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20 May 2016, Volume 11 Issue 5 Previous Issue    Next Issue

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Alzheimer’s disease: the silver tsunami of the 21st century Ankita Sarkar, Madison Irwin, Aditi Singh, Matthew Riccetti, Amit Singh 2016, 11 (5):  693-697.  doi: 10.4103/1673-5374.182680 Abstract ( 282 )   PDF (794KB) ( 540 )   Save Alzheimer’s disease (AD), a fatal progressive neurodegenerative disorder, has no cure to date. One of the causes of AD is the accumulation of amyloid-beta 42 (Aβ42) plaques, which result in the onset of neurodegeneration. It is not known how these plaques trigger the onset of neurodegeneration. There are several animal models developed to (i) study etiology of disease, (ii) look for genetic modifiers, and (iii) identify chemical inhibitors that can block neurodegeneration and help to find cure for this disease. An insect model of Drosophila melanogaster has also provided new insights into the disease. Here we will discuss the utility of the Drosophila eye model to study Alzheimer’s disease. Related Articles | Metrics

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TFP5/TP5 peptide provides neuroprotection in the MPTP model of Parkinson’s disease Binukumar BK, Harish C. Pant 2016, 11 (5):  698-701.  doi: 10.4103/1673-5374.182681 Abstract ( 324 )   PDF (192KB) ( 437 )   Save Cyclin-dependent kinase 5 (Cdk5) is a member of the serine-threonine kinase family of cyclin-dependent kinases. Cdk5 is critical to normal mammalian nervous system development and plays important regulatory roles in multiple cellular functions. Recent evidence indicates that Cdk5 is inappropriately activated in several neurodegenerative conditions, including Parkinson’s disease (PD). PD is a chronic neurodegenerative disorder characterized by the loss of dopamine neurons in the substantia nigra, decreased striatal dopamine levels, and consequent extrapyramidal motor dysfunction. During neurotoxicity, p35 is cleaved to form p25. Binding of p25 with Cdk5 leads deregulation of Cdk5 resulting in number of neurodegenerative pathologies. To date, strategies to specifically inhibit Cdk5 hyperactivity have not been successful without affecting normal Cdk5 activity. Here we show that inhibition of p25/Cdk5 hyperactivation through TFP5/TP5, truncated 24-aa peptide derived from the Cdk5 activator p35 rescues nigrostriatal dopaminergic neurodegeneration induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP/MPP+) in a mouse model of PD. TP5 peptide treatment also blocked dopamine depletion in the striatum and improved gait dysfunction after MPTP administration. The neuroprotective effect of TFP5/TP5 peptide is also associated with marked reduction in neuroinflammation and apoptosis. Here we show inhibition of Cdk5/p25-hyperactivation by TFP5/TP5 peptide, which identifies Cdk5/p25 as a potential therapeutic target to reduce neurodegeneration in PD. Related Articles | Metrics

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Clinical trial perspective for adult and juvenile Huntington’s disease using genetically-engineered mesenchymal stem cells Peter Deng, Audrey Torrest, Kari Pollock, Heather Dahlenburg, Geralyn Annett, Jan A. Nolta, Kyle D. Fink 2016, 11 (5):  702-705.  doi: 10.4103/1673-5374.182682 Abstract ( 334 )   PDF (435KB) ( 460 )   Save "Progress to date from our group and others indicate that using genetically-engineered mesenchymal stem cells (MSC) to secrete brain-derived neurotrophic factor (BDNF) supports our plan to submit an Investigational New Drug application to the Food and Drug Administration for the future planned Phase 1 safety and tolerability trial of MSC/BDNF in patients with Huntington’s disease (HD). There are also potential applications of this approach beyond HD. Our biological delivery system for BDNF sets the precedent for adult stem cell therapy in the brain and could potentially be modified for other neurodegenerative disorders such as amyotrophic lateral sclerosis (ALS), spinocerebellar ataxia (SCA), Alzheimer’s disease, and some forms of Parkinson’s disease. The MSC/BDNF product could also be considered for studies of regeneration in traumatic brain injury, spinal cord and peripheral nerve injury. This work also provides a platform for our future gene editing studies, since we will again use MSCs to deliver the needed molecules into the central nervous system." Related Articles | Metrics

