Neuroscience
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The present study is designed to investigate the role of vagus nerve in the treatments of irritable bowel syndrome (IBS) and the associated central nervous system disorders. ⋯ The intestinal abnormalities and depressive symptoms in IBS rats can be improved by VNS treatment. This positive effect of VNS was achieved through α7nAChR-mediated inflammatory pathway and may also be associated with the decreased of BBB permeability.
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Social interactions between parents and children are closely linked with children's development, and interbrain synchrony has been shown to be a neural marker of social interaction. However, to truly capture the essence of social interactions through interbrain synchrony, it is necessary to simultaneously discuss the parental and child brains and adequately record neurological signals during parent-child interactions in interactive tasks. In the current review, we have reviewed three main contents. ⋯ Last, we have integrated four methods to enhance interbrain synchrony, including communication patterns, nonverbal behavior, music, and multichannel stimulation. A significant correlation exists between parent-child interbrain synchrony and the development of children's cognitive and behavioral abilities. This summary may be useful for expanding researchers' and practitioners' understanding of the ways in which parenting and the parent-child relationship shape children' cognitive and behavioral abilities.
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Diabetes Mellitus (DM) and Alzheimer's disease (AD) have been two of the most common chronic diseases affecting people worldwide. Type 2 DM (T2DM) is a metabolic disease depicted by insulin resistance, dyslipidemia, and chronic hyperglycemia while AD is a neurodegenerative disease marked by Amyloid β (Aβ) accumulation, neurofibrillary tangles aggregation, and tau phosphorylation. Various clinical, epidemiological, and lipidomics studies have linked those diseases claiming shared pathological pathways raising the assumption that diabetic patients are at an increased risk of developing AD later in their lives. ⋯ Lipidomics, an analysis of lipid structure, formation, and interactions, evidently exhibits these lipid changes and their direct and indirect effect on Aβ synthesis, insulin resistance, oxidative stress, and neuroinflammation. In this review, we have discussed the pathophysiology of T2DM and AD, the interconnecting pathological pathways they share, and the lipidomics where different lipids such as cholesterol, phospholipids, sphingolipids, and sulfolipids contribute to the underlying features of both diseases. Understanding their role can be beneficial for diagnostic purposes or introducing new drugs to counter AD.
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Collective self-esteem (CSE) is an important personality variable, defined as self-worth derived from membership in social groups. A study explored the neural basis of CSE using a task-based functional magnetic resonance imaging (fMRI) paradigm; however, task-independent neural basis of CSE remains to be explored, and whether the CSE neural basis of resting-state fMRI is consistent with that of task-based fMRI is unclear. ⋯ Our findings revealed CSE neural basis in the whole-brain RSFC network, and established the concordance between leverage centrality and the activation pattern (evoked during collective self-worth task) of the identified regions in terms of representing CSE.
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Mitophagy plays a significant role in modulating the activation of pyrin domain-containing protein 3 (NLRP3) inflammasome, which is a major contributor to the inflammatory response that exacerbates cerebral ischemia-reperfusion (I/R) injury. Despite this, the transcriptional regulation mechanism that governs mitophagy remains unclear. This study sought to explore the potential mechanism of Forkhead Box P1 (Foxp1) and its impact on cerebral I/R injury. ⋯ Furthermore, we confirmed through chromatin immunoprecipitation (ChIP) and luciferase reporter assays that FUNDC1 is a direct target gene of Foxp1 downstream. Furthermore, the knockdown of FUNDC1 reversed the increased activation of mitophagy and suppressed NLRP3 inflammasome activation induced by Foxp1 overexpression. Collectively, our findings suggest that Foxp1 inhibits NLRP3 inflammasome activation through FUNDC1 to reduce cerebral I/R injury.