Neuroscience
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Central poststroke pain (CPSP) is a neuropathic pain syndrome that usually occurs after cerebrovascular accidents. Currently, the pathogenesis of CPSP is not fully understood. Purinergic P2X4 receptor (P2X4R) is implicated in neuropathic pain including CPSP. ⋯ This mechanism was associated with P2X4R expression and involved the endogenous opioid system. Human patients with CPSP showed decreased plasma levels of miR-133b-3p compared with those of control participants. Logistic regression analysis of our patient cohort showed that determining plasma levels of miR-133b-3p may be useful for CPSP diagnosis and treatment.
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Randomized Controlled Trial
Greater cortical activation and motor recovery following mirror therapy immediately after peripheral nerve repair of the forearm.
Cortical reorganization occurs immediately after peripheral nerve injury, and early sensorimotor training is suggested during nerve regeneration. The effect of mirror therapy and classical sensory relearning on cortical activation immediately after peripheral nerve repair of the forearm is unknown. Six participants were randomly assigned to the mirror-therapy group or the sensory-relearning group. ⋯ All participants showed improvement in the SWM, S-2PD tests, upper extremity function, and grip strength after the intervention at T1, except for the participant who injured both the median and ulnar nerves in the sensory-relearning group. In addition, the mirror-therapy group had better outcomes in finger dexterity and manual dexterity, and fMRIs showed greater activation in the multimodal association cortices and ipsilateral brain areas during motor tasks. This study provides evidence-based results confirming the benefits of early sensorimotor relearning for cortical activation in peripheral nerve injury of the forearm and different neuroplasticity patterns between mirror therapy and classical sensor relearning.
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Astrocytes experience significant metabolic shifts in the "sensitive period" of neurological function recovery following cerebral ischemia. However, the changes in astrocyte lipid metabolism and their implications for neurological recovery remain unknown. In the present study, we employed a mouse middle cerebral artery occlusion model to investigate the changes in de novo lipogenesis and interleukin-33 (IL-33) production in astrocytes and elucidate their role in blood-brain barrier (BBB) repair in the subacute phase of cerebral ischemia. ⋯ Inhibition of lipogenesis in astrocytes decreased IL-33 production in the peri-infarct area, deteriorated BBB damage and interfered with neurological recovery. In addition, supplementation of IL-33 alleviated BBB destruction and improved neurological recovery worsened by lipogenesis inhibition. These findings indicate that astrocyte lipogenesis increases the production of IL-33 in the peri-infarct area, which promotes BBB repair in the subacute phase of cerebral ischemia injury and improves long-term functional recovery.
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It is well known that neuroinflammation plays a key role in neurodegenerative diseases. Hypoxia-inducible factor (HIF) and its hydroxylases-Prolyl-4-hydroxyases (PHDs) have been found to modulate the inflammatory processes. Here, the effects of PHDs enzyme onlipopolysaccharide-induced neuroinflammation and neurocognitive deficits were investigated. ⋯ DMOG and PHD3knockout decreased expression of inflammatory cytokines and improved the metabolic reprogramming caused by LPS treatment. Furthermore, pretreatment of DMOG reversed learning and memory deficits in systemic LPS-exposed mice through anti-neuroinflammation, which is independent of DMOG angiogenesis. These findings suggested that PHD3 may mediate LPS-induced microglial activation and neuroinflammation-associated neurobehavioral deficits.