Table of Content

30 September 2016, Volume 11 Issue 9 Previous Issue    Next Issue

For Selected:

Download Citations EndNote Reference Manager ProCite BibTeX RefWorks

Toggle Thumbnails

Select

Intra-axonal protein synthesis – a new target for neural repair? Jeffery L. Twiss, Ashley L. Kalinski, Rahul Sachdeva, John D. Houle 2016, 11 (9):  1365-1367.  doi: 10.4103/1673-5374.191193 Abstract ( 145 )   PDF (373KB) ( 436 )   Save Although initially argued to be a feature of immature neurons with incomplete polarization, there is clear evidence that neurons in the peripheral nervous system retain the capacity for intra-axonal protein synthesis well into adulthood. This localized protein synthesis has been shown to contribute to injury signaling and axon regeneration in peripheral nerves. Recent works point to potential for protein synthesis in axons of the vertebrate central nervous system. mRNAs and protein synthesis machinery have now been documented in lamprey, mouse, and rat spinal cord axons. Intra-axonal protein synthesis appears to be activated in adult vertebrate spinal cord axons when they are regeneration-competent. Rat spinal cord axons regenerating into a peripheral nerve graft contain mRNAs and markers of activated translational machinery. Indeed, levels of some growth-associated mRNAs in these spinal cord axons are comparable to the regenerating sciatic nerve. Markers of active translation tend to decrease when these axons stop growing, but can be reactivated by a second axotomy. These emerging observations raise the possibility that mRNA transport into and translation within axons could be targeted to facilitate regeneration in both the peripheral and central nervous systems. Related Articles | Metrics

Select

Regeneration-associated macrophages: a novel approach to boost intrinsic regenerative capacity for axon regeneration Min Jung Kwon, Hyuk Jun Yoon Byung Gon Kim 2016, 11 (9):  1368-1371.  doi: 10.4103/1673-5374.191194 Abstract ( 199 )   PDF (385KB) ( 360 )   Save Axons in central nervous system (CNS) do not regenerate spontaneously after injuries such as stroke and traumatic spinal cord injury. Both intrinsic and extrinsic factors are responsible for the regeneration failure. Although intensive research efforts have been invested on extrinsic regeneration inhibitors, the extent to which glial inhibitors contribute to the regeneration failure in vivo still remains elusive. Recent experimental evidence has rekindled interests in intrinsic factors for the regulation of regeneration capacity in adult mammals. In this review, we propose that activating macrophages with pro-regenerative molecular signatures could be a novel approach for boosting intrinsic regenerative capacity of CNS neurons. Using a conditioning injury model in which regeneration of central branches of dorsal root ganglia sensory neurons is enhanced by a preceding injury to the peripheral branches, we have demonstrated that perineuronal macrophages surrounding dorsal root ganglia neurons are critically involved in the maintenance of enhanced regeneration capacity. Neuron-derived chemokine (C-C motif) ligand 2 (CCL2) seems to mediate neuron-macrophage interactions conveying injury signals to perineuronal macrophages taking on a soley pro-regenerative phenotype, which we designate as regeneration-associated macrophages (RAMs). Manipulation of the CCL2 signaling could boost regeneration potential mimicking the conditioning injury, suggesting that the chemokine-mediated RAM activation could be utilized as a regenerative therapeutic strategy for CNS injuries. Related Articles | Metrics

Select

Nanobiomaterials for neural regeneration Nuan Chen, Lingling Tian, Liumin He, Seeram Ramakrishna 2016, 11 (9):  1372-1374.  doi: 10.4103/1673-5374.191195 Abstract ( 282 )   PDF (316KB) ( 423 )   Save Diseases and disorders associated with nervous system such as injuries by trauma and neurodegeneration are shown to be one of the most serious problems in medicine, requiring innovative strategies to trigger and enhance the nerve regeneration. Tissue engineering aims to provide a highly biomimetic environment by using a combination of cells, materials and suitable biological cues, by which the lost body part may be regenerated or even fully rebuilt. Electrospinning, being able to produce extracellular matrix (ECM)-like nanostructures with great ?exibility in design and choice of materials, have demonstrated their great potential for fabrication of nerve tissue engineered scaffolds. The review here begins with a brief description of the anatomy of native nervous system, which provides basic knowledge and ideas for the design of nerve tissue scaffolds, followed by fve main parts in the design of electrospun nerve tissue engineered scaffolds including materials selection, structural design, in vitro bioreactor, functionalization and cellular support. Performances of biomimetic electrospun nanofibrous nerve implant devices are also reviewed. Finally, future directions for advanced electrospun nerve tissue engineered scaffolds are discussed. Related Articles | Metrics

