Table of Content

15 June 2019, Volume 14 Issue 6 Previous Issue    Next Issue

For Selected:

Download Citations EndNote Reference Manager ProCite BibTeX RefWorks

Toggle Thumbnails

Select

The hypothalamic-spinal dopaminergic system: a target for pain modulation Michelino Puopolo 2019, 14 (6):  925-930.  doi: 10.4103/1673-5374.250567 Abstract ( 116 )   PDF (201KB) ( 190 )   Save Nociceptive signals conveyed to the dorsal horn of the spinal cord by primary nociceptors are subject to extensive modulation by local neurons and by supraspinal descending pathways to the spinal cord before being relayed to higher brain centers. Descending modulatory pathways to the spinal cord comprise, among others, noradrenergic, serotonergic, γ-aminobutyric acid (GABA)ergic, and dopaminergic fibers. The contributions of noradrenaline, serotonin, and GABA to pain modulation have been extensively investigated. In contrast, the contributions of dopamine to pain modulation remain poorly understood. The focus of this review is to summarize the current knowledge of the contributions of dopamine to pain modulation. Hypothalamic A11 dopaminergic neurons project to all levels of the spinal cord and provide the main source of spinal dopamine. Dopamine receptors are expressed in primary nociceptors as well as in  spinal neurons located in different laminae in the dorsal horn of the spinal cord, suggesting that dopamine can modulate pain signals by acting at both presynaptic and postsynaptic targets. Here, I will review the literature on the effects of dopamine and dopamine receptor agonists/antagonists on the excitability of primary nociceptors, the effects of dopamine on the synaptic transmission between primary nociceptors and dorsal horn neurons, and the effects of dopamine on pain in rodents. Published data support both anti-nociceptive effects of dopamine mediated by D2-like receptors and pro-nociceptive effects mediated by D1-like receptors. Related Articles | Metrics

Select

Characteristics and advantages of adenoassociated virus vector-mediated gene therapy for neurodegenerative diseases Yuan Qu,Yi Liu,Ahmed Fayyaz Noor,Johnathan Tran,Rui Li 2019, 14 (6):  931-938.  doi: 10.4103/1673-5374.250570 Abstract ( 119 )   PDF (418KB) ( 232 )   Save Common neurodegenerative diseases of the central nervous system are characterized by progressive damage to the function of neurons, even leading to the permanent loss of function. Gene therapy via gene replacement or gene correction provides the potential for transformative therapies to delay or possibly stop further progression of the neurodegenerative disease in affected patients. Adeno-associated virus has been the vector of choice in recent clinical trials of therapies for neurodegenerative diseases due to its safety and efficiency in mediating gene transfer to the central nervous system. This review aims to discuss and summa¬rize the progress and clinical applications of adeno-associated virus in neurodegenerative disease in central nervous system. Results from some clinical trials and successful cases of central neurodegenerative diseases deserve further study and exploration. Related Articles | Metrics

Select

Gene expression changes in dorsal root ganglia following peripheral nerve injury: roles in inflammation, cell death and nociception Sarah L. Martin,Adam J. Reid,Alexei Verkhratsky,Valerio Magnaghi,Alessandro Faroni 2019, 14 (6):  939-947.  doi: 10.4103/1673-5374.250566 Abstract ( 109 )   PDF (493KB) ( 150 )   Save Subsequent to a peripheral nerve injury, there are changes in gene expression within the dorsal root ganglia in response to the damage. This review selects factors which are well-known to be vital for inflammation, cell death and nociception, and highlights how alterations in their gene expression within the dorsal root ganglia can affect functional recovery. The majority of studies used polymerase chain reaction within animal models to analyse the dynamic changes following peripheral nerve injuries. This review aims to highlight the factors at the gene expression level that impede functional recovery and are hence are potential targets for therapeutic approaches. Where possible the experimental model, specific time-points and cellular location of expression levels are reported. Related Articles | Metrics

Select

Nicotinamide adenine dinucleotide phosphate oxidase activation and neuronal death after ischemic strok Jiamei Shen,Radhika Rastogi,Xiaokun Geng,Yuchuan Ding 2019, 14 (6):  948-953.  doi: 10.4103/1673-5374.250568 Abstract ( 106 )   PDF (506KB) ( 152 )   Save Nicotinamide adenine dinucleotide phosphate oxidase (NOX) is a multisubunit enzyme complex that utilizes nicotinamide adenine dinucleotide phosphate to produce superoxide anions and other reactive oxygen species. Under normal circumstances, reactive oxygen species mediate a number of important cellular functions, including the facilitation of adaptive immunity. In pathogenic circumstances, however, excess reactive oxygen species generated by NOX promotes apoptotic cell death. In ischemic stroke, in particular, it has been shown that both NOX activation and derangements in glucose metabolism result in increased apoptosis. Moreover, recent studies have established that glucose, as a NOX substrate, plays a vital role in the pathogenesis of reperfusion injury. Thus, NOX inhibition has the potential to mitigate the deleterious impact of hyperglycemia on stroke. In this paper, we provide an overview of this research, coupled with a discussion of its implications for the development of NOX inhibition as a strategy for the treatment of ischemic stroke. Both inhibition using apocynin, as well as the prospect of developing more specific inhibitors based on what is now understood of the biology of NOX assembly and activation, will be highlighted in the course of our discussion. Related Articles | Metrics

Select

Autophagy: novel insights into therapeutic target of electroacupuncture against cerebral ischemia/reperfusion injury Ya-Guang Huang,Wei Tao,Song-Bai Yang,Jin-Feng Wang,Zhi-Gang Mei,Zhi-Tao Feng 2019, 14 (6):  954-961.  doi: 10.4103/1673-5374.250569 Abstract ( 135 )   PDF (665KB) ( 173 )   Save Electroacupuncture is known as an effective adjuvant therapy in ischemic cerebrovascular disease. How¬ever, its underlying mechanisms remain unclear. Studies suggest that autophagy, which is essential for cell survival and cell death, is involved in cerebral ischemia reperfusion injury and might be modulate by elec¬troacupuncture therapy in key ways. This paper aims to provide novel insights into a therapeutic target of electroacupuncture against cerebral ischemia/reperfusion injury from the perspective of autophagy. Here we review recent studies on electroacupuncture regulation of autophagy-related markers such as UNC-51- like kinase-1 complex, Beclin1, microtubule-associated protein-1 light chain 3, p62, and autophagosomes for treating cerebral ischemia/reperfusion injury. The results of these studies show that electroacupuncture may affect the initiation of autophagy, vesicle nucleation, expansion and maturation of autophagosomes, as well as fusion and degradation of autophagolysosomes. Moreover, studies indicate that electroacupuncture probably modulates autophagy by activating the mammalian target of the rapamycin signaling pathway. This review thus indicates that autophagy is a therapeutic target of electroacupuncture treatment against ischemic cerebrovascular diseases. Related Articles | Metrics

