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20 May 2014, Volume 9 Issue 9 Previous Issue    Next Issue

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Stem cells in neuroinjury and neurodegenerative disorders: challenges and future neurotherapeutic prospects Tarek H. Mouhieddine, Firas H. Kobeissy, Muhieddine Itani, Amaly Nokkari, Kevin K.W. Wang 2014, 9 (9):  901-906.  doi: 10.4103/1673-5374.133129 Abstract ( 285 )   PDF (364KB) ( 758 )   Save Neurodegenerative disorders cause irreversible damage to the brain and affect an increasing number of people worldwide. Although promising, the use of neuronal stem cells requires a better understanding of the process of neurogenesis. Various approaches have been used to control neurogenesis; however, all of these platforms presented major pitfalls. Therefore, an interesting future approach is to leverage the use of stem cell treatment and pharmacological agents such as ROCK inhibitors and growth factors to ameliorate neural deterioration. Related Articles | Metrics

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Delayed neural damage induced by lightning and electrical injury: neural death, vascular necrosis and demyelination? Andrew D. Reisner 2014, 9 (9):  907-908.  doi: 10.4103/1673-5374.133130 Abstract ( 222 )   PDF (132KB) ( 718 )   Save The phenomenon of delayed neurodegenerative syndromes following lighting and electrical injury has been know since the early 1930’s, but to the present day the mechanisms involved have been poorly understood. An initial theory is that the electrical insult causes damage to the vascular structures feeding the spinal cord via damage to vascular endothelial cells. There is evidence suggesting that glutamatergic overstimulation can bring about damaging free radicals and that some of these free radicals can be derived from lipids. Using this evidence, it has been suggested that in cases where delayed demyelinating syndromes occur following electrical and lightning injury, and when vascular damage has not been detected, the electrical overstimulation may create damaging free radicals directly in the lipid-rich myelin cells. Dr. Andrew D. Reisner, who comes from Forensic Diagnostic Center of District Nine in USA, reviewed the literature on the effects of cortisol elevation, glutamatergic over-stimulation, and formation of destructive free radicals, and explanations for both forms of delayed neurological damage were offered. With regard to the electroporation hypothesis, it is unclear as to whether electroporation would cause immediate versus delayed neurological damage. Related Articles | Metrics

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How do corticosteroids influence myelin genesis in the central nervous system? Divya M. Chari 2014, 9 (9):  909-911.  doi: 10.4103/1673-5374.133131 Abstract ( 242 )   PDF (850KB) ( 752 )   Save CS therapy is widely used in the treatment of Multiple Sclerosis (MS) and spinal cord injury. However, several reports have raised serious concerns regarding the adverse neurological consequences of CS use, including significantly delaying the production of new myelin (re-myelination) around axons in adult animal models following induction of experimental myelin loss (demyelination) in the central nervous system (CNS). Dr. Divya M. Chari from Keele University School of Medicine firstly elucidate the specific mechanisms underlying the adverse consequences of CS use, then points out the biological role of myelin and process of myelin genesis, lastly she demonstrates the future directions for CS therapy in myelin genesis, and considers information gained from such research can aid in the identification of factors underpinning remyelination failure and hence nerve fibre damage and repair. It can also assist in the identification of pharmacological targets to promote effective myelination for axon preservation, in turn leading to the development of better classes of therapeutic agents or to refinements to existing treatment regimens in neurological practice. References | Related Articles | Metrics