Select

Blood microRNAs as potential diagnostic and prognostic markers in cerebral ischemic injury Bridget Martinez, Philip V. Peplow 2016, 11 (9):  1375-1378.  doi: 10.4103/1673-5374.191196 Abstract ( 150 )   PDF (358KB) ( 440 )   Save MicroRNAs are a family of small, genome-encoded endogenous RNAs that are transcribed but are not translated into proteins. They serve essential roles in virtually every aspect of brain function, including neurogenesis, neural development, and cellular responses leading to changes in synaptic plasticity. They are also implicated in neurodegeneration and neurological disorders, in responses to hypoxia and ischemia, and in ischemic tolerance induced by ischemic preconditioning. In recent developments, miRNA expression profling has been examined in stroke, and these studies indicate that miRNAs have emerged as key mediators in ischemic stroke biology. Both increased and decreased miRNA levels may be needed either as prevention or treatment of stroke. Novel approaches are being developed to get miRNA related therapeutics into the brain across an intact blood-brain barrier, including chemical modifcation, use of targeting molecules and methods to disrupt the blood-brain barrier." Related Articles | Metrics

Select

Utilizing pharmacotherapy and mesenchymal stem cell therapy to reduce in?ammation following traumatic brain injury Sherwin Mashkouri, Marci G. Crowley, Michael G. Liska, Sydney Corey, Cesar V. Borlongan 2016, 11 (9):  1379-1384.  doi: 10.4103/1673-5374.191197 Abstract ( 133 )   PDF (311KB) ( 417 )   Save The pathologic process of chronic phase traumatic brain injury is associated with spreading in?ammation, cell death, and neural dysfunction. It is thought that sequestration of in?ammatory mediators can facilitate recovery and promote an environment that fosters cellular regeneration. Studies have targeted post-traumatic brain injury in?ammation with the use of pharmacotherapy and cell therapy. These therapeutic options are aimed at reducing the edematous and neurodegenerative in?ammation that have been associated with compromising the integrity of the blood-brain barrier. Although studies have yielded positive results from anti-in?ammatory pharmacotherapy and cell therapy individually, emerging research has begun to target in?ammation using combination therapy. The joint use of anti-in?ammatory drugs alongside stem cell transplantation may provide better clinical outcomes for traumatic brain injury patients. Despite the promising results in this feld of research, it is important to note that most of the studies mentioned in this review have completed their studies using animal models. Translation of this research into a clinical setting will require additional laboratory experiments and larger preclinical trials. Related Articles | Metrics

Select

Cell transplantation for the treatment of spinal cord injury – bone marrow stromal cells and choroid plexus epithelial cells Chizuka Ide, Norihiko Nakano, Kenji Kanekiyo 2016, 11 (9):  1385-1388.  doi: 10.4103/1673-5374.191198 Abstract ( 149 )   PDF (1158KB) ( 721 )   Save Transplantation of bone marrow stromal cells (BMSCs) enhanced the outgrowth of regenerating axons and promoted locomotor improvements of rats with spinal cord injury (SCI). BMSCs did not survive long-term, disappearing from the spinal cord within 2–3 weeks after transplantation. Astrocyte-devoid areas, in which no astrocytes or oligodendrocytes were found, formed at the epicenter of the lesion. It was remarkable that numerous regenerating axons extended through such astrocyte-devoid areas. Regenerating axons were associated with Schwann cells embedded in extracellular matrices. Transplantation of choroid plexus epithelial cells (CPECs) also enhanced axonal regeneration and locomotor improvements in rats with SCI. Although CPECs disappeared from the spinal cord shortly after transplantation, an extensive outgrowth of regenerating axons occurred through astrocyte-devoid areas, as in the case of BMSC transplantation. These fndings suggest that BMSCs and CPECs secret neurotrophic factors that promote tissue repair of the spinal cord, including axonal regeneration and reduced cavity formation. This means that transplantation of BMSCs and CPECs promotes “intrinsic” ability of the spinal cord to regenerate. The treatment to stimulate the intrinsic regeneration ability of the spinal cord is the safest method of clinical application for SCI. It should be emphasized that the generally anticipated long-term survival, proliferation and differentiation of transplanted cells are not necessarily desirable from the clinical point of view of safety. Related Articles | Metrics