Select

Lessons from glaucoma: rethinking the fluid-brain barriers in common neurodegenerative disorders Francisco Javier Carreras 2019, 14 (6):  962-966.  doi: 10.4103/1673-5374.249215 Abstract ( 92 )   PDF (975KB) ( 152 )   Save Glaucoma has been recently characterized as a member of the group of anoikis-related diseases. Anoikis, a form of apoptosis, can be triggered by the unfastening of adherent junctions present in astrocytes. In those areas of the central nervous system in which the soma of the neurons or their axons and dendrites are metabolically dependent on the activity of astrocytes, a derangement of the lactate shuttle caused by a separation between the plasma membranes of neurons and astrocytes would result in metabolic impairment of the neurons themselves. In glaucoma, the triggering event has been attributed to the posterior deviation of aqueous humor towards the astrocyte-rich prelaminar tissue of the optic nerve head. The mean calcium content in the aqueous is able to interfere with calcium-dependent adherent junctions and induce anoikis of the astrocytes. As the cerebrospinal fluid has a similar base calcium concentration, a shunt of cerebrospinal fluid through the cerebral parenchyma would be able to interfere in the astrocytic architecture with dire consequences to the metabolically dependent neurons. Here the similitude between glaucoma, amyotrophic lateral sclerosis and Alzheimer’s disease are discussed and the concept of the break in the fluid-brain barrier, as an event separated from the blood-brain barrier, is stressed. Related Articles | Metrics

Select

Busting the myth: more good than harm in transgenic cells Piñero G, Setton-Avruj P 2019, 14 (6):  967-968.  doi: 10.4103/1673-5374.249219 Abstract ( 102 )   PDF (476KB) ( 109 )   Save Peripheral neuropathy constitutes a highly incidental condition and a major public health concern worldwide. This pathology is triggered by peripheral nervous system damage as a consequence of systemic disease or ischemic-traumatic lesion. In the latter case, nerve crush, partial or total transection and stretch injury interrupt nerve conduction and impair sensitivity and motility of the innervated area, which brings about partial or total functional loss in the affected limb and disabling neuropathic pain. For these reasons, digging into the molecular mechanisms underlying peripheral neuropathy becomes essential for the development of successful therapeutic strategies. Related Articles | Metrics

Select

Muscle secretion of toxic factors, regulated by miR126-5p, facilitates motor neuron degeneration in amyotrophic lateral sclerosis Roy Maimon, Eran Perlson 2019, 14 (6):  969-970.  doi: 10.4103/1673-5374.250571 Abstract ( 96 )   PDF (380KB) ( 166 )   Save Amyotrophic lateral sclerosis (ALS) is a lethal neurodegenerative disease characterized by neuromuscular junction (NMJ) disruption, motor neuron (MN) axon degeneration, and neuronal death. Unfortunately, there is currently no effective treatment available for ALS and consequently, most patients die several years post diagnosis. The neurodegeneration that occurs in ALS is considered to be a non-cell autonomous process involving interactions between the motor neuron and its diverse extracellular microenvironments via an unknown mechanism. Distal Axonopathy is one of the early disease signs; however, the involvement and contribution of neighboring tissues and specifically, the muscle environment to the disease pathology remain controversial. Few works have concluded that muscles play a minor role or none at all in ALS pathology. For example, reducing hSOD G93A directly in the muscles of the SOD G93A mouse model, as well as crossing lipoxygenase (LOX) SOD G37R  with the Cre coding sequence under the control of the muscle creatine kinase (MCK) promoter, or performing manipulations using follistatin did not affect the disease’s onset and survival. Moreover, application of muscle condition media (CM) from SOD G93A -expressing muscles on healthy spinal cord neurons or embryonic stem cell-derived motor neurons in vitro resulted in no appreciable effect. In contrast with these findings, overexpressing SODG93A protein specifically in healthy skeletal muscle results in severe muscle atrophy and induces an ALS phenotype. In addition, expressing hSOD1 with G37A and G93A gene variants only in skeletal muscles led to limb weakness, NMJ abnormalities, MN axon degeneration, and cell death, suggesting a direct role for muscles in ALS physiology. Recently, we have characterized a mechanism by which the diseased muscles contribute to the motor neuron degeneration observed in ALS. Using a simplified micro-fluidic chamber (MFC) for studying muscle and motor neuron interactions, we demonstrated that ALS-mutant muscles affect MN axons. Our results show that ALS-mutant muscles facilitate a delay in axon growth towards the muscle compartment, axon degeneration, and NMJ disruption. However, eventually the connections between axons and muscles are established. Thus, at least in our system, apparently the non-cell autonomous contributions of the muscle are insufficient to recapitulate all the toxic effects observed in ALS. Interestingly, once the MNs also carries an ALS mutation, the axons are more susceptible to degeneration by mutated muscle CM. Therefore, apparently although the muscles have contribution to ALS progression, MNs are key in ALS physiology. Related Articles | Metrics

Select

Preliminary in vitro evaluation of neuroprotective and monoamine oxidase type B inhibitory effects of newly synthesized 8-aminocaffeines Magdalena Kondeva-Burdina,Maya Georgieva, Alexandra Kasabova-Angelova, Virginia Tzankova, Alexander Zlatkov 2019, 14 (6):  971-972.  doi: 10.4103/1673-5374.250573 Abstract ( 95 )   PDF (559KB) ( 121 )   Save The expected growth of the elderly population at highest risk for Parkinson’s disease (PD) in the next decades makes the identification of factors that promote or prevent the disease an important goal. In addition, new therapies - aiming to delay the progression of PD are also needed. However, there have been few clinical trials designed to investigate neuroprotection. Thus the application of an appropriate in vitro model such as the neuroblastoma SH-SY5Y cell line is extremely helpful. These cells were selected due to its human origin, catecholaminergic neuronal properties, and ease of maintenance. Related Articles | Metrics

