Neuroscience
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Previous studies have demonstrated patients with autism spectrum disorder (ASD) are accompanied by alterations of spontaneous brain activity in gray matter. However, whether the alterations of spontaneous brain activity exist in white matter remains largely unclear. In this study, 88 ASD patients and 87 typical controls (TCs) were included and regional homogeneity (ReHo) was calculated to characterize spontaneous brain activity in white matter. ⋯ Compared with TCs, the ASD group showed significantly decreased ReHo in the left superior corona radiata and left posterior limb of internal capsule, and decreased ReHo in the left anterior corona radiata with a trend level of significance. In addition, significantly weaker structural-functional coupling was observed in the left superior corona radiata and left posterior limb of internal capsule in ASD patients. Taken together, these findings highlighted abnormalities of white matter's regional spontaneous brain activity in ASD, which may provide new insights into the pathophysiological mechanisms of this disorder.
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Self-concept clarity (SCC) focuses on the internal consistency and stability of individual self-concept and is assumed to be a critical indicator for one's subjective well-being (SWB), which is assumed to include emotional well-being (EWB) and cognitive well-being (CWB). However, the neurobiological basis of SCC and the neurological mechanisms underlying the relationship between SCC and SWB have not been well defined. Thus, this study explored the neural basis of SCC by correlating the fractional amplitude of low frequency fluctuations (fALFF) and resting-state functional connectivity (RSFC) with the self-reported SCC in 574 healthy first-year university students. ⋯ Additionally, SCC was associated with decreased RSFC of the right PreCG and left inferior parietal lobe (IPL). Furthermore, mediation analysis demonstrated that the fALFF in the right PreCG and PreCG-IPL connectivity strength might be associated with EWB and positive affect through SCC. Our findings contribute to understanding the neurobiological basis of SCC and the neural mechanism underlying the relationship between SCC and EWB.
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Schizophrenia is a neurodevelopmental disorder with dendrite and dendritic spine dysfunction. Dysbindin-1, a protein decreased in the brains of schizophrenia patients, is involved in the development of dendrites and spines. However, it is still unclear how the role of dysbindin-1 in neuronal development is regulated. ⋯ S10 phosphorylation of dysbindin-1A was increased during postnatal neuronal and synapse development stage, and was enriched in postsynaptic densities (PSDs). Furthermore, overexpressing wild type or S10 phospho-mimic mutant (S10D), but not S10 phospho-dead mutant (S10A) of dysbindin-1A rescued the dendrite and spine deficits in dysbindin-1A knockdown neurons. These results indicate S10 phosphorylation of dysbindin-1A by Akt1 is essential for neuronal development, providing a potential regulation mechanism for dysbindin-1A in neuronal development.
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The impacts of early-life adversity (ELA) on cognitive functions including striatal-dependent habit memory and hippocampal-dependent spatial memory were investigated in male mice. The ELA mouse model was generated via an altered cage environment with limited nesting and bedding materials during postnatal days 2-9 (P2-9). The altered cage environment affected the nesting behaviors of dams, creating a stressful condition for their offspring. ⋯ The spine data supported the selective effects of ELA on PSD-95 synapses. Specifically, both thin and mushroom-type spines were increased in DLS, while loss of thin spines was apparent in CA1 radiatum in ELA mice versus controls. The correlation between PSD-95 synapses and memory performances was further analyzed, and the data suggested that increased small (<0.20 μm3) and large (>0.40 μm3) synapses in DLS might drive ELA mice to make decisions largely relying on habit memory, while loss of small synapses in hippocampal CA1 damage the spatial memory of ELA mice.
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Glaucoma is an age-related neurodegenerative disorder characterized by retinal ganglion cell (RGC) degeneration and excavation of the optic nerve head (ONH). It is associated with an increase in intraocular pressure (IOP) and progressive decline in the visual field. Reduction in the retrograde axonal transport of neurotrophic factors such as brain-derived neurotrophic factor (BDNF) from the brain to the neuronal cell bodies in retina, has been suggested as one of the key mechanisms underlying selective degeneration of ganglion cells and optic nerve in glaucoma. ⋯ This study corroborates previous findings and demonstrates that glaucoma is associated with downregulation of TrkB downstream signalling and enhanced levels of amyloid β (Aβ 1-42) accumulation in the retina. 7,8 dihydroxyflavone (7,8 DHF) is a TrkB agonist and regular administration of this compound imparted significant protection against loss of GCL density and preserved inner retinal function in experimental glaucoma models. 7,8 DHF treatment stimulated activation of TrkB intracellular signalling as well as ameliorated the increase in the levels of soluble Aβ (1-42) in the retinas of rats and mice exposed to high IOP. The protective effects of 7,8 DHF were also evident in BDNF+/- mice indicating that TrkB agonist mediated activation of TrkB signalling was not altered upon BDNF allelic impairment. These data support BDNF/TrkB axis as a promising therapeutic target in glaucoma and highlight that the detrimental effects of high IOP exposure can be compensated by the exogenous administration of a TrkB agonist.