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Early expressions of hypoxia-inducible factor 1alpha and vascular endothelial growth factor increase the neuronal plasticity of activated endogenous neural stem cells after focal cerebral ischemia Seung Song, Jong-Tae Park, Joo Young Na, Man-Seok Park, Jeong-Kil Lee, Min-Cheol Lee, Hyung-Seok Kim 2014, 9 (9):  912-918.  doi: 10.4103/1673-5374.133136 Abstract ( 184 )   PDF (1519KB) ( 739 )   Save Endogenous neural stem cells become “activated” after neuronal injury, but the activation sequence and fate of endogenous neural stem cells in focal cerebral ischemia model are little known. We evaluated the relationships between neural stem cells and hypoxia-inducible factor-1α and vascular endothelial growth factor expression in a photothromobotic rat stroke model using immunohistochemistry and western blot analysis. We also evaluated the chronological changes of neural stem cells by 5-bromo-2′-deoxyuridine (BrdU) incorporation. Hypoxia-inducible factor-1α expression was initially increased from 1 hour after ischemic injury, followed by vascular endothelial growth factor expression. Hypoxia-inducible factor-1α immunoreactivity was detected in the ipsilateral cortical neurons of the infarct core and peri-infarct area. Vascular endothelial growth factor immunoreactivity was detected in bilateral cortex, but ipsilateral cortex staining intensity and numbers were greater than the contralateral cortex. Vascular endothelial growth factor immunoreactive cells were easily found along the peri-infarct area 12 hours after focal cerebral ischemia. The expression of nestin increased throughout the microvasculature in the ischemic core and the peri-infarct area in all experimental rats after 24 hours of ischemic injury. Nestin immunoreactivity increased in the subventricular zone during 12 hours to 3 days, and prominently increased in the ipsilateral cortex between 3–7 days. Nestin-labeled cells showed dual differentiation with microvessels near the infarct core and reactive astrocytes in the peri-infarct area. BrdU-labeled cells were increased gradually from day 1 in the ipsilateral subventricular zone and cortex, and numerous BrdU-labeled cells were observed in the peri-infarct area and non-lesioned cortex at 3 days. BrdU-labeled cells rather than neurons, were mainly co-labeled with nestin and GFAP. Early expressions of hypoxia-inducible factor-1α and vascular endothelial growth factor after ischemia made up the microenvironment to increase the neuronal plasticity of activated endogenous neural stem cells. Moreover, neural precursor cells after large-scale cortical injury could be recruited from the cortex nearby infarct core and subventricular zone. References | Related Articles | Metrics

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Intravenous transplantation of bone marrow mesenchymal stem cells promotes neural regeneration after traumatic brain injury Fatemeh Anbari, Mohammad Ali Khalili, Ahmad Reza Bahrami, Arezoo Khoradmehr, Fatemeh Sadeghian, Farzaneh Fesahat, Ali Nabi 2014, 9 (9):  919-923.  doi: 10.4103/1673-5374.133133 Abstract ( 215 )   PDF (601KB) ( 900 )   Save To investigate the supplement of lost nerve cells in rats with traumatic brain injury by intravenous administration of allogenic bone marrow mesenchymal stem cells, this study established a Wistar rat model of traumatic brain injury by weight drop impact acceleration method and administered 3 × 106 rat bone marrow mesenchymal stem cells via the lateral tail vein. At 14 days after cell transplantation, bone marrow mesenchymal stem cells differentiated into neurons and astrocytes in injured rat cerebral cortex and rat neurological function was improved significantly. These findings suggest that intravenously administered bone marrow mesenchymal stem cells can promote nerve cell regeneration in injured cerebral cortex, which supplement the lost nerve cells.  References | Related Articles | Metrics

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Chrysophanol attenuates lead exposure-induced injury to hippocampal neurons in neonatal mice Ji Zhang, Chunlin Yan, Shu Wang, Yong Hou, Guiping Xue, Li Zhang 2014, 9 (9):  924-930.  doi: 10.4103/1673-5374.133141 Abstract ( 226 )   PDF (2340KB) ( 719 )   Save Previous studies have shown that chrysophanol protects against learning and memory impairments in lead-exposed adult mice. In the present study, we investigated whether chrysophanol can alleviate learning and memory dysfunction and hippocampal neuronal injury in lead-exposed neonatal mice. At the end of lactation, chrysophanol (0.1, 1.0, 10.0 mg/kg) was administered to the neonatal mice by intraperitoneal injection for 15 days. Chrysophanol significantly alleviated injury to hippocampal neurons and improved learning and memory abilities in the lead-poisoned neonatal mice. Chrysophanol also significantly decreased lead content in blood, brain, heart, spleen, liver and kidney in the lead-exposed neonatal mice. The levels of malondialdehyde in the brain, liver and kidney were significantly reduced, and superoxide dismutase and glutathione peroxidase activities were significantly increased after chrysophanol treatment. Collectively, these findings indicate that chrysophanol can significantly reduce damage to hippocampal neurons in lead-exposed neonatal mice. References | Related Articles | Metrics