Select

Therapeutic exploitation of the S-nitrosoglutathione/S-nitrosylation mechanism for the treatment of contusion spinal cord injury Mushfiquddin Khan, Inderjit Singh 2019, 14 (6):  973-974.  doi: 10.4103/1673-5374.250572 Abstract ( 106 )   PDF (336KB) ( 118 )   Save Contusion spinal cord injury (SCI) is a major medical and socio-economic problem globally. The incidence of SCI is highest among young adults due to motor vehicle accidents, military or sports injuries, and violence. The elderly and children are also at risk due to falls and accidents. SCI causes neurodegeneration, with profound loss of locomotor and sensory functions. Pain and depression are also prevalent in a majority of SCI patients. Expenses for severe SCI are high: initial hospitalization, rehabilitation, and most likely the continuing need for a caregiver and medical care. SCI survivors with less severe injuries usually face lower but still hefty medical bills. However, people ≥ 50 years old with severe SCI may face medical expenses of over $1.8 million during their lifetimes. These injuries also affect spouses and family members, emotionally and financially, and most injuries jeopardize employment for those affected. In sum, SCI has a lifelong effect on many people; it represents a major challenge for successful health care management. Related Articles | Metrics

Select

The paradigm of protein acetylation in Parkinson’s disease Sokhna M.S. Yakhine-Diop, Guadalupe Martínez-Chacón, Elisabet Uribe-Carretero, Mireia Niso-Santano, Rosa A. González-Polo, José M. Fuentes 2019, 14 (6):  975-976.  doi: 10.4103/1673-5374.250575 Abstract ( 94 )   PDF (485KB) ( 193 )   Save Acetylation is a post-translational modification that is regulated by two antagonistic enzymes, histone acetyltransferases (HATs) and histone deacetylases (HDACs). HATs transfer the acetyl group from acetyl-CoA to lysine residues of proteins while HDACs remove it. The impairment of HAT or HDAC activity elicits changes in the protein acetylation status which disturb several cellular processes, among others, gene expression, autophagy etc., leading finally to cell death. Both enzymes are associated with Parkinson’s disease (PD) pathogenesis. In dopaminergic cells, neurotoxins provoke apoptotic cell death by increasing histone acetylation levels. While paraquat and rotenone reduce HDAC activity, dieldrin enhances HAT activity. However in vivo, paraquat-induced upregulation of α-synuclein triggers histone hypoacetylation. Therefore, in PD models, proteins are hypoacetylated or hyperacetylated in response to a stimulus. All these controversies become a paradigm given that a HDAC inhibitor as well as a HAT inhibitor can be cytoprotective. Most of the studies that link acetylation to PD generally focus on the level of histone acetylation. Recently, a comparative study has been performed in two groups of fibroblasts from PD patients with or without the G2019S leucine-rich repeat kinase 2 (LRRK2) mutation. This is the first time that, by western-blotting, a smear of acetylated proteins as a whole reveals the difference between idiopathic (WT LRRK2) PD (IPD) and genetic (G2019S LRRK2) PD (GPD) under basal conditions. Those changes were more evident with higher molecular weight (MW) proteins displaying a hypoacetylation in IPD and a hyperacetylation in GPD cells. With peptides subjected to LC-MS, we also observed that hypoacetylated peptides were more abundant in IPD cells than in GPD. Related Articles | Metrics

Select

Sympathetic stimulation with norepinephrine may come at a cost Lakshini Y Herat, Markus P Schlaich, Vance B Matthews 2019, 14 (6):  977-978.  doi: 10.4103/1673-5374.250576 Abstract ( 100 )   PDF (759KB) ( 762 )   Save Norepinephrine (NE; also known as noradrenaline) is the body’s primary adrenergic neurotransmitter which belongs to the catecholamine family. Norepinephrine has pharmacologic effects on the α1, α2, β1, β2 and β3 adrenoceptors. In the brain, norepinephrine increases arousal and alertness, promotes vigilance, enhances formation and retrieval of memory, and focuses attention. It also increases restlessness and anxiety. In the remainder of the body, norepinephrine increases heart rate and blood pressure, triggers the release of glucose from energy stores, increases blood flow to skeletal muscle and increases muscle contraction, reduces blood flow to the gastrointestinal system and its motility and lastly, inhibits voiding of the bladder. This last point is particularly interesting in the context of this perspective piece. Related Articles | Metrics

Select

Olfactory proteotyping: towards the enlightenment of the neurodegeneration Joaquín Fernández-Irigoyen, Enrique Santamaría 2019, 14 (6):  979-981.  doi: 10.4103/1673-5374.249220 Abstract ( 81 )   PDF (886KB) ( 114 )   Save Although phylogenetically ancient, the olfactory system has received less attention than other sensorial systems. However, olfactory dysfunction is considered an early prodromal event in neurodegenerative diseases (NDs), which may vary from severe smell loss (e.g., Alzheimer’s and Parkinson’s diseases) to relatively moderate loss (e.g., progressive supranuclear palsy). Recently, a cluster of neuropathological and functional discoveries has evidenced the relevant role of the olfactory bulb (OB) during the neurodegenerative process. For instance, the double-transgenic APP/PS1 mouse model of Alzheimer’s disease (AD) develops early proteomic disturbances accompanied by a specific modulation of the focal adhesion kinase (FAK) and mitogen-ac-tivated protein kinase (MAPK) dynamics at the level of the OB, demonstrating that olfactory molecular alterations occur prior to β-amyloid plaque appearance and memory impairments in APP/ PS1 transgenic mice. Nevertheless, there are currently specific questions which should be addressed in human neurodegeneration: Does the loss of smell precede the onset of ND-specific neuropathological features? What is the metabolic impairment induced by protein inclusions in the OB? Is it disease-specific or tauopathy/synucleinopathy-dependent? How the neuropathological substrates modulate their constitutive interactome at olfactory level? Are there common olfactory targets across different neurological backgrounds? Related Articles | Metrics

Select

The role of degenerative pathways in the development of irreversible consequences after brain ischemia Pluta R, Ułamek-Kozioł M 2019, 14 (6):  982-983.  doi: 10.4103/1673-5374.250574 Abstract ( 98 )   PDF (118KB) ( 105 )   Save Ischemic stroke and irreversible consequences: Ischemic stroke in humans is the second most common cause of death in the world. The outcomes after a stroke are often dependent on complications, including motor disorders, depression and dementia, which causes a high risk of re-hospitalization and/or palliative care. This is also the main reason for long-term disability in people after stroke, with up to half of those who survived the stroke will not regain their independence until the end of their lives. According to epidemiological forecasts, human ischemic stroke will soon become the dominant cause of death worldwide as well as dementia with the phenotype of Alzheimer’s disease. It is suggested that human ischemic stroke and experimental brain ischemia in animals are associated with the possible development of AD neuropathology. Epidemiological observations have shown that brain ischemia is a contributing factor to the development of AD and vice versa. Below we present the latest advances in the investigation of brain ischemia-reperfusion injury, focusing on ischemia-induced of the AD phenotype and genotype in humans and animals. We focus in this report on the very likely association between β-amyloid peptide and tau protein in humans and animals with post-isch-emic irreversible neurodegenerative processes and development dementia. It should be emphasized that despite the fact that stroke in humans is one of the main causes of disability, dementia and death in the world, it has no effective therapy improving outcome of the functional and structural irreversible consequences of this disease. Related Articles | Metrics

