Highlights
  • Review Article | April 30, 2021

    The inflammatory response, by disrupting immunohomeostasis and aggravating brain damage, constitutes a major contributory factor to the pathobiology of stroke. Because the immune system is involved in all stages of stroke, immunosuppressive mechanisms may provide neuroprotection in this setting. The TAM/Gas6 pathway, for instance, has been shown to be involved in modulating post-stroke inflammation, and in the reduction of post-stroke brain injury. In addition to this pathway, those mediated by established immunosuppressive molecules (such as IL-10 and TGF-β), by CD25+CD4+ FoxP3+Tregs, and by the cholinergic anti-inflammatory pathway, also appear to play protective roles in the context of stroke. Taken together, evidence accumulated regarding the function of these mechanisms suggest than an immunoregulatory strategy may prove promising, both as an approach to the study of stroke pathophysiology, and to the discovery of treatments that limit the destructive effects of cerebrovascular disease.

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    The inflammatory response, by disrupting immunohomeostasis and aggravating brain damage, constitutes a major contributory factor to the pathobiology of stroke. Because the immune system is involved in all stages of stroke, immunosuppressive mechanisms may provide neuroprotection in this setting. The TAM/Gas6 pathway, for instance, has been shown to be involved in modulating post-stroke inflammation, and in the reduction of post-stroke brain injury. In addition to this pathway, those mediated by established immunosuppressive molecules (such as IL-10 and TGF-β), by CD25+CD4+ FoxP3+Tregs, and by the cholinergic anti-inflammatory pathway, also appear to play protective roles in the context of stroke. Taken together, evidence accumulated regarding the function of these mechanisms suggest than an immunoregulatory strategy may prove promising, both as an approach to the study of stroke pathophysiology, and to the discovery of treatments that limit the destructive effects of cerebrovascular disease.
    Qian Jiang, Christopher R. Stone, Kenneth Elkin et al.
  • Short Communication | April 30, 2021

    An et al. demonstrate the critical role of astrocytic MAOB in both tonic GABA inhibition of SNpc dopaminergic neurons and parkinsonian motor symptoms in the MPTP PD model.

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    An et al. demonstrate the critical role of astrocytic MAOB in both tonic GABA inhibition of SNpc dopaminergic neurons and parkinsonian motor symptoms in the MPTP PD model.
    Heeyoung An, Jun Young Heo, C. Justin Lee and Min-Ho Nam
  • Original Article | April 30, 2021

    This study shows that Central neurocytoma-derived tumor stem cells have transit-amplifying cell characteristics, and EGFR signaling has a critical role in tumorigenesis of CN.

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    This study shows that Central neurocytoma-derived tumor stem cells have transit-amplifying cell characteristics, and EGFR signaling has a critical role in tumorigenesis of CN.
    Hye Young Shin, Kyung-Seok Han, Hyung Woo Park et al.
  • Original Article | April 30, 2021

    During Morris water maze, the spatial learning and memory (L&M) was impaired, the extracellular concentrations of norepinephrine and field excitatory postsynaptic potential (fEPSP) amplitudes in the hippocampal dentate gyrus (DG) were significantly suppressed in sleep-deprived (SD) rats. Moreover, local activation of β-adrenoceptors by isoproterenol in DG could significantly rescued deficits of spatial L&M, alleviated the fEPSP impairment and increased glutamatergic receptor expression in the DG.

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    During Morris water maze, the spatial learning and memory (L&M) was impaired, the extracellular concentrations of norepinephrine and field excitatory postsynaptic potential (fEPSP) amplitudes in the hippocampal dentate gyrus (DG) were significantly suppressed in sleep-deprived (SD) rats. Moreover, local activation of β-adrenoceptors by isoproterenol in DG could significantly rescued deficits of spatial L&M, alleviated the fEPSP impairment and increased glutamatergic receptor expression in the DG.
    Huan-Jun Lu and Jing lv
Vol.30 No.2 | April 30, 2021

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Subcortical structures in elderly subclinical depression

Structural changes in the subcortical area can affect cognitive function and cause increased vulnerability to mood symptoms such as anxiety and subclinical depression. However, studies on changes in subcortical structures show inconsistencies. This research shows the structural differences in segmented subcortical regions between control and subclinical depression groups and visualizes the pathway between structures based on their connection strength through tractography analysis.