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Zhichan decoction induces differentiation of dopaminergic neurons in Parkinson’s disease rats after neural stem cell transplantation Huifen Shi, Jie Song, Xuming Yang 2014, 9 (9):  931-936.  doi: 10.4103/1673-5374.133135 Abstract ( 173 )   PDF (216KB) ( 822 )   Save The goal of this study was to increase the dopamine content and reduce dopaminergic metabolites in the brain of Parkinson’s disease rats. Using high-performance liquid chromatography, we found that dopamine and dopaminergic metabolite (dihydroxyphenylacetic acid and homovanillic acid) content in the midbrain of Parkinson’s disease rats was increased after neural stem cell transplantation + Zhichan decoction, compared with neural stem cell transplantation alone. Our genetic algorithm results show that dihydroxyphenylacetic acid and homovanillic acid levels achieve global optimization. Neural stem cell transplantation + Zhichan decoction increased dihydroxyphenylacetic acid levels up to 10-fold, while transplantation alone resulted in a 3-fold increment. Homovanillic acid levels showed no apparent change. Our experimental findings show that after neural stem cell transplantation in Parkinson’s disease rats, Zhichan decoction can promote differentiation of neural stem cells into dopaminergic neurons. Related Articles | Metrics

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Repeated febrile convulsions impair hippocampal neurons and cause synaptic damage in immature rats: neuroprotective effect of fructose-1,6-diphosphate Jianping Zhou, Fan Wang, Jun Zhang, Hui Gao, Yufeng Yang, Rongguo Fu 2014, 9 (9):  937-942.  doi: 10.4103/1673-5374.133145 Abstract ( 287 )   PDF (1267KB) ( 869 )   Save Fructose-1,6-diphosphate is a metabolic intermediate that promotes cell metabolism. We hypothesize that fructose-1,6-diphosphate can protect against neuronal damage induced by febrile convulsions. Hot-water bathing was used to establish a repetitive febrile convulsion model in rats aged 21 days, equivalent to 3–5 years in humans. Ninety minutes before each seizure induction, rats received an intraperitoneal injection of low- or high-dose fructose-1,6-diphosphate (500 or 1,000 mg/kg, respectively). Low- and high-dose fructose-1,6-diphosphate prolonged the latency and shortened the duration of seizures. Furthermore, high-dose fructose-1,6-diphosphate effectively reduced seizure severity. Transmission electron microscopy revealed that 24 hours after the last seizure, high-dose fructose-1,6-diphosphate reduced mitochondrial swelling, rough endoplasmic reticulum degranulation, Golgi dilation and synaptic cleft size, and increased synaptic active zone length, postsynaptic density thickness, and synaptic interface curvature in the hippocampal CA1 area. The present findings suggest that fructose-1,6-diphosphate is a neuroprotectant against hippocampal neuron and synapse damage induced by repeated febrile convulsion in immature rats. References | Related Articles | Metrics

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Neuroprotective effects of ginsenoside Rb1 on hippocampal neuronal injury and neurite outgrowth Juan Liu, Jing He, Liang Huang, Ling Dou, Shuang Wu, Qionglan Yuan 2014, 9 (9):  943-950.  doi: 10.4103/1673-5374.133137 Abstract ( 318 )   PDF (950KB) ( 996 )   Save Ginsenoside Rb1 has been reported to exert anti-aging and anti-neurodegenerative effects. In the present study, we investigate whether ginsenoside Rb1 is involved in neurite outgrowth and neuroprotection against damage induced by amyloid beta (25–35) in cultured hippocampal neurons, and explore the underlying mechanisms. Ginsenoside Rb1 significantly increased neurite outgrowth in hippocampal neurons, and increased the expression of phosphorylated-Akt and phosphorylated extracellular signal-regulated kinase 1/2. These effects were abrogated by API-2 and PD98059, inhibitors of the signaling proteins Akt and MEK. Additionally, cultured hippocampal neurons were exposed to amyloid beta (25–35) for 30 minutes; ginsenoside Rb1 prevented apoptosis induced by amyloid beta (25–35), and this effect was blocked by API-2 and PD98059. Furthermore, ginsenoside Rb1 significantly reversed the reduction in phosphorylated-Akt and phosphorylated extracellular signal-regulated kinase 1/2 levels induced by amyloid beta (25–35), and API-2 neutralized the effect of ginsenoside Rb1. The present results indicate that ginsenoside Rb1 enhances neurite outgrowth and protects against neurotoxicity induced by amyloid beta (25–35) via a mechanism involving Akt and extracellular signal-regulated kinase 1/2 signaling. Related Articles | Metrics