Select

Harnessing neural activity to promote repair of the damaged corticospinal system after spinal cord injury John H. Martin 2016, 11 (9):  1389-1391.  doi: 10.4103/1673-5374.191199 Abstract ( 175 )   PDF (378KB) ( 448 )   Save As most spinal cord injuries (SCIs) are incomplete, an important target for promoting neural repair and recovery of lost motor function is to promote the connections of spared descending spinal pathways with spinal motor circuits. Among the pathways, the corticospinal tract (CST) is most associated with skilled voluntary functions in humans and many animals. CST loss, whether at its origin in the motor cortex or in the white matter tracts subcortically and in the spinal cord, leads to movement impairments and paralysis. To restore motor function after injury will require repair of the damaged CST. In this review, I discuss how knowledge of activity-dependent development of the CST—which establishes connectional specifcity through axon pruning, axon outgrowth, and synaptic competition among CST terminals—informed a novel activity-based therapy for promoting sprouting of spared CST axons after injur in mature animals. This therapy, which comprises motor cortex electrical stimulation with and without concurrent trans-spinal direct current stimulation, leads to an increase in the gray matter axon length of spared CST axons in the rat spinal cord and, after a pyramidal tract lesion, restoration of skilled locomotor movements. I discuss how this approach is now being applied to a C4 contusion rat model. Related Articles | Metrics

Select

Sigma-1 receptor and neuroprotection: current outlook and potential therapeutic effects Giovanni Li Volti, Paolo Murabito 2016, 11 (9):  1392-1393.  doi: 10.4103/1673-5374.191200 Abstract ( 304 )   PDF (333KB) ( 943 )   Save Related Articles | Metrics

Select

Function of pioneer neurons specifed by the basic helix-loop-helix transcription factor atonal in neural development Misako Okumura, Takahiro Chihara 2016, 11 (9):  1394-1395.  doi: 10.4103/1673-5374.191201 Abstract ( 225 )   PDF (341KB) ( 481 )   Save Related Articles | Metrics

Select

Possible divergence of serum- and glucocorticoid-inducible kinase function in ischemic brain injury Koichi Inoue 2016, 11 (9):  1396-1397.  doi: 10.4103/1673-5374.191202 Abstract ( 212 )   PDF (260KB) ( 412 )   Save Related Articles | Metrics

Select

Concepts and opportunities for repair in cerebral microvascular disease and white matter stroke Guanxi Xiao, Jason D. Hinman 2016, 11 (9):  1398-1400.  doi: 10.4103/1673-5374.191203 Abstract ( 236 )   PDF (238KB) ( 447 )   Save Related Articles | Metrics

Select

The pleiotropic effects of tissue plasminogen activator in the brain: implications for stroke recovery Julia A. Grummisch, Nafisa M. Jadavji, Patrice D. Smith 2016, 11 (9):  1401-1402.  doi: 10.4103/1673-5374.191204 Abstract ( 178 )   Save Related Articles | Metrics

Select

Stimulating mitochondria to protect the brain following traumatic brain injury Lora Talley Watts 2016, 11 (9):  1403-1404.  doi: 10.4103/1673-5374.191205 Abstract ( 222 )   PDF (353KB) ( 405 )   Save Related Articles | Metrics

Select

The suppressor of cytokine signalling 2 (SOCS2), traumatic brain injury and microglial/macrophage regulation Harleen S. Basrai, Ann M. Turnley 2016, 11 (9):  1405-1406.  doi: 10.4103/1673-5374.191206 Abstract ( 117 )   PDF (289KB) ( 396 )   Save Related Articles | Metrics

Select

Anesthesia-induced neurotoxicity in an animal model of the developing brain: mechanism and therapies Maiko Satomoto, Koshi Makita 2016, 11 (9):  1407-1408.  doi: 10.4103/1673-5374.191207 Abstract ( 191 )   PDF (405KB) ( 589 )   Save Related Articles | Metrics

Select

Central CB2 receptors in in?ammation-driven neurodegeneration: dysregulation and therapeutic potential Ruth M. Concannon, Eilís Dowd 2016, 11 (9):  1409-1410.  doi: 10.4103/1673-5374.191208 Abstract ( 169 )   PDF (368KB) ( 339 )   Save Related Articles | Metrics

Select

Current perspectives on the antidepressant-like effects of guanosine Luis E. B. Bettio, Joana Gil-Mohapel, Ana Lúcia S. Rodrigues 2016, 11 (9):  1411-1413.  doi: 10.4103/1673-5374.191209 Abstract ( 217 )   PDF (343KB) ( 393 )   Save Related Articles | Metrics

Select

Neurodegeneration in branch retinal vein occlusion Rayan A. Alshareef, Jay Chhablani 2016, 11 (9):  1414-1414.  doi: 10.4103/1673-5374.191210 Abstract ( 176 )   PDF (122KB) ( 448 )   Save Related Articles | Metrics