Select

Decreased numbers of circulating endothelial progenitor cells are associated with hyperglycemia in patients with traumatic brain injury Hui-Jie Wei,Li Liu,Fang-Lian Chen,Dong Wang,Liang Wang,Zeng-Guang Wang,Rong-Cai Jiang,Jing-Fei Dong,Jie-Li Chen,Jian-Ning Zhang 2019, 14 (6):  984-990.  doi: 10.4103/1673-5374.250577 Abstract ( 98 )   PDF (444KB) ( 185 )   Save Hyperglycemia reduces the number of circulating endothelial progenitor cells, accelerates their senescence and impairs their function. However, the relationship between blood glucose levels and endothelial progenitor cells in peripheral blood of patients with traumatic brain injury is unclear. In this study, 101 traumatic brain injury patients admitted to the Department of Neurosurgery, Tianjin Medical University General Hospital or the Department of Neurosurgery, Tianjin Huanhu Hospital, China, were enrolled from April 2005 to March 2007. The number of circulating endothelial progenitor cells and blood glucose levels were measured at 1, 4, 7, 14 and 21 days after traumatic brain injury by flow cytometry and automatic biochemical analysis, respectively. The number of circulating endothelial pro¬genitor cells and blood sugar levels in 37 healthy control subjects were also examined. Compared with controls, the number of circulating endothelial progenitor cells in traumatic brain injury patients was decreased at 1 day after injury, and then increased at 4 days after injury, and reached a peak at 7 days after injury. Compared with controls, blood glucose levels in traumatic brain injury patients peaked at 1 day and then decreased until 7 days and then remained stable. At 1, 4, and 7 days after injury, the number of circulating endothelial progen¬itor cells was negatively correlated with blood sugar levels (r =−0.147, P < 0.05). Our results verify that hyperglycemia in patients with traumatic brain injury is associated with decreased numbers of circulating endothelial progenitor cells. This study was approved by Ethical Committee of Tianjin Medical University General Hospital, China (approval No. 200501) on January, 2015. All subjects or guardians pro¬vided informed written consent before enrollment. Related Articles | Metrics

Select

Neurological functional evaluation based on accurate motions in big animals with traumatic brain injury Ji-Peng Jiang,Xue-Gang Niu,Chen Dai,Ke Ma,Hui-You Xu,Shi-Xiang Cheng,Zhi-Wen Zhang,Feng Duan,Xu Zhu,Yu-Ting Wang,Xu-Yi Chen,Sai Zhang 2019, 14 (6):  991-996.  doi: 10.4103/1673-5374.250578 Abstract ( 87 )   PDF (2036KB) ( 149 )   Save An accurate and effective neurological evaluation is indispensable in the treatment and rehabilitation of traumatic brain injury. However, most of the existing evaluation methods in basic research and clinical practice are not objective or intuitive for assessing the neurological function of big animals, and are also difficult to use to qualify the extent of damage and recovery. In the present study, we established a big animal model of traumatic brain injury by impacting the cortical motor region of beagles. At 2 weeks after successful modeling, we detected neurological deficiencies in the animal model using a series of techniques, including three-dimensional motion capture, elec¬tromyogram and ground reaction force. These novel technologies may play an increasingly important role in the field of traumatic brain injury diagnosis and rehabilitation in the future. Related Articles | Metrics

Select

Acute histopathological responses and long-term behavioral outcomes in mice with graded controlled cortical impact injury Si-Yi Xu,Min Liu,Yang Gao,Yang Cao,Jin-Gang Bao,Ying-Ying Lin,Yong Wang,Qi-Zhong Luo,Ji-Yao Jiang,Chun-Long Zhong 2019, 14 (6):  997-1003.  doi: 10.4103/1673-5374.250579 Abstract ( 131 )   PDF (653KB) ( 164 )   Save While animal models of controlled cortical impact often display short-term motor dysfunction after injury, histological examinations do not show severe cortical damage. Thus, this model requires further improvement. Mice were subjected to injury at three severities using a Pin-Point™-controlled cortical impact device to establish secondary brain injury mouse models. Twenty-four hours after injury, hema¬toxylin-eosin staining, Fluoro-Jade B histofluorescence, and immunohistochemistry were performed for brain slices. Compared to the uninjured side, we observed differences of histopathological findings, neuronal degeneration, and glial cell number in the CA2 and CA3 regions of the hippocampus on the injured side. The Morris water maze task and beam-walking test verified long-term (14–28 days) spatial learning/memory and motor balance. To conclude, the histopathological responses were positively correlated with the degree of damage, as were the long-term behavioral manifestations after controlled cortical impact. Related Articles | Metrics

Select

Aphasia rehabilitation based on mirror neuron theory: a randomized-block-design study of neuropsychology and functional magnetic resonance imaging Wen-Li Chen,Qian Ye,Si-Cong Zhang,Yang Xia,Xi Yang,Ti-Fei Yuan,Chun-Lei Shan,Jian-An Li 2019, 14 (6):  1004-1012.  doi: 10.4103/1673-5374.250580 Abstract ( 177 )   PDF (1542KB) ( 550 )   Save When watching someone performs an action, mirror neurons are activated in a way that is very similar to the activation that occurs when actually performing that action. Previous single-sample case studies indicate that hand-action observation training may lead to activation and re¬modeling of mirror neuron systems, which include important language centers, and may improve language function in aphasia patients. In this randomized-block-design experiment, we recruited 24 aphasia patients from, Zhongda Hospital, Southeast University, China. The patients were divided into three groups where they underwent hand-action observation and repetition, dynamic-object observation and repetition, or conven¬tional speech therapy. Training took place 5 days per week, 35 minutes per day, for 2 weeks. We assessed language function via picture naming tests for objects and actions and the Western Aphasia Battery. Among the participants, one patient, his wife and four healthy student volunteers underwent functional magnetic resonance imaging to analyze changes in brain activation during hand-action observation and dynamic-object observation. Results demonstrated that, compared with dynamic-object observation, hand-action observation led to greater performance with respect to the aphasia quotient and affiliated naming sub-tests and a greater Western Aphasia Battery test score. The overall effect was similar to that of conventional aphasia training, yet hand-action observation had advantages compared with conventional training in terms of vocabulary extraction and spontaneous speech. Thus, hand-action observation appears to more strongly activate the mirror neuron system compared with dynamic-object observation. The activated areas included Broca’s area, Wernicke’s area, and the supramarginal gyrus. These results suggest that hand-action observation combined with repetition might better improve language function in aphasia patients compared with dynamic-object observation combined with repetition. The therapeutic mechanism of this intervention may be associated with activation of additional mirror neuron systems, and may have implications for the possible repair and remodeling of damaged nerve networks. The study protocol was ap¬proved by the Ethical Committee of Nanjing Medical University, China (approval number: 2011-SRFA-086) on March 11, 2011. This trial has been registered in the ISRCTN Registry (ISRCTN84827527). Related Articles | Metrics

