Neuroscience
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Understanding the biological basis of cognitive differences between individuals is the goal in human intelligence research. The surface area of the cortex is considered to be a key determinant of human intelligence. Adolescence is a period of development characterized by physiological, emotional, behavioral, and psychosocial changes, which is related to the recombination and optimization of the cerebral cortex, and cognitive ability changes significantly in children and adolescents. ⋯ No correlation was observed between regional surface areas and nonverbal intelligence, except for the occipital lobe and the right hemisphere. In the bivariate twin analyses, the differences in phenotypic correlation between regional surface areas and verbal intelligence were not due to unshared environmental effects or measurement error, but to genetic effects. In summary, the current study has broadened the previous genetic investigations of cognitive ability and cortical surface area.
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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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Spontaneously hypertensive rats (SHR) are the most common animal model used to study attention deficit hyperactivity disorder (ADHD). The purpose of this study was to look at the impact of neuroinflammation and autophagy on blood-brain barrier function in the prefrontal cortex and hippocampus of ADHD rats. The rats were separated into three groups: juvenile SHR (6 weeks), mature SHR (12 weeks), and comparable age WKY groups. ⋯ Moreover, autophagy of cells and the level of MMP2 and MPP9 in the prefrontal cortex and hippocampus increased in SHR rats. In addition, the expression of ZO-1 and occludin was decreased in SHR rats. To sum up, the increase of neuroinflammation and excessive autophagy were essential factors for the damage of blood-brain barrier structure and function.
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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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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.