Select

Glaucoma and amyotrophic lateral sclerosis, two kindred diseases? Francisco Javier Carreras 2016, 11 (9):  1415-1417.  doi: 10.4103/1673-5374.191211 Abstract ( 223 )   PDF (859KB) ( 367 )   Save Related Articles | Metrics

Select

Future directions for using estrogen receptor agonists in the treatment of acute and chronic spinal cord injury Swapan K. Ray, Supriti Samntaray, Naren L. Banik 2016, 11 (9):  1418-1419.  doi: 10.4103/1673-5374.191212 Abstract ( 233 )   PDF (151KB) ( 431 )   Save Related Articles | Metrics

Select

Genetically modifed human umbilical cord blood cells as a promising strategy for treatment of spinal cord injury Yana O. Mukhamedshina, Albert A. Rizvanov 2016, 11 (9):  1420-1421.  doi: 10.4103/1673-5374.191213 Abstract ( 211 )   PDF (403KB) ( 370 )   Save Related Articles | Metrics

Select

Beyond peripheral nerve injury: spinal gliopathy and maladaptive synaptic plasticity Giovanni Cirillo, Michele Papa 2016, 11 (9):  1422-1423.  doi: 10.4103/1673-5374.191214 Abstract ( 332 )   PDF (318KB) ( 430 )   Save Related Articles | Metrics

Select

Regional brain structural abnormality in ischemic stroke patients: a voxel-based morphometry study Ping Wu, Yu-mei Zhou, Fang Zeng, Zheng-jie Li, Lu Luo, Yong-xin Li, Wei Fan, Li-hua Qiu, Wei Qin, Lin Chen, Lin Bai, Juan Nie, San Zhang, Yan Xiong, Yu Bai, Can-xin Yin, Fan-rong Liang 2016, 11 (9):  1424-1430.  doi: 10.4103/1673-5374.191215 Abstract ( 206 )   PDF (920KB) ( 472 )   Save Our previous study used regional homogeneity analysis and found that activity in some brain areas of patients with ischemic stroke changed signifcantly. In the current study, we examined structural changes in these brain regions by taking structural magnetic resonance imaging scans of 11 ischemic stroke patients and 15 healthy participants, and analyzing the data using voxel-based morphometry. Compared with healthy participants, patients exhibited higher gray matter density in the left inferior occipital gyrus and right anterior white matter tract. In contrast, gray matter density in the right cerebellum, left precentral gyrus, right middle frontal gyrus, and left middle temporal gyrus was less in ischemic stroke patients. The changes of gray matter density in the middle frontal gyrus were negatively associated with the clinical rating scales of the Fugl-Meyer Motor Assessment (r = –0.609, P = 0.047) and the left middle temporal gyrus was negatively correlated with the clinical rating scales of the nervous functional defciency scale (r = –0.737, P = 0.010). Our fndings can objectively identify the functional abnormality in some brain regions of ischemic stroke patients. Related Articles | Metrics

Select

13-Methyltetradecanoic acid mitigates cerebral ischemia/reperfusion injury Juan Yu, Li-nan Yang, Yan-yun Wu, Bao-hua Li, Sheng-mei Weng, Chun-lan Hu, Yong-ling Han 2016, 11 (9):  1431-1437.  doi: 10.4103/1673-5374.191216 Abstract ( 319 )   PDF (1265KB) ( 407 )   Save 13-Methyltetradecanoic acid can stabilize cell membrane and have anti-in?ammatory, antioxidant and anti-apoptotic effects. Previous studies mainly focused on peripheral nerve injury, but seldom on the central nervous system. We investigated whether these properties of 13-methyltetradecanoic acid have a neuroprotective effect on focal cerebral ischemia/reperfusion injury, and detected the expression of basic fbroblast growth factor and vascular endothelial growth factor. This study established rat models of middle cerebral artery occlusion/ reperfusion injury by ischemia for 2 hours and reperfusion for 24 hours. At the beginning of reperfusion, 13-methyltetradecanoic acid 10, 40 or 80 mg/kg was injected into the tail vein. Results found that various doses of 13-methyltetradecanoic acid effectively reduced infarct volume, mitigate cerebral edema, and increased the mRNA and protein expression of basic fbroblast growth factor and vascular endothelial growth factor at 24 hours of reperfusion. The effect was most signifcant in the 13-methyltetradecanoic acid 40 and 80 mg/kg groups. The fndings suggest that 13-methyltetradecanoic acid can relieve focal ischemia/reperfusion injury immediately after reperfusion, stimulate the upregulation of basic fbroblast growth factor and vascular endothelial growth factor to exert neuroprotective effects. Related Articles | Metrics