Select

Neuroprotection mediated by the Wnt/Frizzled signaling pathway in early brain injury induced by subarachnoid hemorrhage Yang Wang,De-Jun Bao,Bin Xu,Chuan-Dong Cheng,Yong-Fei Dong,Xiang-pin Wei,Chao-Shi Niu 2019, 14 (6):  1013-1024.  doi: 10.4103/1673-5374.250620 Abstract ( 95 )   PDF (6964KB) ( 100 )   Save The Wnt/Frizzled signaling pathway participates in many inflammation-linked diseases. However, the inflammatory response mediated by the Wnt/Frizzled signaling pathway in experimental subarachnoid hemorrhage has not been thoroughly investigated. Consequently, in this study, we examined the potential role of the Wnt/Frizzled signaling pathway in early brain injury in rat models of subarachnoid hemorrhage. Simultaneously, possible neuroprotective mechanisms were also investigated. Experimental subarachnoid hemorrhage rat models were in¬duced by injecting autologous blood into the prechiasmatic cistern. Experiment 1 was designed to examine expression of the Wnt/Frizzled signaling pathway in early brain injury induced by subarachnoid hemorrhage. In total, 42 adult rats were divided into sham (injection of equivalent volume of saline), 6-, 12-, 24-, 48-, 72-hour, and 1-week subarachnoid hemorrhage groups. Experiment 2 was designed to exam¬ine neuroprotective mechanisms of the Wnt/Frizzled signaling pathway in early brain injury induced by subarachnoid hemorrhage. Rats were treated with recombinant human Wnt1 (rhwnt1), small interfering Wnt1 (siwnt1) RNA, and monoclonal antibody of Frizzled1 (an¬ti-Frizzled1) at 48 hours after subarachnoid hemorrhage. Expression levels of Wnt1, Frizzled1, β-catenin, peroxisome proliferator-activated receptor-γ, CD36, and active nuclear factor-κB were examined by western blot assay and immunofluorescence staining. Microglia type con¬version and inflammatory cytokine levels in brain tissue were examined by immunofluorescence staining and enzyme-linked immunosorbent assay. Our results show that compared with the sham group, expression levels of Wnt1, Frizzled1, and β-catenin were low and reduced to a minimum at 48 hours, gradually returning to baseline at 1 week after subarachnoid hemorrhage. rhwnt1 treatment markedly increased Wnt1 expression and alleviated subarachnoid hemorrhage-induced early brain injury (within 72 hours), including cortical cell apoptosis, brain edema, and neurobehavioral deficits, accompanied by increasing protein levels of β-catenin, CD36, and peroxisome proliferator-activated re¬ceptor-γ and decreasing protein levels of nuclear factor-κB. Of note, rhwnt1 promoted M2-type microglia conversion and inhibited release of inflammatory cytokines (interleukin-1β, interleukin-6, and tumor necrosis factor-α). In contrast, siwnt1 RNA and anti-Frizzled1 treatment both resulted in an opposite effect. In conclusion, the Wnt/Frizzled1 signaling pathway may participate in subarachnoid hemorrhage-induced early brain injury via inhibiting the inflammatory response, including regulating microglia type conversion and decreasing inflammatory cytokine release. The study was approved by Animal Ethics Committee of Anhui Medical University and First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China (approval No. LLSC-20180202) in May 2017. Related Articles | Metrics

Select

Ipsilateral motor evoked potentials in a patient with unihemispheric cortical atrophy due to Rasmussen encephalitis Raffaele Nardone,Patrick B. Langthaler,Andrea Orioli, Viviana Versace,Giuditta Ilaria Scarano,Francesco Brigo,Leopold Saltuari,Luca Carnicelli,Eugen Trinka,Luca Sebastianelli 2019, 14 (6):  1025-1028.  doi: 10.4103/1673-5374.250581 Abstract ( 90 )   PDF (315KB) ( 104 )   Save The role of the ipsilaterally descending motor pathways in the recovery mechanisms after unilateral hemispheric damage is still poorly understood. Motor output reorganization was investigated in a 56-year-old male patient with acquired unilateral hemispheric atrophy due to Rasmussen encephalitis. In particular, the ipsilateral corticospinal pathways were explored using focal transcranial magnetic stimulation. In the first dorsal interosseous and wrist extensors muscles, the median amplitudes of the ipsilateral motor evoked potentials induced by transcranial magnetic stimulation in the patient were higher than those of 10 age-matched healthy control subjects. In the biceps brachii muscle, the median amplitudes of the ipsilateral motor evoked potentials were the second largest in the patient compared to the controls. This study demonstrated a reinforcement of ipsilateral motor projections from the unaffected motor cortex to the hemiparetic hand in a subject with acquired unihemispheric cortical damage. Related Articles | Metrics

