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15 June 2018, Volume 13 Issue 6 Previous Issue    Next Issue

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Role of brain-derived neurotrophic factor during the regenerative response after traumatic brain injury in adult zebrafish Pietro Cacialli, Antonio Palladino, Carla Lucini 2018, 13 (6):  941-944.  doi: 10.4103/1673-5374.233430 Abstract ( 142 )   PDF (249KB) ( 276 )   Save Several mammalian animal models of traumatic brain injury have been used, mostly rodents. However, reparative mechanisms in mammalian brain are very limited, and newly formed neurons do not survive for long time. The brain of adult zebrafish, a teleost fish widely used as vertebrate model, possesses high regenerative properties after injury due to the presence of numerous stem cells niches. The ventricular lining of the zebrafish dorsal telencephalon is the most studied neuronal stem cell niche because its dorso-lateral zone is considered the equivalent to the hippocampus of mammals which contains one of the two constitutive neurogenic niches of mammals. To mimic TBI, stab wound in the dorso-lateral telencephalon of zebrafish was used in studies devoted to fish regenerative properties. Brain-derived neurotrophic factor, which is known to play key roles in the repair process after traumatic brain lesions, persists around the lesioned area of injured telencephalon of adult zebrafish. These results are extensively compared to reparative processes in rodent brain. Considering the complete repair of the damaged area in fish, it could be tempting to consider brain-derived neurotrophic factor as a factor contributing to create a permissive environment that enables the establishment of new neuronal population in damaged brain. Related Articles | Metrics

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Neurological complications of hematopoietic cell transplantation in children and adults Adriana Octaviana Dulamea, Ioana Gabriela Lupescu 2018, 13 (6):  945-954.  doi: 10.4103/1673-5374.233431 Abstract ( 139 )   PDF (822KB) ( 250 )   Save Hematopoietic cell transplantation (HCT) is widely performed for neoplastic and non-neoplastic diseases. HCT involves intravenous infusion of hematopoietic progenitor cells from human leukocyte antigen (HLA)-matched donor (allogeneic) or from the patient (autologous). Before HCT, the patient is prepared with high dose chemotherapy and/or radiotherapy to destroy residual malignant cells and to reduce immunologic resistance. After HCT, chemotherapy is used to prevent graft rejection and graft versus host disease (GvHD). Neurological complications are related to the type of HCT, underlying disease, toxicity of the conditioning regimens, immunosuppression caused by conditioning regimens, vascular complications generated by thrombocytopenia and/or coagulopathy, GvHD and inappropriate immune response. In this review, neurological complications are presented according to time of onset after HCT: (1) early complications (in the first month) - related to harvesting of stem cells, during conditioning (drug toxicity, posterior reversible encephalopathy syndrome), related to pancytopenia, (2) intermediate phase complications (second to sixth month) - central nervous system infections caused by prolonged neutropenia and progressive multifocal leukoencephalopathy due to JC virus, (3) late phase complications (after sixth month) - neurological complications of GvHD, second neoplasms and relapses of the original disease. Related Articles | Metrics

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Natural polyphenols effects on protein aggregates in Alzheimer’s and Parkinson’s prion-like diseases Aline Freyssin, Guylène Page, Bernard Fauconneau, Agnès Rioux Bilan 2018, 13 (6):  955-961.  doi: 10.4103/1673-5374.233432 Abstract ( 142 )   PDF (598KB) ( 241 )   Save Alzheimer’s and Parkinson’s diseases are the most common neurodegenerative diseases. They are characterized by protein aggregates and so can be considered as prion-like disease. The major components of these deposits are amyloid peptide and tau for Alzheimer’s disease, α-synuclein and synphilin-1 for Parkinson’s disease. Drugs currently proposed to treat these pathologies do not prevent neurodegenerative processes and are mainly symptomatic therapies. Molecules inducing inhibition of aggregation or disaggregation of these proteins could have beneficial effects, especially if they have other beneficial effects for these diseases. Thus, several natural polyphenols, which have antioxidative, anti-inflammatory and neuroprotective properties, have been largely studied, for their effects on protein aggregates found in these diseases, notably in vitro. In this article, we propose to review the significant papers concerning the role of polyphenols on aggregation and disaggregation of amyloid peptide, tau, α-synuclein, synphilin-1, suggesting that these compounds could be useful in the treatments in Alzheimer’s and Parkinson’s diseases. Related Articles | Metrics

