pathophysiology of viral tropism.