Select

Protective effects of carnosine on white matter damage induced by chronic cerebral hypoperfusion Jing Ma, Shu-hong Bo, Xiao-tong Lu, A-jing Xu, Jian Zhang 2016, 11 (9):  1438-1444.  doi: 10.4103/1673-5374.191217 Abstract ( 318 )   PDF (3381KB) ( 533 )   Save Carnosine is a dipeptide that scavenges free radicals, inhibits in?ammation in the central nervous system, and protects against ischemic and hypoxic brain damage through its anti-oxidative and anti-apoptotic actions. Therefore, we hypothesized that carnosine would also protect against white matter damage caused by subcortical ischemic injury. White matter damage was induced by right unilateral common carotid artery occlusion in mice. The animals were treated with 200, 500 or 750 mg/kg carnosine by intraperitoneal injection 30 minutes before injury and every other day after injury. Then, 37 days later, Klüver-Barrera staining, toluidine blue staining and immuno?uorescence staining were performed. Carnosine (200, 500 mg/kg) substantially reduced damage to the white matter in the corpus callosum, internal capsule and optic tract, and it rescued expression of myelin basic protein, and alleviated the loss of oligodendrocytes. However, carnosine at the higher dose of 750 mg/kg did not have the same effects as the 200 and 500 mg/kg doses. These fndings show that carnosine, at a particular dose range, protects against white matter damage caused by chronic cerebral ischemia in mice, likely by reducing oligodendroglial cell loss. Related Articles | Metrics

Select

Neuroprotection of hyperbaric oxygen therapy in sub-acute traumatic brain injury: not by immediately improving cerebral oxygen saturation and oxygen partial pressure Jing Ma, Shu-hong Bo, Xiao-tong Lu, A-jing Xu, Jian Zhang 2016, 11 (9):  1445-1449.  doi: 10.4103/1673-5374.191218 Abstract ( 284 )   PDF (241KB) ( 403 )   Save Although hyperbaric oxygen (HBO) therapy can promote the recovery of neural function in patients who have suffered traumatic brain injury (TBI), the underlying mechanism is unclear. We hypothesized that hyperbaric oxygen treatment plays a neuroprotective role in TBI by increasing regional transcranial oxygen saturation (rSO2) and oxygen partial pressure (PaO2). To test this idea, we compared two groups: a control group with 20 healthy people and a treatment group with 40 TBI patients. The 40 patients were given 100% oxygen of HBO for 90 minutes. Changes in rSO2 were measured. The controls were also examined for rSO2 and PaO2, but received no treatment. rSO2 levels in the patients did not differ signifcantly after treatment, but levels before and after treatment were signifcantly lower than those in the control group. PaO2 levels were signifcantly decreased after the 30-minute HBO treatment. Our fndings suggest that there is a disorder of oxygen metabolism in patients with sub-acute TBI. HBO does not immediately affect cerebral oxygen metabolism, and the underlying mechanism still needs to be studied in depth. Related Articles | Metrics

Select

Erythropoietin reduces apoptosis of brain tissue cells in rats after cerebral ischemia/reperfusion injury: a characteristic analysis using magnetic resonance imaging Chun-juan Jiang, Zhong-juan Wang, Yan-jun Zhao, Zhui-yang Zhang, Jing-jing Tao, Jian-yong Ma 2016, 11 (9):  1450-1455.  doi: 10.4103/1673-5374.191219 Abstract ( 262 )   PDF (1326KB) ( 443 )   Save Some in vitro experiments have shown that erythropoietin (EPO) increases resistance to apoptosis and facilitates neuronal survival following cerebral ischemia. However, results from in vivo studies are rarely reported. Perfusion-weighted imaging (PWI) and diffusion-weighted imaging (DWI) have been applied successfully to distinguish acute cerebral ischemic necrosis and penumbra in living animals; therefore, we hypothesized that PWI and DWI could be used to provide imaging evidence in vivo for the conclusion that EPO could reduce apoptosis in brain areas injured by cerebral ischemia/reperfusion. To validate this hypothesis, we established a rat model of focal cerebral ischemia/ reperfusion injury, and treated with intra-cerebroventricular injection of EPO (5,000 U/kg) 20 minutes before injury. Brain tissue in the ischemic injury zone was sampled using MRI-guided localization. The relative area of abnormal tissue, changes in PWI and DWI in the ischemic injury zone, and the number of apoptotic cells based on TdT-mediated dUTP-biotin nick end-labeling (TUNEL) were assessed. Our fndings demonstrate that EPO reduces the relative area of abnormally high signal in PWI and DWI, increases cerebral blood volume, and decreases the number of apoptotic cells positive for TUNEL in the area injured by cerebral ischemia/reperfusion. The experiment provides imaging evidence in vivo for EPO treating cerebral ischemia/reperfusion injury. Related Articles | Metrics

