Neuroscience
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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.
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Astrocytes are implicated in stress-induced neuroinflammatory responses in depression. This paper was to explore the molecular mechanism of the E3 ubiquitin ligase NEDD4L (NEDD4 like E3 ubiquitin protein ligase) in depressed mice by regulating astrocyte activation, and to find a new target for depression. A mouse model of depression was established by CUMS (chronic mild unpredictable stress) in 48 6-week male C57BL/6 mice and injected with sh-NEDD4L vector for testing behavioral and cognitive abilities, histopathological changes, and the number of GFAP-positive cells. ⋯ NEDD4L inhibition increased GFAP-positive cells, increased PAX6 protein levels and decreased P2X7R mRNA and protein levels, and decreased inflammatory factor secretion in brain tissue and in vitro cells. PAX6 knockdown or P2X7R overexpression partially reversed the effects of NEDD4L inhibition on astrocyte activation and neuroinflammation. To conclude, highly-expressed NEDD4L in depression-like mouse brain inhibits astrocyte activation and exacerbates neuroinflammation by ubiquitinating PAX6 and promoting P2X7R level.
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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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Motor imagery based brain-computer interfaces (MI-BCIs) have excellent application prospects in motor enhancement and rehabilitation. However, MI-induced electroencephalogram features applied to MI-BCI usually vary from person to person. This study aimed to investigate whether the motor ability of the individual upper limbs was associated with these features, which helps understand the causes of inter-subject variability. ⋯ The results demonstrate that hand dexterity and fine motor coordination are significantly related to MI-induced neural activities. In addition, the method of imagining is also relevant to MI features. Therefore, this study is meaningful for understanding individual differences and the design of user-centered MI-BCI.