Brain research
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The filum terminale (FT) is a potential source of ependymal cells for transplantation. The present study was performed to clarify the characteristics of ependymal cells of the central canal (CC) of the FT in rats. The FT was a thin strand continuous with the conus medullaris (CM), a caudal end of the main spinal cord, situated at the L3-4 level in adult rats. ⋯ Almost all ependymal cells were immunostained for Sox2, Sox9, FoxJ1, and CD133, generally recognized immunochemical markers for ependymal cells of the CC in the spinal cord. Ependymal cells of the CC of FT exhibited almost the same structural and immunohistochemical characteristics as those of the CC of the main spinal cord. Ependymal cells of FTI covered by a thin layer of connective tissue are considered appropriate for transplantation.
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Alzheimer's disease (AD) is characterized by the classical hallmarks of Aβ-deposition and tau-pathology that are thought to ultimately lead to synapse and neuron loss. Although long known, neuroinflammation has recently attracted a substantial amount of attention by researchers due to genome wide association studies (GWAS) that identified microglia associated genes to be correlated with sporadic AD. Besides that, cholinergic degeneration and gamma-aminobutyric acid (GABA) abnormalities have been identified in the brains of AD patients already decades ago, but have not received much attention over the last ten years. ⋯ In this context, an imbalance between excitation and inhibition has been hypothesized to contribute to neuronal network dysfunction. Here, disturbances of cholinergic and GABAergic transmission might play a crucial role. In this review, we will focus on GABAergic dysfunction in AD and mouse models of AD and how those might relate to neuronal network aberration and memory impairment.
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The present study was designed to investigate the mechanism by which lncRNA NEAT1 regulates survival and angiogenesis in oxygen-glucose deprivation (OGD)-induced brain microvascular endothelial cells (BMECs). ⋯ lncRNA NEAT1 facilitated the survival and angiogenesis of OGD-induced BMECs via targeting miR-377 and promoting the expression of VEGFA, SIRT1, and BCL-XL, suggesting that lncRNA NEAT1 could be a promising target for cerebral ischaemia treatment.
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Diabetes induces neurovascular dysfunction leading to peripheral neuropathy. MicroRNAs (miRNAs) affect many biological processes and the development of diabetic peripheral neuropathy. In the present study, we investigated whether thymosin-β4 (Tβ4) ameliorates diabetic peripheral neuropathy and whether miR-146a mediates the effect of Tβ4 on improved neurovascular function. ⋯ Tβ4 treatment significantly increased intraepidermal nerve fiber density and augmented local blood flow and the density of fluorescein isothiocyanate (FITC)-dextran perfused vessels in the sciatic nerve tissue. In vitro, treatment of dorsal root ganglion (DRG) neurons and mouse dermal endothelial cells (MDEs) with Tβ4 significantly increased axonal outgrowth and capillary-like tube formation, whereas blocking miR-146a attenuated Tβ4-induced axonal outgrowth and capillary tube formation, respectively. Our data indicate that miR-146a may mediate Tβ4-induced neurovascular remodeling in diabetic mice, by suppressing pro-inflammatory signals.