Select

Transplantation of vascular endothelial growth factor-modifed neural stem/progenitor cells promotes the recovery of neurological function following hypoxic-ischemic brain damage Yue Yao, Xiang-rong Zheng, Shan-shan Zhang, Xia Wang, Xiao-he Yu, Jie-lu Tan, Yu-jia Yang 2016, 11 (9):  1456-1463.  doi: 10.4103/1673-5374.191220 Abstract ( 324 )   PDF (1137KB) ( 702 )   Save Related Articles | Metrics

Select

Rhesus monkey neural stem cell transplantation promotes neural regeneration in rats with hippocampal lesions Li-juan Ye, Hui Bian, Yao-dong Fan, Zheng-bo Wang, Hua-lin Yu, Yuan-ye Ma, Feng Chen 2016, 11 (9):  1464-1470.  doi: 10.4103/1673-5374.191221 Abstract ( 267 )   PDF (1570KB) ( 777 )   Save Related Articles | Metrics

Select

Serotonin regulates brain-derived neurotrophic factor expression in select brain regions during acute psychological stress De-guo Jiang, Shi-li Jin, Gong-ying Li, Qing-qing Li, Zhi-ruo Li, Hong-xia Ma, Chuan-jun Zhuo, Rong-huan Jiang, Min-jie Ye 2016, 11 (9):  1471-1479.  doi: 10.4103/1673-5374.191222 Abstract ( 269 )   PDF (5394KB) ( 497 )   Save Previous studies suggest that serotonin (5-HT) might interact with brain-derived neurotrophic factor (BDNF) during the stress response. However, the relationship between 5-HT and BDNF expression under purely psychological stress is unclear. In this study, one hour before psychological stress exposure, the 5-HT1A receptor agonist 8-OH-DPAT or antagonist MDL73005, or the 5-HT2A receptor agonist DOI or antagonist ketanserin were administered to rats exposed to psychological stress. Immunohistochemistry and in situ hybridization revealed that after psychological stress, with the exception of the ventral tegmental area, BDNF protein and mRNA expression levels were higher in the 5-HT1A and the 5-HT2A receptor agonist groups compared with the solvent control no-stress or psychological stress group in the CA1 and CA3 of the hippocampus, prefrontal cortex, central amygdaloid nucleus, dorsomedial hypothalamic nucleus, dentate gyrus, shell of the nucleus accumbens and the midbrain periaqueductal gray. There was no signifcant difference between the two agonist groups. In contrast, after stress exposure, BDNF protein and mRNA expression levels were lower in the 5-HT1A and 5-HT2A receptor antagonist groups than in the solvent control non-stress group, with the exception of the ventral tegmental area. Our fndings suggest that 5-HT regulates BDNF expression in a rat model of acute psychological stress. Related Articles | Metrics

Select

Protective effect of tetrahydroxy stilbene glucoside on learning and memory by regulating synaptic plasticity Hong-bo Luo, Yun Li, Zun-jing Liu, Li Cao, Zhi-qiang Zhang, Yong Wang, Xiao-yan Zhang, Zhao Liu, Xiang-qun Shi 2016, 11 (9):  1480-1486.  doi: 10.4103/1673-5374.191223 Abstract ( 268 )   PDF (886KB) ( 490 )   Save Damage to synaptic plasticity induced by neurotoxicity of amyloid-beta is regarded to be one of the pathological mechanisms of learning and memory disabilities in Alzheimer’s disease patients. This study assumed that the damage of amyloid-beta to learning and memory abilities was strongly associated with the changes in the Fyn/N-methyl-D-aspartate receptor 2B (NR2B) expression. An APP695V7171 transgenic mouse model of Alzheimer’s disease was used and treatment with tetrahydroxy-stilbene glucoside was administered intragastrically. Results showed that intragastric administration of tetrahydroxy-stilbene glucoside improved the learning and memory abilities of the transgenic mice through increasing NR2B receptors and Fyn expression. It also reversed parameters for synaptic interface structure of gray type I. These fndings indicate that tetrahydroxy stilbene glucoside has protective effects on the brain, and has prospects for its clinical application to improve the learning and memory abilities and treat Alzheimer’s disease. Related Articles | Metrics