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Adenosine A2A receptors in neuronal outgrowth: a target for nerve regeneration? Filipa F. Ribeiro, Ana M. Sebastião 2016, 11 (5):  706-708.  doi: 10.4103/1673-5374.182683 Abstract ( 339 )   PDF (1401KB) ( 507 )   Save Related Articles | Metrics

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Coordination of the axonal cytoskeleton during the emergence of axon collateral branches Gianluca Gallo 2016, 11 (5):  709-711.  doi: 10.4103/1673-5374.182684 Abstract ( 319 )   PDF (679KB) ( 579 )   Save Related Articles | Metrics

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Antibody-based neuronal and axonal delivery vectors for targeted ligand delivery Kazim A. Sheikh, Gang Zhang 2016, 11 (5):  712-714.  doi: 10.4103/1673-5374.182685 Abstract ( 155 )   PDF (343KB) ( 464 )   Save Related Articles | Metrics

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Possible application of apolipoprotein E-containing lipoproteins and polyunsaturated fatty acids in neural regeneration Michinori Matsuo 2016, 11 (5):  715-716.  doi: 10.4103/1673-5374.182686 Abstract ( 244 )   PDF (407KB) ( 489 )   Save Related Articles | Metrics

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Self-assembling peptide nanofibrous hydrogel as a promising strategy in nerve repair after traumatic injury in the nervous system Na Zhang, Liumin He, Wutian Wu 2016, 11 (5):  717-718.  doi: 10.4103/1673-5374.182687 Abstract ( 297 )   PDF (269KB) ( 807 )   Save Related Articles | Metrics

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Cross tolerance: a tread to decipher the code of endogenous global cerebral resistance Ashish Sharma, Rohit Goyal 2016, 11 (5):  719-720.  doi: 10.4103/1673-5374.182688 Abstract ( 313 )   PDF (165KB) ( 478 )   Save Related Articles | Metrics

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Focusing on the protective effects of metallothionein-I/II in cerebral ischemia Abass Eidizadeh, George Trendelenburg 2016, 11 (5):  721-722.  doi: 10.4103/1673-5374.182689 Abstract ( 260 )   PDF (366KB) ( 507 )   Save Related Articles | Metrics

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Comparative insights into mitochondrial adaptations to anoxia in brain Matthew E. Pamenter 2016, 11 (5):  723-724.  doi: 10.4103/1673-5374.182690 Abstract ( 271 )   PDF (279KB) ( 454 )   Save Related Articles | Metrics

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Iron metabolism, oxidative stress, and neonatal brain injury Qing Lu, Stephen M. Black 2016, 11 (5):  725-726.  doi: 10.4103/1673-5374.182691 Abstract ( 183 )   PDF (275KB) ( 492 )   Save Related Articles | Metrics

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Induced pluripotent stem cells for modeling and cell therapy of Parkinson’s disease Mária Csöbönyeiová, Ľuboš Danišovič, Štefan Polák 2016, 11 (5):  727-728.  doi: 10.4103/1673-5374.182692 Abstract ( 161 )   PDF (273KB) ( 719 )   Save Related Articles | Metrics

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Cholinergic input from the pedunculopontine nucleus to the cerebellum: implications for deep brain stimulation in Parkinson’s disease Eugenio Scarnati, Flora Vitale, Annamaria Capozzo, Paolo Mazzone 2016, 11 (5):  729-730.  doi: 10.4103/1673-5374.182693 Abstract ( 228 )   PDF (217KB) ( 519 )   Save Related Articles | Metrics

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Do we need a new levodopa? Thomas Müller 2016, 11 (5):  731-732.  doi: 10.4103/1673-5374.182694 Abstract ( 180 )   PDF (294KB) ( 454 )   Save Related Articles | Metrics

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Programmed cell death and natural killer cells in multiple sclerosis: new potential therapeutic targets? Beatrice Macchi, Antonio Mastino 2016, 11 (5):  733-734.  doi: 10.4103/1673-5374.182695 Abstract ( 215 )   PDF (201KB) ( 555 )   Save Related Articles | Metrics

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Neurotrophic factors: promising candidates in tissue regeneration Nan Xiao 2016, 11 (5):  735-736.  doi: 10.4103/1673-5374.182696 Abstract ( 159 )   PDF (189KB) ( 450 )   Save Related Articles | Metrics