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How random is the random forest ? Random forest algorithm on the service of structural imaging biomarkers for Alzheimer’s disease: from Alzheimer’s disease neuroimaging initiative (ADNI) database Stavros I. Dimitriadis, Dimitris Liparas, for the Alzheimer’s Disease Neuroimaging Initiative 2018, 13 (6):  962-970.  doi: 10.4103/1673-5374.233433 Abstract ( 163 )   PDF (951KB) ( 466 )   Save Neuroinformatics is a fascinating research field that applies computational models and analytical tools to high dimensional experimental neuroscience data for a better understanding of how the brain functions or dysfunctions in brain diseases. Neuroinformaticians work in the intersection of neuroscience and informatics supporting the integration of various sub-disciplines (behavioural neuroscience, genetics, cognitive psychology, etc.) working on brain research. Neuroinformaticians are the pathway of information exchange between informaticians and clinicians for a better understanding of the outcome of computational models and the clinical interpretation of the analysis. Machine learning is one of the most significant computational developments in the last decade giving tools to neuroinformaticians and finally to radiologists and clinicians for an automatic and early diagnosis-prognosis of a brain disease. Random forest (RF) algorithm has been successfully applied to high-dimensional neuroimaging data for feature reduction and also has been applied to classify the clinical label of a subject using single or multi-modal neuroimaging datasets. Our aim was to review the studies where RF was applied to correctly predict the Alzheimer’s disease (AD), the conversion from mild cognitive impairment (MCI) and its robustness to overfitting, outliers and handling of non-linear data. Finally, we described our RF-based model that gave us the 1st position in an international challenge for automated prediction of MCI from MRI data. Related Articles | Metrics

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Protective effects of gonadal hormones on spinal motoneurons following spinal cord injury Dale R. Sengelaub, Xiao-Ming Xu 2018, 13 (6):  971-976.  doi: 10.4103/1673-5374.233434 Abstract ( 167 )   PDF (1062KB) ( 223 )   Save Spinal cord injury (SCI) results in lesions that destroy tissue and disrupt spinal tracts, producing deficits in locomotor and autonomic function. The majority of treatment strategies after SCI have concentrated on the damaged spinal cord, for example working to reduce lesion size or spread, or encouraging regrowth of severed descending axonal projections through the lesion, hoping to re-establish synaptic connectivity with caudal targets. In our work, we have focused on a novel target for treatment after SCI, surviving spinal motoneurons and their target musculature, with the hope of developing effective treatments to preserve or restore lost function following SCI. We previously demonstrated that motoneurons, and the muscles they innervate, show pronounced atrophy after SCI. Importantly, SCI-induced atrophy of motoneuron dendrites can be attenuated by treatment with gonadal hormones, testosterone and its active metabolites, estradiol and dihydrotestosterone. Similarly, SCI-induced reductions in muscle fiber cross-sectional areas can be prevented by treatment with androgens. Together, these findings suggest that regressive changes in motoneuron and muscle morphology seen after SCI can be ameliorated by treatment with gonadal hormones, further supporting a role for steroid hormones as neurotherapeutic agents in the injured nervous system. Related Articles | Metrics

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Role of presynaptic calcium stores for neural network dysfunction in Alzheimer’s disease Chommanad Lerdkrai, Olga Garaschuk 2018, 13 (6):  977-978.  doi: 10.4103/1673-5374.233435 Abstract ( 112 )   PDF (302KB) ( 245 )   Save Alzheimer’s disease (AD) is the most common form of dementia representing a major problem for public health. In 2017 there were an estimated 50 million patients worldwide and this number is expected to almost double every 20 years, reaching 75 million in 2030 and 131.5 million in 2050 (https://www.alz.co.uk/research/statistics). Clinically there are two forms of the disease: the sporadic form (also called late onset AD, LOAD) and the familial form (FAD).LOAD is the most common form. Its prevalence increases with advancing age from 1% in the 65–70 years old cohort to more that 30% after the age of 85. It is characterized by moderate to extreme severity with the advancing age being the main risk factor for LOAD. Familiar AD represents some 5–10% of all AD cases. FAD is linked to mutations in a specific set of genes, most often in the genes encoding amyloid precursor protein (APP) and the presenilins (PS) 1 and 2. Interestingly, the vast majority of AD related mutations are located on PS1 thus identifying this protein as one of the main targets for FAD-modifying therapies. Here we address the role of AD-related presenilin mutations for Ca2+ dyshomeostasis and in vivo neural network dysfunction in AD. Related Articles | Metrics

