Neuroscience
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Meta Analysis
Effect of Mirror Therapy on Recovery of Stroke Survivors: A Systematic Review and Network Meta-analysis.
Mirror therapy (MT) as a relatively new rehabilitation technique has been widely applied in stroke patients. A number of randomized controlled trials (RCTs) have investigated the effects of MT for stroke survivors. The main purpose of this network meta-analysis was to investigate the effects of MT on motor function, activities of daily living (ADL), and pain perception in stroke survivors. ⋯ Network meta-analysis showed that MT combined with electrical stimulation (ES) for less than 4 weeks along with conventional rehabilitation therapy (CT), and MT accompanied with CT for less than 4 weeks might be the most suitable interventions for improvement of motor function and ADL, respectively. Overall, MT could effectively improve motor function and ADL, as well as relieve pain for stroke survivors. The study was registered at PROSPERO (CRD42017081742).
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We aimed to investigate the role of dorsal and ventral visual systems in rapid naming of simple Chinese characters. Twenty college students (10 female; Mage = 22.5 years) were required to covertly read a character- and a cross-matrix during an fMRI experiment. A basic prosaccade and a prosaccade-naming task were also performed to confirm the functional significance of the findings. ⋯ Moreover, in the character-matrix reading, we found a negative correlation between the reaction time of naming in the prosaccade-naming task and the EC strength from visual word form area to superior temporal gyrus and a positive correlation between the reaction time in the basic prosaccade task and the EC strength from middle frontal gyrus to intraparietal sulcus. The cross-matrix scanning did not show any brain-behavior relationship. These results suggest that while the dorsal visual system is mainly engaged in eye-movement control, the ventral system is associated more with orthographic processing and orthography-phonology mapping.
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Activation of the inflammasome complex contributes to the inflammatory response and cell death under pathologic conditions. The nucleotide-binding oligomerization domain-like receptor pyrin domain-containing 2 (NLRP2) inflammasome is activated in astrocytes after cerebral ischemia, which can aggravate ischemic damage. Apoptosis signal-regulating kinase 1 (ASK1) is an early activator and immune-regulator after ischemic injury, that can lead to cell death. ⋯ ASK1 silencing or inhibition efficiently reduced NLRP2 inflammasome components and pro-inflammatory cytokine levels in mice and cultured astrocytes. Our findings identify a key role for ASK1 in regulating astroglial inflammasomes after cerebral ischemia. We suggest ASK1 as one of the main targets for astroglial inflammasomes in ischemic stroke.
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Localization of apelin and its receptor APJ in limbic structures such as the hippocampus suggests potential involvement of apelin/APJ signaling in stress-related emotional responses. We have recently reported that apelin-13 exerts antidepressant-like actions in acute stressed rats, and that the hippocampus is a critical brain region mediating its actions. However, the neural mechanism underling antidepressant-like actions of apelin-13 is still largely unknown. ⋯ Moreover, apelin-13 ameliorated hypothalamic-pituitary-adrenal (HPA) axis hyperactivity, and hippocampal BDNF expression deficit and glucocorticoid receptor (GR) nucleus translocation hypoactivity in chronic stressed rats. Finally, apelin-13-mediated effects were blocked by the selective TrkB receptor antagonist ANA-12. These results suggest that apelin-13 upregulates BDNF against chronic stress-induced depression-like phenotypes by ameliorating HPA axis and hippocampal GR dysfunctions.
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Adolescence is a window of vulnerability to environmental factors such as chronic stress that can disrupt brain development and cause long-lasting behavioral dysfunction, as seen in disorders like depression, anxiety, and schizophrenia. There are also sex differences in the prevalence of these disorders across the lifespan. However, the mechanisms of how adolescent stress contributes to neuropsychiatric phenotypes are not well understood, nor are the mediating effects of sex. ⋯ PFC-dependent cognitive functioning was also impaired in adult males stressed in adolescence. Adolescent stress disrupted expression patterns of parvalbumin (PV) and perineuronal nets (PNNs) in the PFC, as well as NMDA receptor subunit composition, in a sex- and age-specific manner. The findings presented here contribute to understanding how adolescent stress may lead to neuropsychiatric disorders such as anxiety by disrupting the development of the PFC and emotional behaviors.