Neuroscience
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Stress is an independent risk factor for cognitive impairment, with elevated plasma homocysteine (HCY) levels playing a crucial role in stress-induced cognitive decline. While the rise in plasma HCY levels is linked to abnormal peripheral catabolism, the impact of stress on HCY catabolism in the brain remains unclear. This study investigated the effect of stress on HCY metabolism in the brain by analyzing HCY and its metabolic enzymes in the hippocampus and prefrontal cortex. ⋯ Immunofluorescence double-labeling revealed the downregulation of HCY metabolic enzymes in neurons of stressed mice. The transcription factor KLF4 (Kruppel-likefactor4), known for its inhibitory role, increased after stress or glucocorticoid treatment and suppressed the expression of MS, CBS, and CSE, contributing to elevated HCY levels in the brain. These findings offer new insights into the impairment of HCY catabolism in the stressed brain, suggesting that the downregulation of HCY metabolic enzymes may underlie HCY accumulation and exacerbate stress-induced cognitive dysfunction.
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Neural stem cells and/or progenitor cells (NSCs/NPCs) in the subventricular and subgranular zones of the adult mammal forebrain generate new neurons and are involved in partial repair after injury. Recently, NSCs/NPCs were identified in the area postrema (AP) of the medulla oblongata of the hindbrain. In this study, we used the properties of fenestrate capillaries to observe specific neuronal elimination in the AP of adult mice and investigated subsequent neuronal regeneration by neurogenesis. ⋯ Within 7 days of MSG administration, the number of BrdU+ Sox2+ and BrdU+ Math1+ cells increased markedly, and at least the BrdU+ Math1+ cells similarly increased for the next following 7 days. A remarkable number of HuC/D+ neurons with BrdU+ nuclei were observed 35 days after MSG administration. This study reveals that neurogenesis occurs in the AP of adult mice, recovering and maintaining normal neuronal density after neuronal death.
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Essential tremor with resting tremor (rET) and tremor-dominant Parkinson's disease (tPD) share many similar clinical symptoms, leading to frequent misdiagnoses. Functional connectivity (FC) matrix analysis derived from resting-state functional MRI (Rs-fMRI) offers a promising approach for early diagnosis and for exploring FC network pathogenesis in rET and tPD. However, methods relying solely on a single connection pattern may overlook the complementary roles of different connectivity patterns, resulting in reduced diagnostic differentiation. ⋯ Compared with single-pattern GCN, our proposed MCGCN model demonstrated superior classification accuracy, underscoring the advantages of integrating multiple connectivity modes. Specifically, the model achieved an average accuracy of 88.0% for distinguishing rET from HC, 88.8% for rET from tPD, and 89.6% for tPD from HC. Our findings indicate that combining graph convolutional networks with multi-connection patterns can not only effectively discriminate between tPD, rET, and HC but also enhance our understanding of the functional network mechanisms underlying rET and tPD.
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With the increased availability and sophistication of digital devices in the last decade, young people have become mainstream mobile phone users. Heavy mobile phone dependence causes affective problems (depression, anxiety) and loss of attention on current activities, leading to more cluttered thoughts. Problematic mobile phone use has been found to increase the occurrence of mind wandering, but the neural mechanism underlying this relationship remains unclear. ⋯ FC between the frontoparietal and motor networks, between the default mode network and cerebellar network, and within the cerebellar network mediated the relationship between mobile phone addiction and mind wandering. The findings confirm that mobile phone addiction is a risk factor for increased mind wandering and reveal that FC in several brain networks underlies this relationship. They contribute to research on behavioral addiction, education, and mental health among young adults.
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While mounting evidence suggests that scalp acupuncture (SA) may be effective in alleviating neurological deficits in patients with acute ischemic stroke (IS), its effect on remote hippocampal damage in acute IS and the underlying mechanisms remain elusive. Thus, proteomics analysis was conducted to identify potential targets of SA therapy in acute IS. SA significantly reduced cerebral infarct volume and attenuated neuronal damage in the ischemic penumbra and hippocampus, as well as alleviated neurological deficits in rats with middle cerebral artery occlusion (MCAO). ⋯ Proteomic analysis suggested that this effect is related to the modulation of the acute inflammatory response. SA attenuated remote hippocampal damage after IS by inhibiting microglia activation and neuroinflammation. Lastly, Kng1, Brd9, and Magl were identified as potential targets that mediate the anti-inflammatory effects of SA.