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Ischemic penumbra in retina endures: vascular neuropathology is reconciled David McLeod 2016, 11 (5):  737-739.  doi: 10.4103/1673-5374.181367 Abstract ( 270 )   PDF (385KB) ( 510 )   Save Related Articles | Metrics

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Complementary research in mammals and fish indicates MMP-2 as a pleiotropic contributor to optic nerve regeneration Kim Lemmens, Inge Van Hove, Lieve Moons 2016, 11 (5):  740-742.  doi: 10.4103/1673-5374.182697 Abstract ( 348 )   PDF (706KB) ( 390 )   Save Related Articles | Metrics

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Viral-mediated gene therapy for spinal cord injury (SCI) from a translational neuroanatomical perspective Andrew P Tosolini, Renée Morris 2016, 11 (5):  743-744.  doi: 10.4103/1673-5374.182698 Abstract ( 140 )   PDF (192KB) ( 477 )   Save Related Articles | Metrics

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Bumetanide promotes neural precursor cell regeneration and dendritic development in the hippocampal dentate gyrus in the chronic stage of cerebral ischemia Wang-shu Xu, Xuan Sun, Cheng-guang Song, Xiao-peng Mu, Wen-ping Ma, Xing-hu Zhang, Chuan-sheng Zhao 2016, 11 (5):  745-751.  doi: 10.4103/1673-5374.182700 Abstract ( 207 )   PDF (2853KB) ( 812 )   Save "Bumetanide has been shown to lessen cerebral edema and reduce the infarct area in the acute stage of cerebral ischemia. Few studies focus on the effects of bumetanide on neuroprotection and neurogenesis in the chronic stage of cerebral ischemia. We established a rat model of cerebral ischemia by injecting endothelin-1 in the left cortical motor area and left corpus striatum. Seven days later, bumetanide 200 μg/kg/day was injected into the lateral ventricle for 21 consecutive days with a mini-osmotic pump. Results demonstrated that the number of neuroblasts cells and the total length of dendrites increased, escape latency reduced, and the number of platform crossings increased in the rat hippocampal dentate gyrus in the chronic stage of cerebral ischemia. These findings suggest that bumetanide promoted neural precursor cell regeneration, dendritic development and the recovery of cognitive function, and protected brain tissue in the chronic stage of ischemia." Related Articles | Metrics

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Inhibition of TYRO3/Akt signaling participates in hypoxic injury in hippocampal neurons Tyro 3/Akt信号受抑制为海马神经元缺氧性损伤的2个重要事件 2016, 11 (5):  752-757.  doi: 10.4103/1673-5374.182701 Abstract ( 235 )   PDF (1183KB) ( 475 )   Save "In this study, we investigated the role of the TYRO3/Akt signaling pathway in hypoxic injury to hippocampal neurons. 3-(4,5-Dimethylthiazol- 2-yl)-2,5-diphenyltetrazolium bromide assay showed that hypoxia inhibited the proliferation and viability of hippocampal neurons. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assay demonstrated that hypoxia induced neuronal apoptosis in a time-dependent manner, with a greater number of apoptotic cells with longer hypoxic exposure. Immunofluorescence labeling revealed that hypoxia suppressed TYRO3 expression. Western blot assay showed that hypoxia decreased Akt phosphorylation levels in a time-dependent manner. Taken together, these findings suggest that hypoxia inhibits the proliferation of hippocampal neurons and promotes apoptosis, and that the inhibition of the TYRO3/Akt signaling pathway plays an important role in hypoxia-induced neuronal injury." Related Articles | Metrics