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Protective effect of alpha-synuclein knockdown on methamphetamine-induced neurotoxicity in dopaminergic neurons Yunchun Tai, Ling Chen, Enping Huang, Chao Liu, Xingyi Yang, Pingming Qiu, Huijun Wang 2014, 9 (9):  951-958.  doi: 10.4103/1673-5374.133146 Abstract ( 242 )   PDF (1073KB) ( 1044 )   Save The over-expression of α-synuclein is a major factor in the death of dopaminergic neurons in a methamphetamine-induced model of Parkinson’s disease. In the present study, α-synuclein knockdown rats were created by injecting α-synuclein-shRNA lentivirus stereotaxically into the right striatum of experimental rats. At 2 weeks post-injection, the rats were injected intraperitoneally with methamphetamine to establish the model of Parkinson’s disease. Expression of α-synuclein mRNA and protein in the right striatum of the injected rats was significantly downregulated. Food intake and body weight were greater in α-synuclein knockdown rats, and water intake and stereotyped behavior score were lower than in model rats. Striatal dopamine and tyrosine hydroxylase levels were significantly elevated in α-synuclein knockdown rats. Moreover, superoxide dismutase activity was greater in α-synuclein knockdown rat striatum, but the levels of reactive oxygen species, malondialdehyde, nitric oxide synthase and nitrogen monoxide were lower compared with model rats. We also found that α-synuclein knockdown inhibited methamphetamine-induced neuronal apoptosis. These results suggest that α-synuclein has the capacity to reverse methamphetamine-induced apoptosis of dopaminergic neurons in the rat striatum by inhibiting oxidative stress and improving dopaminergic system function. Related Articles | Metrics

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Neuropeptide Y protects cerebral cortical neurons by regulating microglial immune function Qijun Li, Changzheng Dong, Wenling Li, Wei Bu, Jiang Wu, Wenqing Zhao 2014, 9 (9):  959-967.  doi: 10.4103/1673-5374.133140 Abstract ( 236 )   PDF (682KB) ( 1067 )   Save Neuropeptide Y has been shown to inhibit the immunological activity of reactive microglia in the rat cerebral cortex, to reduce N-methyl-D-aspartate current (INMDA) in cortical neurons, and protect neurons. In this study, after primary cultured microglia from the cerebral cortex of rats were treated with lipopolysaccharide, interleukin-1β and tumor necrosis factor-α levels in the cell culture medium increased, and mRNA expression of these cytokines also increased. After primary cultured cortical neurons were incubated with the lipopolysaccharide-treated microglial conditioned medium, peak INMDA in neurons increased. These effects of lipopolysaccharide were suppressed by neuropeptide Y. After addition of the neuropeptide Y Y1 receptor antagonist BIBP3226, the effects of neuropeptide Y completely disappeared. These results suggest that neuropeptide Y prevents excessive production of interleukin-1β and tumor necrosis factor-α by inhibiting microglial reactivity. This reduces INMDA in rat cortical neurons, preventing excitotoxicity, thereby protecting neurons. References | Related Articles | Metrics