Select

Can long-term thiamine treatment improve the clinical outcomes of myotonic dystrophy type 1? Antonio Costantini, Erika Trevi, Maria Immacolata Pala, Roberto Fancellu 2016, 11 (9):  1487-1491.  doi: 10.4103/1673-5374.19 Abstract ( 314 )   PDF (214KB) ( 484 )   Save Myotonic dystrophy type 1, also known as Steinert’s disease, is an autosomal dominant disorder with multisystemic clinical features affecting the skeletal and cardiac muscles, the eyes, and the endocrine system. Thiamine (vitamin B1) is a cofactor of fundamental enzymes involved in the energetic cell metabolism; recent studies described its role in oxidative stress, protein processing, peroxisomal function, and gene expression. Thiamine defciency is critical mainly in the central and peripheral nervous system, as well as in the muscular cells. Our aim was to investigate the potential therapeutical effects of long-term treatment with thiamine in myotonic dystrophy type 1 in an observational open-label pilot study. We described two patients with myotonic dystrophy type 1 treated with intramuscular thiamine 100 mg twice a week for 12 or 11 months. We evaluated the patients using the grading of muscle strength according to Medical Research Council (MRC), the Muscular Impairment Rating Scale (MIRS), and the Modifed Barthel index. High-dose thiamine treatment was well tolerated and effective in improving the motor symptomatology, particularly the muscle strength evaluated with the MRC scale, and the patients’ activities of daily living using the Modifed Barthel Index. At the end of treatment, the MRC score was 5 in the proximal muscles and 2–4 in the distal muscles (the MRC score before the treatment was 3–4 and 1–3, respectively). The MIRS grade improved by 25% compared to baseline for both patients. In patient #1, the Modifed Barthel Index improved by 44%, and in patient #2 by 29%. These fndings suggest that clinical outcomes are improved by long-term thiamine treatment. Related Articles | Metrics

Select

Effects of triptolide on hippocampal microglial cells and astrocytes in the APP/PS1 double transgenic mouse model of Alzheimer’s disease Jian-ming Li, Yan Zhang, Liang Tang, Yong-heng Chen, Qian Gao, Mei-hua Bao, Ju Xiang, De-liang Lei 2016, 11 (9):  1492-1498.  doi: 10.4103/1673-5374.191224 Abstract ( 277 )   PDF (1361KB) ( 452 )   Save The principal pathology of Alzheimer’s disease includes neuronal extracellular deposition of amyloid-beta peptides and formation of senile pl aques, which in turn induce neuroin?ammation in the brain. Triptolide, a natural extract from the vine-like herb Tripterygium wilfordii Hook F, has potent anti-in?ammatory and immunosuppressive effcacy. Therefore, we determined if triptolide can inhibit activation and proliferation of microglial cells and astrocytes in the APP/PS1 double transgenic mouse model of Alzheimer’s disease. We used 1 or 5 μg/kg/d triptolide to treat APP/PS1 double transgenic mice (aged 4–4.5 months) for 45 days. Unbiased stereology analysis found that triptolide dose-dependently reduced the total number of microglial cells, and transformed microglial cells into the resting state. Further, triptolide (5 μg/kg/d) also reduced the total number of hippocampal astrocytes. Our in vivo test results indicate that triptolide suppresses activation and proliferation of microglial cells and astrocytes in the hippocampus of APP/PS1 double transgenic mice with Alzheimer’s disease. Related Articles | Metrics

Select

Does crossover innervation really affect the clinical outcome? A comparison of outcome between unilateral and bilateral digital nerve repair Melike Oruç, Kadri Ozer, Özlem Çolak, Yüksel Kankaya, Uğur Koçer 2016, 11 (9):  1499-1505.  doi: 10.4103/1673-5374.191226 Abstract ( 253 )   PDF (391KB) ( 521 )   Save Digital nerve injuries are the mostly detected nerve injury in the upper extremity. However, since the clinical phenomenon of crossover innervation at some degree from uninjured digital nerve to the injured side occurs after digital nerve injuries is sustained, one could argue that this concept might even result in the overestimation of the outcome of the digital nerve repair. With this knowledge in mind, this study aimed to present novel, pure, focused and valuable clinical data by comparing the outcomes of bilateral and unilateral digital nerve repair. A retrospective review of 28 fngers with unilateral or bilateral digital nerve repair using end-to-end technique in 19 patients within 2 years was performed. Weber’s two-point discrimination, sharp/dull discrimination, warm/cold sensation and Visual Analog Scale scoring were measured at final 12-month follow ups in all patients. There was no significant difference in recovery of sensibility after unilateral and bilateral digital nerve repairs. Though there is crossover innervation microscopically, it is not important in the clinical evaluation period. According to clinical fndings from this study, crossover innervations appear to be negligible in the estimation of outcomes of digital neurorrhaphy. Related Articles | Metrics

