Neuroscience
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Parkinson's disease (PD) is a common neurodegeneration disease associated with the abnormal deposition and spread of misfolded proteins (α-synuclein and Tau protein), which progressively damages the glymphatic system. This research intended to investigate the activity of the glymphatic system in PD individuals with freezing of gait (PD-FOG) and PD patients without it (PD-nFOG), as well as their relationship to the clinical neural scale. Diffusion tensor imaging (DTI) was performed in 28 PD-FOG individuals, 31 PD-nFOG individuals, and 34 healthy controls (HC). ⋯ In addition, the DTI-ALPS index of PD-nFOG patients were positively correlated with disease duration, Unified Parkinson's Disease Rating-III Right (UPDRS-III R), UPDRS-III TOTAL, UPDRS-IV. Taken together, these findings highlighted the weakening of function of the glymphatic system in PD individuals, which is associated with motor symptoms and treatment complications. We speculate that treatment aimed at enhancing the flow and clearance of the glymphatic system may alleviate clinical symptoms of PD.
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Neuronal necroptosis and apoptosis are the most important pathways for programmed cell death after brain ischaemic stroke. Although apoptosis signalling pathways have been extensively studied, molecular mechanisms underlying necroptosis remain unclear. In this study, we found that receptor-interacting protein 3 (RIP3) deficiency reduced cerebral infarction volume, neurological deficits, and neuronal ultrastructural damage in a mouse model of brain ischaemic stroke by inhibiting programmed cell death. ⋯ We further confirmed that RIP3 deficiency inhibited the decrease of mitochondrial membrane potential, the increase of calcium influx and reactive oxygen species (ROS) production. In addition, compared with WT primary cortical neurons, the decreased expression of CaMKII and Pyk2 was further verified in a Ripk3-/- primary cortical neurons underlying oxygen and glucose deprivation/reoxygenation (OGD/R) model. In conclusion, we first identified that the RIP3/CaMKII/Pyk2 pathway is involved in programmed cell death after brain ischaemic stroke, which suggests it is a promising therapeutic target in ischaemia-induced neuronal injury.
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Cervical spinal cord injury (cSCI) impairs neural drive to the respiratory muscles, causing life- threatening complications such as respiratory insufficiency and diminished airway protection. Repetitive "low dose" acute intermittent hypoxia (AIH) is a promising strategy to restore motor function in people with chronic SCI. Conversely, "high dose" chronic intermittent hypoxia (CIH; ∼8 h/night), such as experienced during sleep apnea, causes pathology. ⋯ However, CIH exerted complex effects depending on injury status. Whereas CIH increased A1 receptor expression in intact (not injured) rats, it increased A2A receptor expression in spinally injured (not intact) rats. The differential impact of CIH reinforces the concept that the injured spinal cord behaves in distinct ways from intact spinal cords, and that these differences should be considered in the design of experiments and/or new treatments for chronic cSCI.
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Studies of scalp electroencephalography (EEG) had shown altered topological organization of functional brain networks in patients with major depressive disorder (MDD). However, most previous EEG-based network analyses were performed at sensor level, while the interpretation of obtained results was not straightforward due to volume conduction effect. To reduce the impact of this defect, the whole cortical functional brain networks of MDD patients were studied during resting state based on EEG-source estimates in this paper. ⋯ Furthermore, patients with MDD exhibited increased nodal clustering coefficients in the left lingual gryus and left precuneus in α band. In addition, β band global clustering coefficient was positively correlated with the scores of depression severity. Therefore, the findings indicated the cortical functional brain networks in MDD patients were disruptions, which suggested it would be one of potential causes of depression.
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The reading of action verbs has been shown to activate motor areas, whereby sentence context may serve to either globally strengthen this activation or to selectively sharpen it. To investigate this issue, we manipulated the presence of manual actions and sentence context, assessing the level of corticospinal excitability by means of transcranial magnetic stimulation. We hypothesized that context would serve to sharpen the neural representation of the described actions in the motor cortex, reflected in context-specific modulation of corticospinal excitability. ⋯ The coil was positioned over the cortical representation of the right first dorsal interosseous (pointer finger). We observed a general increase of corticospinal excitability while reading both manual action and non-manual verbs in minimal context, whereas the modulation was action-specific in rich context: corticospinal excitability increased while reading manual verbs, but did not differ from baseline for non-manual verbs. These findings suggest that sentence context sharpens motor representations, activating the motor cortex when relevant and eliminating any residual motor activation when no action is present.