Select

Inhibition of α5 GABAA receptors has preventive but not therapeutic effects on isoflurane-induced memory impairment in aged rats Zi-Fang Zhao,Lei Du,Teng Gao,Lin Bao,Yuan Luo,Yi-Qing Yin,Yong-An Wang 2019, 14 (6):  1029-1036.  doi: 10.4103/1673-5374.250621 Abstract ( 99 )   PDF (1180KB) ( 151 )   Save The α5 subunit-containing gamma-amino butyric acid type A receptors (α5 GABAARs) are a distinct subpopulation that are specifically distributed in the mammalian hippocampus and also mediate tonic inhibitory currents in hippocampal neurons. These tonic currents can be enhanced by low-dose isoflurane, which is associated with learning and memory impairment. Inverse agonists of α5 GABAARs, such as L-655,708, are able to reverse the short-term memory deficit caused by low-dose isoflurane in young animals. However, whether these negative allosteric modulators have the same effects on aged rats remains unclear. In the present study, we mainly investigated the effects of L-655,708 on low-dose (1.3%) isoflurane-induced learning and memory impairment in elderly rats. Young (3-month-old) and aged (24-month-old) Wistar rats were randomly assigned to receive L-655,708 0.5 hour before or 23.5 hours after 1.3% isoflurane anesthesia. The Morris Water Maze tests demonstrated that L-655,708 injected before or after anesthesia could reverse the memory deficit in young rats. But in aged rats, application of L-655,708 only before anesthesia showed similar effects. Reverse transcription-polymerase chain reac¬tion showed that low-dose isoflurane decreased the mRNA expression of α5 GABAARs in aging hippocampal neurons but increased that in young animals. These findings indicate that L-655,708 prevented but could not reverse 1.3% isoflurane-induced spatial learning and memory impairment in aged Wistar rats. All experimental procedures and protocols were approved by the Experimental Animal Ethics Committee of Academy of Military Medical Science of China (approval No. NBCDSER-IACUC-2015128) in December 2015. Related Articles | Metrics

Select

Glutamate receptor delocalization in postsynaptic membrane and reduced hippocampal synaptic plasticity in the early stage of Alzheimer’s disease Ning Li,Yang Li,Li-Juan Li,Ke Zhu,Yan Zheng,Xiao-Min Wang 2019, 14 (6):  1037-1045.  doi: 10.4103/1673-5374.250625 Abstract ( 129 )   PDF (1304KB) ( 147 )   Save Mounting evidence suggests that synaptic plasticity provides the cellular biological basis of learning and memory, and plasticity deficits play a key role in dementia caused by Alzheimer’s disease. However, the mechanisms by which synaptic dysfunction contributes to the pathogenesis of Alzheimer’s disease remain unclear. In the present study, Alzheimer’s disease transgenic mice were used to determine the relationship between decreased hippocampal synaptic plasticity and pathological changes and cognitive-behavioral deterioration, as well as possible mechanisms underlying decreased synaptic plasticity in the early stages of Alzheimer’s disease-like diseases. APP/PS1 double transgenic (5XFAD; Jackson Laboratory) mice and their littermates (wild-type, controls) were used in this study. Additional 6-week-old and 10-week-old 5XFAD mice and wild-type mice were used for electrophysiological recording of hippocampal dentate gyrus. For 10-week-old 5XFAD mice and wild-type mice, the left hippocampus was used for electrophysiological recording, and the right hippocam¬pus was used for biochemical experiments or immunohistochemical staining to observe synaptophysin levels and amyloid beta deposition levels. The results revealed that, compared with wild-type mice, 6-week-old 5XFAD mice exhibited unaltered long-term potentiation in the hippocampal dentate gyrus. Another set of 5XFAD mice began to show attenuation at the age of 10 weeks, and a large quantity of amyloid beta protein was accumulated in hippocampal cells. The location of α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor and N-methyl-D-aspartic acid receptor subunits in synaptosomes was decreased. These findings indicate that the delocalization of postsynaptic glutamate receptors and an associated decline in synaptic plasticity may be key mechanisms in the early onset of Alzheimer’s disease. The use and care of animals were in strict accordance with the ethical standards of the animal ethics committee of the Capital Medical Univer¬sity, China on December 17, 2015 (ethics No. AEEI-2015-182). Related Articles | Metrics

Select

Rapid transport of insulin to the brain following intranasal administration in rats Lir-Wan Fan, Kathleen Carter, Abhay Bhatt, Yi Pang 2019, 14 (6):  1046-1051.  doi: 10.4103/1673-5374.250624 Abstract ( 93 )   PDF (2746KB) ( 157 )   Save We previously reported that intranasal insulin protects substantia nigra dopaminergic neurons against 6-hydroxydopamine neurotoxicity in rats. This study aimed to assess insulin pharmacokinetics in the rat brain following intranasal application. Recombinant human insulin (rh-Ins) or phosphate buffer solution was administered to both nostrils of rats. Animals were sacrificed at 15 minutes, 1, 2, and 6 hours to determine insulin levels in different brain regions by an ultrasensitive, human-specific enzyme-linked immunosorbent assay kit. For fluorescence tracing study, rats were administered with intranasal florescence-tagged insulin (Alex546-Ins), and brains were fixed at 10 and 30 minutes to prepare sagittal sections. rh-Ins was detected in all brain regions examined except the cerebral cortex. The highest levels were detected in the brainstem, followed by the cerebellum, substantia nigra/ventral tegmental area, olfactory bulb, striatum, hippocampus, and thalamus/hypothalamus. Insulin levels reached a peak at 15 minutes and then declined gradually overtime, but remained significantly higher than baseline levels at 6 hours in most regions. Consistently, widespread Alex546-Ins-binding cells were detected in the brain at 10 and 30 minutes, with the olfactory bulb and brainstem showing the highest while the cerebral cortex showing lowest fluorescence signals. Double-immunostaining showed that Alex546-Ins-bindings were primarily co-localized with neuronal nuclei-positive neurons. In the subtantia nigra, phospho-Akt was found to be activated in a subset of Alex546-Ins and tyrosine hydroxylase double-labeled cells, suggesting activation of the Akt/PI3K pathway in these dopaminergic neurons. Data from this study suggest that intranasal insulin could effectively reach deep brain structures including the nigrostriatal pathways, where it binds to dopaminergic neurons and activates intracellular cell survival signaling. This study was approved by the Institutional Animal Care Committee at the University of Mississippi Medical Center (protocol 1333A) on June 29, 2015. Related Articles | Metrics

Select

A method to deliver patterned electrical impulses to Schwann cells cultured on an artificial axon Antonio Merolli,Yong Mao,Gregory Voronin,Joseph A.M. Steele,N. Sanjeeva Murthy,Joachim Kohn 2019, 14 (6):  1052-1059.  doi: 10.4103/1673-5374.250626 Abstract ( 104 )   PDF (1628KB) ( 184 )   Save Information from the brain travels back and forth along peripheral nerves in the form of electrical impulses generated by neurons and these impulses have repetitive patterns. Schwann cells in peripheral nerves receive molecular signals from axons to coordinate the process of myelination. There is evidence, however, that non-molecular signals play an important role in myelination in the form of patterned electrical impulses generated by neuronal activity. The role of patterned electrical impulses has been investigated in the literature using co-cultures of neurons and myelinating cells. The co-culturing method, however, prevents the uncoupling of the direct effect of patterned electrical impulses on myelinating cells from the indirect effect mediated by neurons. To uncouple these effects and focus on the direct response of Schwann cells, we developed an in vitro model where an electroconductive carbon fiber acts as an artificial axon. The fiber provides only the biophysical characteristics of an axon but does not contribute any molecular signaling. In our “suspended wire model”, the carbon fiber is suspended in a liquid media supported by a 3D printed scaffold. Patterned electrical impulses are generated by an Arduino 101 microcontroller. In this study, we describe the technology needed to set-up and eventually replicate this model. We also report on our initial in vitro tests where we were able to document the adherence and ensheath of human Schwann cells to the carbon fiber in the presence of patterned electrical impulses (hSCs were purchased from ScienCell Research Laboratories, Carlsbad, CA, USA; ScienCell fulfills the ethic requirements, including donor’s consent). This technology will likely make feasible to investigate the response of Schwann cells to patterned electrical impulses in the future. Related Articles | Metrics