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Potential utility of aldose reductasedeficient Schwann cells IKARS1 for the study of axonal degeneration and regeneration Naoko Niimi, Kazunori Sango 2018, 13 (6):  979-980.  doi: 10.4103/1673-5374.233436 Abstract ( 126 )   PDF (317KB) ( 190 )   Save Diabetic peripheral neuropathy (DPN) is one of the most common and intractable complications of diabetes mellitus. Its irritating symptoms, such as paresthesia, hyperalgesia and allodynia, can be causes of insomnia and depression; whereas its progression to more advanced stages can result in serious consequences, such as lower limb amputations and lethal arrhythmias. The pathogenesis of DPN remains largely unknown, but long-term exposure to hyperglycemia is likely to play a major role in metabolic and vascular abnormalities in the peripheral nervous system (PNS). In the PNS,blood glucose is transported into the cells in an insulin-independent manner. Under normoglycemic conditions, most of the cellular glucose is converted into pyruvate through the glycolytic pathway, and further metabolized in the cytosol or mitochondria.Under hyperglycemic conditions, however, saturation of the glycolytic pathway and augmentation of glucose flux into the several collateral pathways (e.g., polyol pathway, hexosamine pathway, protein kinase C (PKC) pathway, and advanced glycation endproduct (AGE) pathway) appears to be detrimental to the PNS constituents,in particular, neurons, Schwann cells and blood vessels. Aldose reductase (AR), the first  and rate-limiting enzyme in the polyol pathway, is predominantly localized to Schwann cells in the PNS. AR catalyzes the conversion of glucose to sorbitol using reduced nicotinamide adenine dinucleotide phosphate (NADPH) as a cofactor, and sorbitol dehydrogenase (SDH) catalyzes the conversion of sorbitol to fructose using nicotinamide adenine dinucleotide (NAD+). The enhanced AR activity in Schwann cells under high glucose environments is thought to affect nerve functions through various mechanisms, e.g.,osmotic stress and impaired uptake of myo-inositol and taurine due to sorbitol accumulation, acceleration of AGE synthesis from fructose and its metabolites, and reduced activity of nitric oxide synthase (NOS) and glutathione reductase (GR) due to NADPH consumption by AR. Depletion of nitric oxide resulting from NOS inhibition can be a cause of diminished nerve blood flow, whereas a decrease in reduced glutathione (GSH) levels resulting from GR inhibition can trigger oxidative stress.AR-deficient (AR–/–) mice exhibited no obvious phenotypes in the PNS, and they were protected from diabetes-induced reduction of nerve conduction velocity (NCV) and GSH levels in sciatic nerves. In contrast, transgenic mice overexpressing human AR in Schwann cells displayed more advanced neurological manifestations than non-transgenic littermates under diabetic conditions. These findings support the idea that AR hyperactivity is a major contributing factor in the development and progression of DPN. Related Articles | Metrics