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Immediate effects of scalp acupuncture with twirling reinforcing manipulation on hemiplegia following acute ischemic stroke: a hidden association study Xiao-zheng Du, Chun-ling Bao, Gui-rong Dong, Xu-ming Yang 2016, 11 (5):  758-764.  doi: 10.4103/1673-5374.182702 Abstract ( 212 )   PDF (289KB) ( 441 )   Save "Data mining has the potential to provide information for improving clinical acupuncture strategies by uncovering hidden rules between acupuncture manipulation and therapeutic effects in a data set. In this study, we performed acupuncture on 30 patients with hemiplegia due to acute ischemic stroke. All participants were pre-screened to ensure that they exhibited immediate responses to acupuncture. We used a twirling reinforcing acupuncture manipulation at the specific lines between the bilateral Baihui (GV20) and Taiyang (EX-HN5). We collected neurologic deficit score, simplified Fugl-Meyer assessment score, muscle strength of the proximal and distal hemiplegic limbs, ratio of the maximal H-reflex to the maximal M-wave (Hmax/Mmax), muscle tension at baseline and immediately after treatment, and the syndromes of traditional Chinese medicine at baseline. We then conducted data mining using an association algorithm and an artificial neural network backpropagation algorithm. We found that the twirling reinforcing manipulation had no obvious therapeutic difference in traditional Chinese medicine syndromes of “Deficiency and Excess”. The change in the muscle strength of the upper distal and lower proximal limbs was one of the main factors affecting the immediate change in Fugl-Meyer scores. Additionally, we found a positive correlation between the muscle tension change of the upper limb and Hmax/Mmax immediate change, and both positive and negative correlations existed between the muscle tension change of the lower limb and immediate Hmax/Mmax change. Additionally, when the difference value of muscle tension for the upper and lower limbs was > 0 or < 0, the difference value of Hmax/Mmax was correspondingly positive or negative, indicating the scalp acupuncture has a bidirectional effect on muscle tension in hemiplegic limbs. Therefore, acupuncture with twirling reinforcing manipulation has distinct effects on acute ischemic stroke patients with different symptoms or stages of disease. Improved muscle tension in the upper and lower limbs, reflected by the variation in the Hmax/Mmax ratio, is crucial for recovery of motor function from hemiplegia." Related Articles | Metrics

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Ischemic preconditioning protects against ischemic brain injury Xiao-meng Ma, Mei Liu, Ying-ying Liu, Li-li Ma, Ying Jiang, Xiao-hong Chen 2016, 11 (5):  765-770.  doi: 10.4103/1673-5374.182703 Abstract ( 187 )   PDF (1691KB) ( 523 )   Save "In this study, we hypothesized that an increase in integrin αvβ3 and its co-activator vascular endothelial growth factor play important neuroprotective roles in ischemic injury. We performed ischemic preconditioning with bilateral common carotid artery occlusion for 5 minutes in C57BL/6J mice. This was followed by ischemic injury with bilateral common carotid artery occlusion for 30 minutes. The time interval between ischemic preconditioning and lethal ischemia was 48 hours. Histopathological analysis showed that ischemic preconditioning substantially diminished damage to neurons in the hippocampus 7 days after ischemia. Evans Blue dye assay showed that ischemic preconditioning reduced damage to the blood-brain barrier 24 hours after ischemia. This demonstrates the neuroprotective effect of ischemic preconditioning. Western blot assay revealed a significant reduction in protein levels of integrin αvβ3, vascular endothelial growth factor and its receptor in mice given ischemic preconditioning compared with mice not given ischemic preconditioning 24 hours after ischemia. These findings suggest that the neuroprotective effect of ischemic preconditioning is associated with lower integrin αvβ3 and vascular endothelial growth factor levels in the brain following ischemia." Related Articles | Metrics

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Neuroprotective effects of cold-inducible RNA-binding protein during mild hypothermia on traumatic brain injury Guan Wang, Jian-ning Zhang, Jia-kui Guo, Ying Cai,Hong-sheng Sun, Kun Dong, Cheng-gang Wu 2016, 11 (5):  771-778.  doi: 10.4103/1673-5374.182704 Abstract ( 262 )   PDF (2453KB) ( 814 )   Save "Cold-inducible RNA-binding protein (CIRP), a key regulatory protein, could be facilitated by mild hypothermia in the brain, heart and liver. This study observed the effects of mild hypothermia at 31 ± 0.5°C on traumatic brain injury in rats. Results demonstrated that mild hypothermia suppressed apoptosis in the cortex, hippocampus and hypothalamus, facilitated CIRP mRNA and protein expression in these regions, especially in the hypothalamus. The anti-apoptotic effect of mild hypothermia disappeared after CIRP silencing. There was no correlation between mitogen-activated extracellular signal-regulated kinase activation and CIRP silencing. CIRP silencing inhibited extracellular signal-regulated kinase-1/2 activation. These indicate that CIRP inhibits apoptosis by affecting extracellular signal-regulated kinase-1/2 activation, and exerts a neuroprotective effect during mild hypothermia for traumatic brain injury." Related Articles | Metrics

