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19 December 2019, Volume 14 Issue 13 Previous Issue    Next Issue

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Glutamate receptors delocalization and impairment of hippocampal long-term potentiation precedes local extracellular Aβ deposition in asymptomatic 5XFAD mouse model Ning Li, Yang Li, Lijuan Li, Ke Zhu, Yan Zheng, Xiaomin Wang 2019, 14 (13):  2400-2407.  Abstract ( 83 )   PDF (442KB) ( 272 )   Save Alzheimer disease(AD) is the most common form of dementia. Since the synaptic plasticity is considered the cellular mechanism of memory formation and its impairment is found involve in dementia, it is necessary to clarify the checkpoint of synaptic plasticity decline and associated mechanism in early stage of AD process. Mice at age of 12 weeks were subjected to spatial learning test in Morris water maze. The 6-10 weeks old 5XFAD mice and their age-matched littermates were used to record long-term potentiation (LTP) in dentate gyrus (DG) of hippocampus. In addition, mice at age of 10 weeks were applied in observation of Aβ immunostaining and synaptic subcellular fractionation. Deficit in reversal learning was not developed in the AD mice until 14 weeks old. The impairment of LTP in DG of 5XFAD mice at 10 weeks old occurred, accompanying with synaptic delocalization of AMPA and NMDA receptor subunits. Meanwhile, Aβ was found accumulated intracellularly in hippocampus of the mouse model with no extracellular Aβ deposition. However, no changes in basal synaptic transmission in hippocampus of these AD mice compared to wild type control were detected. The delocalization of postsynaptic glutamate receptors and its associated decline in synaptic plasticity may be a leading event within the AD pathological context, even preceding the senile plaque formation in the 5XFAD mouse model. This study provides a referable checkpoint for studying pathogenesis of AD. Related Articles | Metrics

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Screening for the key mRNA SNP targets associated with pathogenesis of neonatal hypoxia-ischemic brain damage by RNA sequencing Liu-Lin Xiong,Lu-Lu Xue,Mohammed Al-Hawwas,Jin Huang,Rui-Ze Niu,Ya-Xin Tan,Yang Xu,Ying-Ying Su,Jia Liu,Ting-Hua Wang 2019, 14 (13):  2408-2417.  Abstract ( 62 )   PDF (3086KB) ( 338 )   Save Single-nucleotide polymorphisms (SNPs) were involved in certain diseases. However, the influences of SNPs on the pathogenesis of neonatal hypoxia-ischemic brain damage (HIBD) remain elusive. This study aimed to investigate the differential expression of mRNAs and the relatedness of SNPs with neonatal HIBD to identify potential etiological targets for HIBD. Seven-day postnatal rats were used to establish HIBD model, and the expression profiles of mRNA and SNP were analyzed in HI-brains using RNA sequencing and compared to control-brains. Genes exhibiting SNPs associated with HIBD were identified and studied by gene ontology (GO) and pathway analysis to identify their possible mechanism to initiate the disease. The results revealed 89 up-regulated genes exhibiting SNPs that mainly located on chromosome 1 and 2. Additionally, GO analysis indicated that the SNPs exhibiting up-regulated genes are mainly involved with angiogenesis, wound healing and glutamatergic synapse and biological processing of calcium-activated chloride channels. Signaling pathways analysis indicated that deferentially expressed genes play a role in glutamatergic synapse, longterm depression and oxytocin signaling pathway. Moreover, the intersection analysis of high throughput screening via Pubmed and gene sequencing for SNP showed that CSRNP1, DUSP5 and LRRC25 were most innovative and relative to HIE. They were verified to significantly up-regulate by qPCR in human neurons with OGD. Thus, the CSRNP1, DUSP5 and LRRC25 displaying SNPs may be accountable for the pathogenesis of HIBD, and are closely relevant to the development of HIBD. It is possible that our finding may be considered as a novel direction for further research on HIBD. Related Articles | Metrics