Select

Use of a combination strategy to improve neuroprotection and neuroregeneration in a rat model of acute spinal cord injury Elisa García,Roxana Rodríguez-Barrera,Vinnitsa Buzoianu-Anguiano,Adrian Flores-Romero,Emanuel Malagón-Axotla,Marco Guerrero-Godinez,Estefanía De la Cruz-Castillo,Laura Castillo-Carvajal,Monserrat Rivas-Gonzalez,Paola Santiago-Tovar,Ivis Morales,Cesar Borlongan,Antonio Ibarra 2019, 14 (6):  1060-1068.  doi: 10.4103/1673-5374.250627 Abstract ( 112 )   PDF (1570KB) ( 145 )   Save Spinal cord injury is a very common pathological event that has devastating functional consequences in patients. In recent years, several research groups are trying to find an effective therapy that could be applied in clinical practice. In this study, we analyzed the combination of different strategies as a potential therapy for spinal cord injury. Immunization with neural derived peptides (INDP), inhibition of glial scar formation (dipyridyl: DPY), as well as the use of biocompatible matrix (fibrin glue: FG) impregnated with bone marrow mesenchymal stem cells (MSCs) were combined and then its beneficial effects were evaluated in the induction of neuroprotection and neuroregeneration after acute SCI. Sprague-Dawley female rats were subjected to a moderate spinal cord injury and then randomly allocated into five groups: 1) phosphate buffered saline; 2) DPY; 3) INDP + DPY; 4) DPY+ FG; 5) INDP + DPY + FG + MSCs. In all rats, intervention was performed 72 hours after spinal cord injury. Locomotor and sensibility recovery was assessed in all rats. At 60 days after treatment, histological examinations of the spinal cord (hematoxylin-eosin and Bielschowsky staining) were performed. Our results showed that the combination therapy (DPY+ INDP + FG + MSCs) was the best strategy to promote motor and sensibility recovery. In addition, significant increases in tissue preservation and axonal density were observed in the combination therapy group. Findings from this study suggest that the combination theapy (DPY+ INDP + FG + MSCs) exhibits potential effects on the protection and regeneration of neural tissue after acute spinal cord injury. All procedures were approved by the Animal Bioethics and Welfare Committee (aproval number: 178544; CSNBTBIBAJ 090812960) on August 15, 2016. Related Articles | Metrics

Select

Effect of lentiviral vector-mediated overexpression of hypoxia-inducible factor 1 alpha delivered by pluronic F-127 hydrogel on brachial plexus avulsion in rats Tao Wang,Li-Ni Zeng,Zhe Zhu,Yu-Hui Wang,Lu Ding,Wei-Bin Luo,Xiao-Min Zhang,Zhi-Wei He,Hong-Fu Wu 2019, 14 (6):  1069-1078.  doi: 10.4103/1673-5374.250629 Abstract ( 102 )   PDF (2275KB) ( 143 )   Save Brachial plexus avulsion often results in massive motor neuron death and severe functional deficits of target muscles. However, no satisfactory treatment is currently available. Hypoxia-inducible factor 1α is a critical molecule targeting several genes associated with ischemia-hypoxia damage and angiogenesis. In this study, a rat model of brachial plexus avulsion-reimplantation was established, in which C5–7 ventral nerve roots were avulsed and only the C6 root reimplanted. Different implants were immediately injected using a microsyringe into the avulsion-reimplantation site of the C6 root post-brachial plexus avulsion. Rats were randomly divided into five groups: phosphate-buffered saline, negative control of lentivirus, hypoxia-inducible factor 1α (hypoxia-inducible factor 1α overexpression lentivirus), gel (pluronic F-127 hydrogel), and gel + hypoxia-inducible factor 1α (pluronic F-127 hydrogel + hypoxia-inducible factor 1α overexpression lentivirus). The Terzis grooming test was performed to assess recovery of motor function. Scores were higher in the hypox¬ia-inducible factor 1α and gel + hypoxia-inducible factor 1α groups (in particular the gel + hypoxia-inducible factor 1α group) compared with the phosphate-buffered saline group. Electrophysiology, fluorogold retrograde tracing, and immunofluorescent staining were further performed to investigate neural pathway reconstruction and changes of neurons, motor endplates, and angiogenesis. Compared with the phosphate-buffered saline group, action potential latency of musculocutaneous nerves was markedly shortened in the hypoxia-inducible factor 1α and gel + hypoxia-inducible factor 1α groups. Meanwhile, the number of fluorogold-positive cells and ChAT-positive neurons, neovascular area (labeled by CD31 around avulsed sites in ipsilateral spinal cord segments), and the number of motor endplates in biceps brachii (identified by α-bungarotoxin) were all visibly increased, as well as the morphology of motor endplate in biceps brachil was clear in the hypoxia-inducible factor 1α and gel + hypoxia-inducible factor 1α groups. Taken together, delivery of hypoxia-inducible factor 1α overexpression lentiviral vectors mediated by pluronic F-127 effectively promotes spinal root regeneration and functional recovery post-brachial plexus avulsion. All animal procedures were approved by the Institutional Animal Care and Use Committee of Guangdong Medical University, China. Related Articles | Metrics