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ZD7288, a selective hyperpolarizationactivated cyclic nucleotide-gated channel blocker, inhibits hippocampal synaptic plasticity Xiao-xue Zhang, Xiao-chun Min, Xu-lin Xu, Min Zheng, Lian-jun Guo 2016, 11 (5):  779-786.  doi: 10.4103/1673-5374.182705 Abstract ( 363 )   PDF (991KB) ( 1253 )   Save "The selective hyperpolarization-activated cyclic nucleotide-gated (HCN) channel blocker 4-(N-ethyl-N-phenylamino)-1,2-dimethyl- 6-(methylamino) pyrimidinium chloride (ZD7288) blocks the induction of long-term potentiation in the perforant path–CA3 region in rat hippocampus in vivo. To explore the mechanisms underlying the action of ZD7288, we recorded excitatory postsynaptic potentials in perforant path–CA3 synapses in male Sprague-Dawley rats. We measured glutamate content in the hippocampus and in cultured hippocampal neurons using high performance liquid chromatography, and determined intracellular Ca2+ concentration ([Ca2+]i) using Fura- 2. ZD7288 inhibited the induction and maintenance of long-term potentiation, and these effects were mirrored by the nonspecific HCN channel blocker cesium. ZD7288 also decreased glutamate release in hippocampal tissue and in cultured hippocampal neurons. Furthermore, ZD7288 attenuated glutamate-induced rises in [Ca2+]i in a concentration-dependent manner and reversed 8-Br-cAMP-mediated facilitation of these glutamate-induced [Ca2+]i rises. Our results suggest that ZD7288 inhibits hippocampal synaptic plasticity both glutamate release and resultant [Ca2+]i increases in rat hippocampal neurons." Related Articles | Metrics

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Responses from two firing patterns in inferior colliculus neurons to stimulation of the lateral lemniscus dorsal nucleus Xiao-ting Li, Ning-yu Wang, Yan-jun Wang, Zhi-qing Xu, Jin-feng Liu, Yun-fei Bai, Jin-sheng Dai, Jing-yi Zhao 2016, 11 (5):  787-794.  doi: 10.4103/1673-5374.182706 Abstract ( 285 )   PDF (802KB) ( 441 )   Save "The γ-aminobutyric acid neurons (GABAergic neurons) in the inferior colliculus are classified into various patterns based on their intrinsic electrical properties to a constant current injection. Although this classification is associated with physiological function, the exact role for neurons with various firing patterns in acoustic processing remains poorly understood. In the present study, we analyzed characteristics of inferior colliculus neurons in vitro, and recorded responses to stimulation of the dorsal nucleus of the lateral lemniscus using the wholecell patch clamp technique. Seven inferior colliculus neurons were tested and were classified into two firing patterns: sustained-regular (n = 4) and sustained-adapting firing patterns (n = 3). The majority of inferior colliculus neurons exhibited slight changes in response to stimulation and bicuculline. The responses of one neuron with a sustained-adapting firing pattern were suppressed after stimulation, but recovered to normal levels following application of the γ-aminobutyric acid receptor antagonist. One neuron with a sustained-regular pattern showed suppressed stimulation responses, which were not affected by bicuculline. Results suggest that GABAergic neurons in the inferior colliculus exhibit sustained-regular or sustained-adapting firing patterns. Additionally, GABAergic projections from the dorsal nucleus of the lateral lemniscus to the inferior colliculus are associated with sound localization. The different neuronal responses of various firing patterns suggest a role in sound localization. A better understanding of these mechanisms and functions will provide better clinical treatment paradigms for hearing deficiencies." Related Articles | Metrics