Select

Changes in microtubule-associated protein tau during peripheral nerve injury and regeneration Guang-bin Zha, Mi Shen, Xiao-song Gu, Sheng Yi 2016, 11 (9):  1506-1511.  doi: 10.4103/1673-5374.191227 Abstract ( 291 )   PDF (1257KB) ( 511 )   Save Tau, a primary component of microtubule-associated protein, promotes microtubule assembly and/or disassembly and maintains the stability of the microtubule structure. Although the importance of tau in neurodegenerative diseases has been well demonstrated, whether tau is involved in peripheral nerve regeneration remains unknown. In the current study, we obtained sciatic nerve tissue from adult rats 0, 1, 4, 7, and 14 days after sciatic nerve crush and examined tau mRNA and protein expression levels and the location of tau in the sciatic nerve following peripheral nerve injury. The results from our quantitative reverse transcription polymerase chain reaction analysis showed that compared with the uninjured control sciatic nerve, mRNA expression levels for both tau and tau tubulin kinase 1, a serine/ threonine kinase that regulates tau phosphorylation, were decreased following peripheral nerve injury. Our western blot assay results suggested that the protein expression levels of tau and phosphorylated tau initially decreased 1 day post nerve injury but then gradually increased. The results of our immunohistochemical labeling showed that the location of tau protein was not altered by nerve injury. Thus, these results showed that the expression of tau was changed following sciatic nerve crush, suggesting that tau may be involved in peripheral nerve repair and regeneration. Related Articles | Metrics

Select

Stem Cell Ophthalmology Treatment Study (SCOTS)：improvement in serpiginous choroidopathy following autologous bone marrow derived stem cell treatment Jeffrey N. Weiss, Susan C. Benes, Steven Levy 2016, 11 (9):  1512-1516.  doi: 10.4103/1673-5374.191229 Abstract ( 323 )   PDF (1653KB) ( 447 )   Save We report results in a 77-year-old male patient with visual loss from long-standing serpiginous choroidopathy treated with bone marrow derived stem cells (BMSC) within the Stem Cell Ophthalmology Treatment Study (SCOTS). SCOTS is an Institutional Review Board approved clinical trial and the largest ophthalmology stem cell study registered at the National Institutes of Health to date (ClinicalTrials.gov Identifer: NCT01920867). Eight months after treatment by a combination of retrobulbar, subtenon, intravitreal and intravenous injection of BMSC, the patient’s best corrected Snellen acuity improved from 20/80– to 20/60+1 in the right eye and from 20/50– to 20/20–3 in the left eye. The Early Treatment of Diabetic Retinopathy Study (ETDRS) visual acuity continued to improve over the succeeding 8 months and the optical coherence tomography macular volume increased. The increases in visual acuity and macular volume are encouraging and suggest that the use of BMSC as provided in SCOTS may be a viable approach to treating serpiginous choroidopathy. Related Articles | Metrics

Select

Galanin and its receptor system promote the repair of injured sciatic nerves in diabetic rats Xiao-feng Xu, Dan-dan Zhang, Jin-chi Liao, Li Xiao, Qing Wang, Wei Qiu 2016, 11 (9):  1517-1526.  doi: 10.4103/1673-5374.191228 Abstract ( 356 )   PDF (4210KB) ( 418 )   Save Various studies have reported that galanin can promote axonal regeneration of dorsal root ganglion neurons in vitro and inhibit neuropathic pain. However, little is known about its effects on diabetic peripheral neuropathy, and in vivo experimental data are lacking. We hypothesized that repeated applications of exogenous galanin over an extended time frame may also repair nerve damage in diabetic peripheral neuropathy, and relieve pain in vivo. We found that neuropathic pain occurred in streptozotocin-induced diabetic rats and was more severe after sciatic nerve pinch injury at 14 and 28 days than in diabetic sham-operated rats. Treatment with exogenous galanin alleviated the neuropathic pain and promoted sciatic nerve regeneration more effectively in diabetic rats than in non-diabetic rats after sciatic nerve pinch injury. This was accompanied by changes in the levels of endogenous galanin, and its receptors galanin receptor 1 and galanin receptor 2 in the dorsal root ganglia and the spinal dorsal horn when compared with nerve pinch normal rats. Our results show that application of exogenous galanin daily for 28 days can promote the regeneration of injured sciatic nerves, and alleviate neuropathic pain in diabetic rats. Related Articles | Metrics

Select

Recovery of corticospinal tract injured by traumatic axonal injury at the subcortical white matter: a case report Sung Ho Jang, Seong Ho Kim, Woo Hyuk Jang 2016, 11 (9):  1527-1528.  doi: 10.4103/1673-5374.19123 Abstract ( 283 )   PDF (1068KB) ( 847 )   Save Related Articles | Metrics