Neuroreport
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Microglial activation plays a critical role in spinal cord ischemic reperfusion injury. Spinal cord stimulation preconditioning and postconditioning has shown spinal cord protection in ischemic reperfusion injury in animal studies. However, whether spinal cord stimulation could reduce microglial activation is still unclear. ⋯ Microglial activation was accompanied with up-regulated p-ERK1/2, and microglial inhibition by 2 Hz spinal cord stimulation was associated with down-regulated p-ERK1/2. Spinal cord stimulation increased the expression of IL-1β. Our results revealed, for the first time, that spinal cord stimulation postconditioning suppresses microglial activation during spinal cord ischemic reperfusion by down-regulation of p-ERK1/2, which may be the protective mechanism of spinal cord stimulation.
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To explore alterations in γ-aminobutyric acid (GABA) levels in response to levetiracetam (LEV) treatment in patients with migraine. Patients with migraine (N=14) were treated with LEV for 12 weeks. The levels of GABA+ in the anterior cingulate cortex/medial prefrontal cortex (ACC/mPFC) and the posterior cingulate cortex (PCC) were examined by proton magnetic resonance spectroscopy before (baseline) and after treatment. ⋯ ACC/mPFC GABA+ was assessed by proton magnetic resonance spectroscopy in eight patients with migraine. LEV had no significant effect on GABA+ levels in the ACC/mPFC region. The decreased GABA+ levels after LEV treatment in patients with migraine suggest that GABA is a migraine biomarker.
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This study aims to identify and characterize neurobiological markers for major depressive disorder (MDD) from resting-state brain functional MRI. We examined the abnormality in the regional homogeneity (ReHo) and amplitude of low-frequency fluctuation (ALFF) in first-episode, drug-naive major depressive disorder (fMDD), and remitted major depressive disorder (rMDD) and correlated these fluctuations with clinical markers of MDD. We conducted a retrospective study and reviewed the medical records of 43 patients with fMDD. ⋯ The temporal gyrus may play a critical role in depressive symptomatology. Abnormal right fusiform gyrus, left middle temporal gyrus, and right superior temporal gyrus alterations were present only in patients with rMDD but not in patients with fMDD, indicating that these alterations may be a therapeutic target for MDD. Abnormal right supramarginal, right precuneus, right lingual gyrus and left superior frontal lobe alterations were present only in patients with rMDD and not in healthy control, and thus may be used as a state marker of MDD.
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High myopia (HM) was associated with impaired long-distance vision. Previous neuroimaging studies showed that abnormal visual experience leads to dysfunction in brain activity in HM even corrected. However, whether alterations in brain structure occur in HM remains unknown. ⋯ No significantly different white matter volume values were found between the two groups. Moreover, in the HM group, the mean retinal nerve fiber layer of the left eye showed a negative correlation with the mean GMV values of the brain stem (r=-0.218; P=0.049), right parahippocampal gyrus/thalamus (r=-0.262; P=0.017), left parahippocampal gyrus/thalamus (r=-0.249; P=0.024), and left putamen (r=-0.232; P=0.036). We found that HM patients showed an altered brain structure in the visual pathway regions and the limbic system, which may provide useful information to explore the neural mechanisms of impaired long-distance vision in HM.
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Diffuse axonal injury (DAI) accounts for more than 50% of all traumatic brain injury. In response to the mechanical damage associated with DAI, the abnormal proteins produced in the neurons and axons, namely, β-APP and p-tau, induce endoplasmic reticulum (ER) stress. Curcumin, a major component extracted from the rhizome of Curcuma longa, has shown potent anti-inflammatory, antioxidant, anti-infection, and antitumor activity in previous studies. ⋯ Further investigation showed that the protective effect of curcumin in DAI was mediated by the PERK/Nrf2 pathway. Curcumin promoted PERK phosphorylation, and then Nrf2 dissociated from Keap1 and was translocated to the nucleus, which activated ATF4, an important bZIP transcription factor that maintains intracellular homeostasis, but inhibited the CHOP, a hallmark of ER stress and ER-associated programmed cell death. In summary, we demonstrate for the first time that curcumin confers protection against abnormal proteins and neuronal apoptosis after DAI, that the process is mediated by strengthening of the unfolded protein response to overcome ER stress, and that the protective effect of curcumin against DAI is dependent on the activation of Nrf2.