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Cyanidin suppresses amyloid beta-induced neurotoxicity by inhibiting reactive oxygen species-mediated DNA damage and apoptosis in PC12 cells Yi Wang, Xiao-ting Fu, Da-wei Li, Kun Wang, Xin-zhi Wang, Yuan Li, Bao-liang Sun, Xiao-yi Yang, Zun-cheng Zheng, Nam Chun Cho 2016, 11 (5):  795-800.  doi: 10.4103/1673-5374.182707 Abstract ( 298 )   PDF (1526KB) ( 462 )   Save "Amyloid beta (Aβ)-induced oxidative stress is a major pathologic hallmark of Alzheimer’s disease. Cyanidin, a natural flavonoid compound, is neuroprotective against oxidative damage-mediated degeneration. However, its molecular mechanism remains unclear. Here, we investigated the effects of cyanidin pretreatment against Aβ-induced neurotoxicity in PC12 cells, and explored the underlying mechanisms. Cyanidin pretreatment significantly attenuated Aβ-induced cell mortality and morphological changes in PC12 cells. Mechanistically, cyanidin effectively blocked apoptosis induced by Aβ, by restoring the mitochondrial membrane potential via upregulation of Bcl-2 protein expression. Moreover, cyanidin markedly protected PC12 cells from Aβ-induced DNA damage by blocking reactive oxide species and superoxide accumulation. These results provide evidence that cyanidin suppresses Aβ-induced cytotoxicity, by preventing oxidative damage mediated by reactive oxide species, which in turn inhibits mitochondrial apoptosis. Our study demonstrates the therapeutic potential of cyanidin in the prevention of oxidative stress-mediated Aβ neurotoxicity." Related Articles | Metrics

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High-frequency electroacupuncture evidently reinforces hippocampal synaptic transmission in Alzheimer’s disease rats Wei Li, Li-hong Kong, Hui Wang, Feng Shen, Ya-wen Wang, Hua Zhou, Guo-jie Sun 2016, 11 (5):  801-806.  doi: 10.4103/1673-5374.182708 Abstract ( 249 )   PDF (750KB) ( 562 )   Save "The frequency range of electroacupuncture in treatment of Alzheimer’s disease in rats is commonly 2–5 Hz (low frequency) and 50–100 Hz (high frequency). We established a rat model of Alzheimer’s disease by injecting β-amyloid 1–42 (Aβ1–42) into the bilateral hippocampal dentate gyrus to verify which frequency may be better suited in treatment. Electroacupuncture at 2 Hz or 50 Hz was used to stimulate Baihui (DU20) and Shenshu (BL23) acupoints. The water maze test and electrophysiological studies demonstrated that spatial memory ability was apparently improved, and the ranges of long-term potentiation and long-term depression were increased in Alzheimer’s disease rats after electroacupuncture treatment. Moreover, the effects of electroacupuncture at 50 Hz were better than that at 2 Hz. These findings suggest that high-frequency electroacupuncture may enhance hippocampal synaptic transmission and potentially improve memory disorders in Alzheimer’s disease rats." Related Articles | Metrics

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Moderate exercise prevents neurodegeneration in D-galactose-induced aging mice Li Li, Meng Xu, Bo Shen, Man Li, Qian Gao, Shou-gang Wei 2016, 11 (5):  807-815.  doi: 10.4103/1673-5374.182709 Abstract ( 344 )   PDF (837KB) ( 556 )   Save "D-galactose has been widely used in aging research because of its efficacy in inducing senescence and accelerating aging in animal models. The present study investigated the benefits of exercise for preventing neurodegeneration, such as synaptic plasticity, spatial learning and memory abilities, in mouse models of aging. D-galactose-induced aging mice were administered daily subcutaneous injections of D-galactose at the base of the neck for 10 consecutive weeks. Then, the mice were subjected to exercise training by running on a treadmill for 6 days a week. Shortened escape latency in a Morris water maze test indicated that exercise improved learning and memory in aging mice. The ameliorative changes were likely induced by an upregulation of Bcl-2 and brain-derived neurotrophic factor, the repression of apoptosis factors such as Fas and Bax, and an increase in the activity of glucose transporters-1 and 4. The data suggest moderate exercise may retard or inhibit neurodegeneration in D-galactose-induced aging mice." Related Articles | Metrics

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Repetitive magnetic stimulation affects the microenvironment of nerve regeneration and evoked potentials after spinal cord injury Jin-lan Jiang, Xu-dong Guo, Shu-quan Zhang, Xin-gang Wang, Shi-feng Wu 2016, 11 (5):  816-822.  doi: 10.4103/1673-5374.182710 Abstract ( 290 )   PDF (1190KB) ( 826 )   Save "Repetitive magnetic stimulation has been shown to alter local blood flow of the brain, excite the corticospinal tract and muscle, and induce motor function recovery. We established a rat model of acute spinal cord injury using the modified Allen’s method. After 4 hours of injury, rat models received repetitive magnetic stimulation, with a stimulus intensity of 35% maximum output intensity, 5-Hz frequency, 5 seconds for each sequence, and an interval of 2 minutes. This was repeated for a total of 10 sequences, once a day, 5 days in a week, for 2 consecutive weeks. After repetitive magnetic stimulation, the number of apoptotic cells decreased, matrix metalloproteinase 9/2 gene and protein expression decreased, nestin expression increased, somatosensory and motor-evoked potentials recovered, and motor function recovered in the injured spinal cord. These findings confirm that repetitive magnetic stimulation of the spinal cord improved the microenvironment of neural regeneration, reduced neuronal apoptosis, and induced neuroprotective and repair effects on the injured spinal cord." Related Articles | Metrics