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Normal tension glaucoma: from the brain to the eye or the inverse? Hui-Jun Zhang,Xue-Song M,Kwok-Fai So 2019, 14 (13):  2418-2423.  Abstract ( 44 )   PDF (367KB) ( 218 )   Save Glaucoma is a chronic, progressive optic neuropathy characterized by the loss of peripheral vision first and then cen-tral vision. Clinically, normal tension glaucoma is considered a special subtype of glaucoma, in which the patient’s intraocular pressure is within the normal range, but the patient experiences typical glaucomatous changes. However, increasing evidence has challenged the traditional pathophysiological view of normal tension glaucoma, which is based only on intraocular pressure, and breakthroughs in central nervous system imaging may now greatly increase our knowledge about the mechanisms underlying normal tension glaucoma. In this article, we review the latest pro-gress in understanding the pathogenesis of normal tension glaucoma and in developing imaging techniques to detect it, to strengthen the appreciation for the connection between normal tension glaucoma and the brain. Related Articles | Metrics

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A Comparative Proteome Study of MicroRNA-21a-5p within the Mouse Model After Spinal Cord Injury, and its Possible Role in Different Pathways Almaghalsa-Ziad Mohammed,HongXia Du, Bin Ning, Jia Tang Hong 2019, 14 (13):  2424-2432.  Abstract ( 79 )   PDF (3025KB) ( 215 )   Save Spinal cord injury (SCI) is considered to be one of the most devastating effects of all neurological diseases. The pathophysiological mechanisms of SCI involve central nervous system injury of the various signaling pathways. During our previous study, we found that microRNA-21a-5p (miR-21a-5p) plays a significant role in SCI to improve the recovery of motor function after spinal cord injury in a mouse model. In this study, we utilized the proteomics approach to understand the role of different proteins expressed in miR-21a-5p knockdown (KD) and their functions as compare to the negative control group (NC). We found that after introducing miR-21a-5p, most of the proteins that play an essential role in regulation of inflammatory processes, cell protection against oxidative stress, cell redox homeostasis and cell maintenance were upregulated in comparison to the NC group. We investigated different enriched pathways generated via the Kyoto Encyclopedia of Genes and Genomes (KEGG). Enriched pathways were found in both groups, such as the oxidative phosphorylation pathway, which is relevant to Parkinson’s disease, Huntington’s disease, Alzheimer’s disease and cardiac muscle contraction. We also found that miR-21a-5p could be a potential biomarker in the amyotrophic lateral sclerosis pathway (ALS), as miR-21a-5p becomes deregulated in this pathway. This study helps to give an overview of the significant proteins and their potential role in SCI. It will be helpful gateway to study these proteins and their co-relation in the recovery of spinal cord injury and can be a useful biomarker in future studies. Related Articles | Metrics

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Lycium barbarum polysaccharides protected retinal ganglion cells against oxidative stress injury Lian Liu,Xiao-Yuan Sha,Yi-Ning Wu,Meng-Ting Chen,Jing-Xiang Zhong 2019, 14 (13):  2433-2438.  Abstract ( 50 )   PDF (1735KB) ( 205 )   Save AIM: To investigate the protective effect and its mechanism of Lycium barbarum polysaccharides (LBP) against oxidative stress injury in retinal ganglion cells-5 (RGC-5). METHODS: RGC-5 cells were exposed to different concentrations of CoCl 2 for 24 hours, then cell viability was measured to get the properly concentration of CoCl 2 which can induce half apoptosis of RGC-5. With different concentrations of LBP pretreatment, the RGC-5 cells were then exposed to appropriate concentration of CoCl 2 , cell apoptosis was detected by flow cytometric analysis. ROS and mitochondrial membrane potential(MMP) were test by the kits. RSULTS: LBP could effectively reduce the CoCl 2 -induced RGC-5 cells’ apoptosis. LBP inhibited ROS generation and the reduction of the mitochondrial membrane potential(MMP). CONCLUSION: LBP could protect RGC-5 cells from CoCl 2 -induced apoptosis. MMP and ROS had relationship with the protective effects of LBP. Related Articles | Metrics