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Alzheimer's disease (AD) is a common neurodegenerative disease, which is mainly caused by brain lesions. The activation of complement system plays an important role in the process of AD lesions. The activated complement can bind to cell membrane receptors and regulate downstream signals. Therefore, inhibiting complement activation provides a new idea for AD treatment. This article reviews the progress in the mechanism and drug development of complement activation in AD, which may provide a new perspective for the diagnosis, treatment and drug development of AD. [ABSTRACT FROM AUTHOR]

Sepsis associated encephalopathy (SAE) is a common complication in patients with sepsis. It is characterized by brain dysfunction, and a considerable proportion of patients have long-term cognitive impairment. The central nervous system is one of earliest regions affected by peripheral inflammation caused by sepsis. As resident immune cells of central nervous system, microglia can coordinate inflammatory responses in brain and play an important role in the innate and adaptive immune responses of brain. Therefore, it plays a crucial role in the occurrence and development of SAE. In this paper, the functional phenotypes of microglia and their role in SAE are reviewed to explore the potential value of microglia in the prevention and treatment of SAE. [ABSTRACT FROM AUTHOR]

Cognitive impairment refers to one or more impairments in feeling, learning and memory, speech, attention and execution, which seriously affects the quality of life of patients. Studies have shown that high fat diet (HFD) can cause neuronal damage and cerebrovascular dysfunction, thus causing cognitive impairment. This article reviews the relevant mechanisms and treatment progress of HFD induced cognitive impairment, with a view to providing new ideas for effective prevention and treatment of cognitive impairment. [ABSTRACT FROM AUTHOR]

Synaptic plasticity is closely related to the development and repair after injury in the nervous system. Glial cells maintain close communication with neurons through energy transportation and signal transduction, which is an important way to promote synaptic plasticity. Astrocytes are closely related to synapses in morphology and function, and are an important factor in regulating synaptic plasticity. Microglia carry out two-way information interaction with synapses, which is a key regulator of synaptic plasticity during development and adulthood. Oligodendrocytes participate in the formation of myelin sheaths, provide metabolic substrates for synaptic transmission, which is a potential force to promote synaptic plasticity. This paper reviews the research progress on the relationship between astrocytes, microglia, oligodendrocytes and synaptic plasticity, in order to provide the reference for further understanding the relationship between glial cells and synaptic plasticity. [ABSTRACT FROM AUTHOR]

BACKGROUND: Glial cell line derived neurotrophic factor (GDNF) plays an important role in inducing the differentiation of bone marrow mesenchymal stem cells (BMSCs) in vitro and promoting the regeneration of neuron axons. OBJECTIVE: To observe BMSCs differentiation induced by over-expression of GDNF gene, detect synaptic function of cells and expression of Wnt signaling pathway components after differentiation, and preliminarily explore the mechanism of BMSCs differentiation into mature neurons. METHODS: Rat BMSCs were isolated and cultured, and further divided into recombinant adenovirus-containing GDNF gene transfection group (Ad-GDNFBMSCs), adenovirus transfection control group (Ad-BMSCs), and untransfected control group. The relative expression of GDNF gene in BMSCs of each group was detected by Q-PCR, and the expression of β-catenin, cyclin D1, NeuN and MAP-2 was detected by immunofluorescence technology in each group. High K+ stimulation induced cell depolarization response after differentiation, and FM4-64 marks synaptic vesicle activity of differentiated cells. RESULTS AND CONCLUSION: (1) The adenovirus-transfected gene had no significant negative effect on the proliferation of BMSCs. BMSCs could express endogenous GDNF gene continuously and at high levels. (2) Under the induction of GDNF gene, BMSCs could express neuron-specific protein NeuN after 3 days cultivation in vitro. The expression of β-catenin protein also could be detected in the cytoplasm of cells. After 7 days cultivation in vitro culture, BMSCs expressed the mature neuronal marker protein MAP-2, and the cell body contracted significantly. Neuron axon-like structures appeared around the cell body. Moreover, β-catenin and cyclin D1 were respectively detected in the cell cytoplasm and the nucleus, while the expression levels of NeuN, MAP-2, β-catenin, and cyclin D1 were not observed in Ad-BMSCs and untransfected control groups, and the cells remained spindle-shaped. (3) After 11 days of in vitro culture, the cells in the Ad-GDNF-BMSCs group showed typical neuronal processes or axons and connected to each other into a network structure, which could be labeled with FM4-64 to show red fluorescence, and induced by high K+ stimulation to induce action potentials in the cells. Synaptic vesicle activity in posterior axons showed FM4-64 red fluorescence gradually decaying. Under the same conditions, cells in the Ad-GDNF-BMSCs group and untransfected control group did not present FM4-64 fluorescently labeled synaptic vesicle activity. (4) Continuous GDNF induction can promote BMSCs differentiated into mature neurons with synaptic cycle function, and may be carried out through the classic Wnt/β-catenin signaling pathway. [ABSTRACT FROM AUTHOR]