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Methylprednisolone exerts neuroprotective effects by regulating autophagy and apoptosis Wei Gao, Shu-rui Chen, Meng-yao Wu, Kai Gao, Yuan-long Li, Hong-yu Wang, Chen-yuan Li, Hong Li 2016, 11 (5):  823-828.  doi: 10.4103/1673-5374.182711 Abstract ( 130 )   PDF (1566KB) ( 763 )   Save "Methylprednisolone markedly reduces autophagy and apoptosis after secondary spinal cord injury. Here, we investigated whether pretreatment of cells with methylprednisolone would protect neuron-like cells from subsequent oxidative damage via suppression of autophagy and apoptosis. Cultured N2a cells were pretreated with 10 μM methylprednisolone for 30 minutes, then exposed to 100 μM H2O2 for 24 hours. Inverted phase contrast microscope images, MTT assay, flow cytometry and western blot results showed that, compared to cells exposed to 100 μM H2O2 alone, cells pretreated with methylprednisolone had a significantly lower percentage of apoptotic cells, maintained a healthy morphology, and showed downregulation of autophagic protein light chain 3B and Beclin-1 protein expression. These findings indicate that methylprednisolone exerted neuroprotective effects against oxidative damage by suppressing autophagy and apoptosis." Related Articles | Metrics

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A self-made, low-cost infrared system for evaluating the sciatic functional index in mice Lukas Fricker, Vincenzo Penna, Florian Lampert, G. Bjoern Stark, Christian Witze, Georgios Koulaxouzidis 2016, 11 (5):  829-834.  doi: 10.4103/1673-5374.182712 Abstract ( 277 )   PDF (1008KB) ( 491 )   Save "The sciatic functional index (SFI) is a popular parameter for peripheral nerve evaluation that relies on footprints obtained with ink and paper. Drawbacks include smearing artefacts and a lack of dynamic information during measurement. Modern applications use digitized systems that can deliver results with less analytical effort and fewer mice. However, the systems are expensive (€40,000). This study aimed to evaluate the applicability and precision of a self-made, low-cost infrared system for evaluating SFI in mice. Mice were subjected to unilateral sciatic nerve crush injury (crush group; n = 7) and sham operation (sham group; n = 4). They were evaluated on the day before surgery, the 2nd, 4th and 6th days after injury, and then every day up to the 23rd day after injury. We compared two SFI evaluation methods, i.e., conventional inkand- paper SFI (C-SFI) and our infrared system (I-SFI). Our apparatus visualized footprints with totally internally reflected infrared light (950 nm) and a camera that can only detect this wavelength. Additionally we performed an analysis with the ladder beam walking test (LBWT) as a reference test. I-SFI assessment reduced the standard deviation by about 33 percent, from 11.6 to 7.8, and cut the variance around the baseline to 21 percent. The system thus requires fewer measurement repetitions and fewer animals, and cuts the cost of keeping the animals. The apparatus cost €321 to build. Our results show that the process of obtaining the SFI can be made more precise via digitization with a self-made, low-cost infrared system." Related Articles | Metrics

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Methylprednisolone microsphere sustained-release membrane inhibits scar formation at the site of peripheral nerve lesion Qiang Li, Teng Li, Xiang-chang Cao, De-qing Luo, Ke-jian Lian 2016, 11 (5):  835-841.  doi: 10.4103/1673-5374.182713 Abstract ( 299 )   PDF (1293KB) ( 513 )   Save "Corticosteroids are widely used for the treatment of acute central nervous system injury. However, their bioactivity is limited by their short half-life. Sustained release of glucocorticoids can prolong their efficacy and inhibit scar formation at the site of nerve injury. In the present study, we wrapped the anastomotic ends of the rat sciatic nerve with a methylprednisolone sustained-release membrane. Compared with methylprednisone alone or methylprednisone microspheres, the methylprednisolone microsphere sustained-release membrane reduced tissue adhesion and inhibited scar tissue formation at the site of anastomosis. It also increased sciatic nerve function index and the thickness of the myelin sheath. Our findings show that the methylprednisolone microsphere sustained-release membrane effectively inhibits scar formation at the site of anastomosis of the peripheral nerve, thereby promoting nerve regeneration." Related Articles | Metrics

