Neuroscience
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Subarachnoid Hemorrhage (SAH) is a cerebrovascular disorder that has been found to have severe consequences, including a high mortality and disability rate. Research has indicated that neuronal death, particularly apoptosis, plays a major role in the neurological impairment that follows SAH. RNA-binding protein Pum2 can interfere with translation or other biological functions by connecting to the UGUAHAUA sequence on RNA. ⋯ Subsequent overexpression of Pum2 and Norad knockdown is found to reduce SAH-induced oxidative stress, neuronal apoptosis, and ultimately improve behavioral and cognitive changes in SAH mice. Our study indicates that Norad-Pum2 acts as a neuromodulator in SAH, and that by increasing Pum2 and decreasing Norad levels, SAH-induced neuronal apoptosis can be reduced and neurological deficits alleviated. Consequently, Norad-Pum2 may be a promising therapeutic target for SAH.
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Depressive disorder is a psychiatric condition that is characterized by the core symptoms of anhedonia and learned helplessness. Myelination loss was recently found in the prefrontal cortex (PFC) of patients with depression and animal models, but the mechanism of this loss is unclear. In our previous study, chronic restraint stress (CRS) mice showed depressive-like symptoms. ⋯ Rapamycin also increased myelination in the PFC of CRS mice. In summary, we found that CRS enhanced mTOR signaling and reduced myelination in the PFC and that rapamycin could prevent it. Our study provides the etiology of reduced myelin in depressive symptoms and suggests that mTOR signaling could be a target for treating depression or improving myelination deficits in depressive disorders.
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Meta Analysis
Altered functional connectivity in working memory network after acute sleep deprivation.
Acute sleep deprivation (SD) has a detrimental effect on working memory (WM). However, prior functional magnetic resonance imaging (fMRI) studies have failed to reach consistent results on brain functions underlying WM decline after acute SD. Thus, we aimed to identify convergent patterns of abnormal brain functions due to WM decline after acute SD. ⋯ The increased FC between the left declive and right sub-gyral, left cuneus and left lingual gyrus, and left cuneus and right post cingulate were found. Furthermore, the impaired WM performance negatively correlated with increased FC. Taken together, our findings highlight that the altered FC in WM network may be the underlying mechanisms of WM decline after acute SD.
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The prevalence of the novel coronavirus (COVID-19) has been considered a major threat to physical and mental health around the world, causing great pressure and mortality threat to most people. The current study aimed to investigate the neurological markers underlying the relationship between perceived mortality threat (PMT) and negative affect (NA). ⋯ Furthermore, longitudinal mediation models showed that ALFF in the cerebellum, medial occipital gyrus, medial frontal gyrus, and angular gyrus (wave 1) predicted PMT (wave 2) through NA (wave 2). These findings revealed functional neural markers of PMT and suggest candidate mechanisms for explaining the complex relationship between NA and mental/neural processing related to PMT in the circumstance of a major crisis.
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Recent studies have explored the circuitry involving the ventral hippocampus (vHPC), the amygdala, and the prefrontal cortex, a pathway mainly activated to store contextual information efficiently. Lesions in the vHPC impair remote memory, but not in the short term. However, how the vHPC is affected by distinct memory strength or its role in systems consolidation has not yet been elucidated. ⋯ The vHPC is required for the expression of remote fear memory and may control contextual fear generalization, a view corroborated by the fact that inactivation of the vHPC suppresses generalized fear expression, making memory more precise again. Systems consolidation occurs concomitantly with greater activation of the vHPC, which is accelerated in stronger fear memories. These findings lead us to propose that greater activation of the vHPC could be used as a marker for memory generalization.