BACKGROUND: Olfactory ensheathing cell transplantation for treating spinal cord injury is an issue of concern, which mainly explores the changes of microenvironment after spinal cord injury. However, the effect of olfactory ensheathing cell transplantation on the ultrastructure of spinal cord after spinal cord injury is never reported. OBJECTIVE: To investigate the ultrastructure alterations of neurocytes, axons, myelin sheaths, synapses, and glial scar after spinal cord injury, and the effect of olfactory ensheathing cell transplantation on the protection and regeneration of nerve repair after spinal cord injury. METHODS: The study was approved by the Ethical Committee of Biomedicine of Medical Department of Xi'an Jiaotong University, approval No. 2018-2048. Twenty female Sprague-Dawley rats ware divided into three groups: blank control group (n=4, complete laminectomy of T10, partial laminectomy of T9and T11), DF12 group (n=8, cordotomy+injection of DF12 solution), and olfactory ensheathing cell transplantation group (n=8, cordotomy+olfactory ensheathing cell transplantation). The spinal cord was removed under anesthesia to observe the ultrastructure alterations of neurocytes under transmission electron microscope at 1, 7, 28 and 56 days after injury. RESULTS AND CONCLUSION: (1) Compared with the blank control group, the organelles in the neurons of the injured lesions were significantly reduced, and the obvious changes were found in the ultrastructure of axon, synapses and myelin sheath in the DF12 group. In the olfactory ensheathing cell transplantation group, the organelles in the neurons of the injured lesions were significantly increased with obvious nucleolus, the regeneration of axon, myelin sheath and synapses were significantly promoted, and the glial scar was significantly decreased. (2) The degree of reaction of the astrocytes and perlcytes in the olfactory ensheathing cell transplantation group was light. (3) These findings suggest that olfactory ensheathing cell transplantation can effectively protect the nerve tissues in the lesions after spinal cord injury, promote the regeneration of axon, myelin sheath and synapses, and inhibit the hyperplasia of astrocytes and pericytes, so that the post-injury microenvironment is available for the regeneration of neurons, axons and synapses. [ABSTRACT FROM AUTHOR]

Objective To investigate the effect of dexmedetomidine (Dex) preconditioning on the long-term synaptic plasticity damage induced by repeated exposure of sevoflurane in neonatal rats. Methods Forty-eight rats were randomly assigned into sevoflurane group (group S), sevoflurane preconditioning group (group DS) and control group (group C), with 16 rats in each group. Rats in group S were intraperitoneally injected with 3 mL/kg normal saline before inhaling sevoflurane for 4 h at d7, d14 and d21. Rats in group DS were injected intraperitoneally with 20 μg/kg Dex dissolved in 3 mL/kg normal saline before 4 h sevoflurane inhalation at the same time points. Rats in group C inhaled carrier gas for 4 h after injecting 3 mL/kg normal saline. Eight rats were randomly selected from each group at d37 and d97 to detect learning and memory ability by Morris water maze. Thereafter, in vivo electrophysiological experiments were implemented to compare the longterm potentiation (LTP) and paired-pulse facilitation (PPF) ratio in hippocampal neurons between three groups. Results At both juvenile and adult rats, comparing with rats in group C and group DS, the escape latency was remarkably prolonged in rats of group S, and the number of crossing through the target quadrant was reduced (P＜0.05). The increments of field excitatory postsynaptic potential (fEPSP) slope at all time points after high frequency stimulation were remarkably lower in rats of group S than those of group C and group DS (P＜0.05), while PPF ratio was significantly higher at multiple stimulus intervals in group S than group C and group DS (P＜0.05). As compared to group S at juvenile age, the escape latency at adult age was shortened in the first and second day in group S, and the number of crossing was increased. Meanwhile in the group S at adult age, the increment of fEPSP after high frequency stimulation was higher, and the PPF ratios induced by paired stimulation with interstimulus interval of 50 ms,100 ms,150 ms and 200 ms were obviously lower than those of group S at juvenile age (P＜0.05). Conclusion Dexmedetomidine can ameliorate the abnormal changes on the long-term and shortterm synaptic plasticity, as well as learning and memory ability, which could provide a new strategy for prevention and treatment of adverse effects on the developing brain induced by sevoflurane in clinical practice. [ABSTRACT FROM AUTHOR]