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Acupuncture and moxibustion reduces neuronal edema in Alzheimer’s disease rats Hua Zhou, Guojie Sun, Lihong Kong, Yanjun Du, Feng Shen, Shuju Wang, Bangguo Chen, Xiaoling Zeng 2014, 9 (9):  968-972.  doi: 10.4103/1673-5374.133148 Abstract ( 209 )   PDF (2497KB) ( 840 )   Save To examine the possible correlation of aberrant Wnt signaling and pathological changes in Alzheimer’s disease, we established a rat model of Alzheimer’s disease and measured axin and β-catenin expression in the hippocampus. Rats were pretreated with moxibustion or electroacupuncture, or both, at Baihui (GV20) and Shenshu (BL23). Axin expression was lower, β-catenin expression was greater, and neuronal cytoplasmic edema was visibly prevented in the rats that had received the pretreatments. Our results suggest that the mechanism underlying the neuroprotective effect of acupuncture and moxibustion in Alzheimer’s disease is associated with axin and β-catenin expression in the Wnt signal transduction pathway. References | Related Articles | Metrics

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The apparent diffusion coefficient does not reflect cytotoxic edema on the uninjured side after traumatic brain injury Hong Lu, Xiaoyan Lei 2014, 9 (9):  973-977.  doi: 10.4103/1673-5374.133150 Abstract ( 237 )   PDF (919KB) ( 1336 )   Save After traumatic brain injury, vasogenic and cytotoxic edema appear sequentially on the involved side. Neuroimaging investigations of edema on the injured side have employed apparent diffusion coefficient measurements in diffusion tensor imaging. We investigated the changes occurring on the injured and uninjured sides using diffusion tensor imaging/apparent diffusion coefficient and histological samples in rats. We found that, on the injured side, that vasogenic edema appeared at 1 hour and intracellular edema appeared at 3 hours. Mixed edema was observed at 6 hours, worsening until 12–24 hours post-injury. Simultaneously, microglial cells proliferated at the trauma site. Apparent diffusion coefficient values increased at 1 hour, decreased at 6 hours, and increased at 12 hours. The uninjured side showed no significant pathological change at 1 hour after injury. Cytotoxic edema appeared at 3 hours, and vasogenic edema was visible at 6 hours. Cytotoxic edema persisted, but vasogenic edema tended to decrease after 12–24 hours. Despite this complex edema pattern on the uninjured side with associated pathologic changes, no significant change in apparent diffusion coefficient values was detected over the first 24 hours. Apparent diffusion coefficient values accurately detected the changes on the injured side, but did not detect the changes on the uninjured side, giving a false-negative result. Related Articles | Metrics

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Sequential expression of cyclooxygenase-2, glutamate receptor-2, and platelet activating factor receptor in rat hippocampal neurons after fluid percussion injury Zhiqiang Li, Qingming Shu, Lingzhi Li, Maolin Ge, Yongliang Zhang 2014, 9 (9):  978-985.  doi: 10.4103/1673-5374.133151 Abstract ( 218 )   PDF (819KB) ( 814 )   Save Traumatic brain injury causes gene expression changes in different brain regions. Occurrence and development of traumatic brain injury are closely related, involving expression of three factors, namely cyclooxygenase-2, glutamate receptor-2, and platelet activating factor receptor. However, little is known about the correlation of these three factors and brain neuronal injury. In this study, primary cultured rat hippocampal neurons were subjected to fluid percussion injury according to Scott’s method, with some modifications. RT-PCR and semi-quantitative immunocytochemical staining was used to measure the expression levels of cyclooxygenase-2, glutamate receptor-2, and platelet activating factor receptor. Our results found that cyclooxygenase-2 expression were firstly increased post-injury, and then decreased. Both mRNA and protein expression levels reached peaks at 8 and 12 hours post-injury, respectively. Similar sequential changes in glutamate receptor 2 were observed, with highest levels mRNA and protein expression at 8 and 12 hours post-injury respectively. On the contrary, the expressions of platelet activating factor receptor were firstly decreased post-injury, and then increased. Both mRNA and protein expression levels reached the lowest levels at 8 and 12 hours post-injury, respectively. Totally, our findings suggest that these three factors are involved in occurrence and development of hippocampal neuronal injury. References | Related Articles | Metrics

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Age-related changes of lateral  ventricular width and periventricular white matter in the human brain: a diffusion tensor imaging study Yong Hyun Kwon, Sung Ho Jang, Sang Seok Yeo 2014, 9 (9):  986-989.  doi: 10.4103/1673-5374.133152 Abstract ( 241 )   PDF (870KB) ( 1698 )   Save References | Related Articles | Metrics