Select

Chitosan tubes enriched with fresh skeletal muscle fibers for delayed repair of peripheral nerve defects Alessandro Crosio,Benedetta Elena Fornasari, Giovanna Gambarotta,Stefano Geuna,Stefania Raimondo,Bruno Battiston,Pierluigi Tos,Giulia Ronchi 2019, 14 (6):  1079-1084.  doi: 10.4103/1673-5374.250628 Abstract ( 97 )   PDF (1440KB) ( 132 )   Save Nerve regeneration after delayed nerve repair is often unsuccessful. Indeed, the expression of genes associated with regeneration, including neurotrophic and gliotrophic factors, is drastically reduced in the distal stump of chronically transected nerves; moreover, Schwann cells undergo atrophy, losing their ability to sustain regeneration. In the present study, to provide a three-dimensional environment and trophic factors supporting Schwann cell activity and axon re-growth, we combined the use of an effective conduit (a chitosan tube) with a promising intraluminal structure (fresh longitudinal skeletal muscle fibers). This enriched conduit was used to repair a 10-mm rat median nerve gap after 3-month delay and functional and morphometrical analyses were performed 4 months after nerve reconstruction. Our data show that the enriched chitosan conduit is as effective as the hollow chitosan conduit in promoting nerve regeneration, and its efficacy is not statistically different from the autograft, considered the “gold standard” technique for nerve reconstruction. Since hollow tubes not always lead to good results after long defects (> 20 mm), we believe that the conduit enriched with fresh muscle fibers could be a promising strategy to repair longer gaps, as muscle fibers create a favorable three-dimensional environment and release trophic factors. All procedures were approved by the Bioethical Committee of the University of Torino and by the Italian Ministry of Health (approval number: 864/2016/PR) on September 14, 2016. Related Articles | Metrics

Select

Neural-like cells from adipose-derived stem cells for cavernous nerve injury in rats Cheng-Cheng Ying,Mei Yang,Yong Wang,Yong-Lian Guo,Wan-Li Hu,Xin-Min Zheng 2019, 14 (6):  1085-1090.  doi: 10.4103/1673-5374.250630 Abstract ( 107 )   PDF (1357KB) ( 162 )   Save Although the remaining nerve tissue can regenerate and partly restore erectile function when the cavernous nerve is compressed/severed and function lost, the limited regenerative ability of these nerve tissues often fails to meet clinical needs. Adipose-derived stem cells are easy to obtain and culture, and can differentiate into neural cells. Their proliferation rate is easy to control and they may be used to help restore injured cavernous nerve function. Sprague-Dawley male rats (n = 45) were equally randomized into three groups: fifteen rats as a sham-op¬erated group, fifteen rats as a bilateral nerve crush (BINC) group (with no further intervention), fifteen rats as a BINC with intracavernous injection of one million neural-like cells from adipose-derived stem cells (NAS) (BINC + NAS) group. After 4 weeks, erectile function was assessed by stimulating the cavernous body. The number of myelinated axons in the dorsal cavernous nerve was determined by toluidine blue staining. The area of neuronal nitric oxide synthase-positive fibers in the dorsal penile nerve was measured by immunohistochemical staining. Masson staining was used to analyze the ratio of smooth muscle to collagen in penile tissue. The results demonstrate that maxi¬mal intracavernous pressure, the ratio of maximal intracavernous pressure to mean arterial pressure, the numbers of myelinated axons and neuronal nitric oxide synthase-positive fibers in the dorsal penile nerve, and the ratio of smooth muscle to collagen could be increased after cell transplantation. These findings indicate that neural-like cells from adipose-derived stem cells can effectively alleviate cavernous nerve injury and improve erectile function. Related Articles | Metrics

Select

Mechanism of persistent hyperalgesia in neuropathic pain caused by chronic constriction injury Qin-Yi Chen,Chao-Yang Tan,Yang Wang,Ke-Tao Ma,Li Li,Jun-Qiang Si 2019, 14 (6):  1091-1098.  doi: 10.4103/1673-5374.250631 Abstract ( 120 )   PDF (1137KB) ( 140 )   Save Transmembrane member 16A (TMEM16A) is involved in many physiological functions, such as epithelial secretion, sensory conduction, nociception, control of neuronal excitability, and regulation of smooth muscle contraction, and may be important in peripheral pain transmission. To explore the role of TMEM16A in the persistent hyperalgesia that results from chronic constriction injury-induced neuro¬pathic pain, a rat model of the condition was established by ligating the left sciatic nerve. A TMEM16A selective antagonist (10 μg T16Ain h-A01) was intrathecally injected at L5–6. For measurement of thermal hyperalgesia, the drug was administered once at 14 days and ther¬mal withdrawal latency was recorded with an analgesia meter. For measurement of other indexes, the drug was administered at 12 days, once every 6 hours, totally five times. The measurements were performed at 14 days. Western blot assay was conducted to analyze TME¬M16A expression in the L4–6 dorsal root ganglion. Immunofluorescence staining was used to detect the immunoreactivity of TMEM16A in the L4–6 dorsal root ganglion on the injured side. Patch clamp was used to detect electrophysiological changes in the neurons in the L4–6 dorsal root ganglion. Our results demonstrated that thermal withdrawal latency was shortened in the model rats compared with con¬trol rats. Additionally, TMEM16A expression and the number of TMEM16A positive cells in the L4–6 dorsal root ganglion were higher in the model rats, which induced excitation of the neurons in the L4–6 dorsal root ganglion. These findings were inhibited by T16Ainh-A01 and confirm that TMEM16A plays a key role in persistent chronic constriction injury-induced hyperalgesia. Thus, inhibiting TMEM16A might be a novel pharmacological intervention for neuropathic pain. Related Articles | Metrics

Select

Comparative study of microarray and experimental data on Schwann cells in peripheral nerve degeneration and regeneration: big data analysis Ulfuara Shefa,Junyang Jung 2019, 14 (6):  1099-1104.  doi: 10.4103/1673-5374.250632 Abstract ( 85 )   PDF (892KB) ( 134 )   Save A Schwann cell has regenerative capabilities and is an important cell in the peripheral nervous system. This microarray study is part of a bioinformatics study that focuses mainly on Schwann cells. Microarray data provide information on differences between microarray-based and experiment-based gene expression analyses. According to microarray data, several genes exhibit increased expression (fold change) but they are weakly expressed in experimental studies (based on morphology, protein and mRNA levels). In contrast, some genes are weakly expressed in microarray data and highly expressed in experimental studies; such genes may represent future target genes in Schwann cell studies. These studies allow us to learn about additional genes that could be used to achieve targeted results from experimental studies. In the current big data study by retrieving more than 5000 scientific articles from PubMed or NCBI, Google Scholar, and Google, 1016 (up- and downregulated) genes were determined to be related to Schwann cells. However, no experiment was performed in the laboratory; rather, the present study is part of a big data analysis. Our study will contribute to our understanding of Schwann cell biology by aiding in the identification of genes. Based on a comparative analysis of all microarray data, we conclude that the microarray could be a good tool for predicting the expression and intensity of different genes of interest in actual experiments. Related Articles | Metrics