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Vitamin B complex and vitamin B12 levels after peripheral nerve injury Idiris Altun, Ergül Belge Kurutaş 2016, 11 (5):  842-845.  doi: 10.4103/1673-5374.177150 Abstract ( 372 )   PDF (351KB) ( 1133 )   Save "The aim of the present study was to evaluate whether tissue levels of vitamin B complex and vitamin B12 were altered after crush-induced peripheral nerve injury in an experimental rat model. A total of 80 male Wistar rats were randomized into one control (n = 8) and six study groups (1, 6, 12, 24 hours, 3, and 7 days after experimental nerve injury; n = 12 for each group). Crush-induced peripheral nerve injury was performed on the sciatic nerves of rats in six study groups. Tissue samples from the sites of peripheral nerve injury were obtained at 1, 6, 12, 24 hours, 3 and 7 days after experimental nerve injury. Enzyme-linked immunosorbent assay results showed that tissue levels of vitamin B complex and vitamin B12 in the injured sciatic nerve were significantly greater at 1 and 12 hours after experimental nerve injury, while they were significantly lower at 7 days than in control group. Tissue level of vitamin B12 in the injured sciatic nerve was significantly lower at 1, 6, 12 and 24 hours than in the control group. These results suggest that tissue levels of vitamin B complex and vitamin B12 vary with progression of crush-induced peripheral nerve injury, and supplementation of these vitamins in the acute period may be beneficial for acceleration of nerve regeneration." Related Articles | Metrics

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Gender difference in the neuroprotective effect of rat bone marrow mesenchymal cells against hypoxia-induced apoptosis of retinal ganglion cells Jing Yuan, Jian-xiong Yu 2016, 11 (5):  846-853.  doi: 10.4103/1673-5374.182764 Abstract ( 201 )   Save "Bone marrow mesenchymal stem cells can reduce retinal ganglion cell death and effectively prevent vision loss. Previously, we found that during differentiation, female rhesus monkey bone marrow mesenchymal stem cells acquire a higher neurogenic potential compared with male rhesus monkey bone marrow mesenchymal stem cells. This suggests that female bone marrow mesenchymal stem cells have a stronger neuroprotective effect than male bone marrow mesenchymal stem cells. Here, we first isolated and cultured bone marrow mesenchymal stem cells from female and male rats by density gradient centrifugation. Retinal tissue from newborn rats was prepared by enzymatic digestion to obtain primary retinal ganglion cells. Using the transwell system, retinal ganglion cells were co-cultured with bone marrow mesenchymal stem cells under hypoxia. Cell apoptosis was detected by flow cytometry and caspase-3 activity assay. We found a marked increase in apoptotic rate and caspase-3 activity of retinal ganglion cells after 24 hours of hypoxia compared with normoxia. Moreover, apoptotic rate and caspase-3 activity of retinal ganglion cells significantly decreased with both female and male bone marrow mesenchymal stem cell co-culture under hypoxia compared with culture alone, with more significant effects from female bone marrow mesenchymal stem cells. Our results indicate that bone marrow mesenchymal stem cells exert a neuroprotective effect against hypoxia-induced apoptosis of retinal ganglion cells, and also that female cells have greater neuroprotective ability compared with male cells." Related Articles | Metrics

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Recovery of injured fornical crura following neurosurgical operation of a brain tumor: a case report Sung Ho Jang, You Sung Seo 2016, 11 (5):  854-855.  doi: 10.4103/1673-5374.182714 Abstract ( 415 )   PDF (1092KB) ( 432 )   Save Related Articles | Metrics

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Amyotrophic lateral sclerosis: promising therapeutic outcome–not far away? Adrija Hajra, Dhrubajyoti Bandyopadhyay, Shyamal Kumar Hajra 2016, 11 (5):  856-856.  doi: 10.4103/1673-5374.182715 Abstract ( 186 )   PDF (127KB) ( 440 )   Save Related Articles | Metrics