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Promoting functional recovery by inhibition of repulsive guidance molecule-a after spinal cord injury Hiroshi Nakagawa, Masahiko Takada 2018, 13 (6):  981-982.  doi: 10.4103/1673-5374.233437 Abstract ( 128 )   PDF (210KB) ( 387 )   Save Spinal cord injury (SCI) leads to permanent disability with motor and sensory dysfunctions. The mature mammalian central nervous system (CNS) possesses a limited capacity to regenerate/regrow after injury. Research works on functional restoration from SCI via enhanced sprouting of injured/spared fibers based on molecular mechanisms have greatly increased in recent years, especially using small animal models such as anamniotes and rodents. These results allow us to understand the advanced mechanisms of axonal remodeling after SCI. However,for a successful translation of the mechanisms into human patients with SCI, we have to consider certain anatomical and physiological differences in neural circuits between small animals and humans. For example, the corticospinal tract (CST)has been focused as a therapeutic target to enhance motor functions after SCI. The CST fibers originating from the motor cortex directly connect with spinal interneurons and/or motoneurons, to transmit motor commands to them for achieving voluntary movement. Less dexterous animals such as rodents and cats do not physiologically have a direct connectivity of the CST fibers with spinal motoneurons. Thus, it is generally considered that the CST closely relates to the development of manual dexterity through evolution.Recently, at least part of the CST fibers originating from the contralesional primary motor cortex (MI) in a primate SCI model have been reported to extend into the spinal medial gray matter and the motoneuron pool in conjunction with spontaneous recovery from impaired manual dexterity. The relative number of sprouting CST fibers increased in the motoneuron pool as compared to a normal control. However, such an event is not observed in a rodent SCI model. This indicates that the reorganization pattern of CST fibers below the lesioned site in primates differs from that in rodents.To promote axonal sprouting and regrowth as the strategy for functional recovery in human patients with SCI, the CST fibers are needed to extend over a long distance beyond the lesioned site and connect properly with target spinal neurons. For considering such a therapeutic strategy for human patients, it is essential to understand the mechanisms underlying neural network remodeling to achieve functional recovery in primate animals who are characterized by manual dexterity using precision grip. Related Articles | Metrics

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The brain-derived neurotrophic factor in neuronal plasticity and neuroregeneration: new pharmacological concepts for old and new drugs Solomon Habtemariam 2018, 13 (6):  983-984.  doi: 10.4103/1673-5374.233438 Abstract ( 156 )   PDF (315KB) ( 210 )   Save Neurotrophins are peptides or proteins that are known to regulate neuronal viability, development, and function.Beyond synaptic plasticity, neurotrophins protect neurons from apoptosis and also promote neurogenesis to recover neuronal deficit even in adulthood. For various reasons that we have highlighted previously (Habtemariam, 2016a), neuronal cells in the brain are highly susceptible to oxidative stress and hence efficient cell survival mechanisms must be maintained at all times. Many age-related and other neurodegenerative diseases (NDs) in the brain are also associated with excessive oxidative damage resulting from either high production of reactive oxygen species generated by neurotoxic agents (e.g.,amyloid beta (Aβ)) or suppressed level of antioxidant defenses. Our progress in understanding neurotrophins in recent years has now offered more insight into therapeutic options for various NDs where neuroregeneration is considered the best therapeutic approach. This include traumatic brain injury (TBI), Alzheimer’s disease (AD) and Parkinson’s disease (PD), among others. Neurotrophins that have been well-characterised to date include the nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and neurotrophin-4/5 (NT-4/5). Among the neurotrophins,BDNF is the best studied with explosive number of publications appeared in the last decade to establish its functional role in the brain and targeting it to treat for many diseases. Upon binding to its receptor,a signal transduction pathway that is common to the process of cell proliferation promotion and/or inhibition of the apoptosis cascade has been shown to be activated. Not surprisingly, the common mitogen activated protein kinase (MAPK) pathway, particularly the extracellular signal-regulated kinase (ERK) pathway, that regulates cell growth and differentiation is involved. Details of the signal transduction pathway including the ERK, phosphatidylinositide 3-kinase (PI3K) and phosphoinositide phospholipase C-γ (PLCγ) pathway-mediated calcium ion mobilization and cellular events have been illustrated in a review by Numakawa et al. Related Articles | Metrics

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What triggers tauopathy in chronic traumatic encephalopathy? Liam Chen 2018, 13 (6):  985-986.  doi: 10.4103/1673-5374.233439 Abstract ( 109 )   PDF (244KB) ( 260 )   Save Chronic traumatic encephalopathy (CTE) is a neuropathologically defined tauopathy: CTE is closely related with repetitive,traumatic brain injury. In a most recent study of 202 deceased players of American football from a brain donation program,CTE was neuropathologically diagnosed in 177 players across all levels of play (87%), including 110 of 111 former National Football League players (99%) . Consistent with a progressive and neurodegenerative nature, the CTE presentation does not appear until midlife, usually decades after the repetitive brain trauma, and are not simply the aggravation of symptoms from earlier concussions or injuries. At early stage, patient may complain about headache and loss of attention, short-term memory difficulties, depression and impulse control problems. As the disease progresses, symptoms become more severe, with worsening memory impairment, worsening executive dysfunction, language difficulties,and motor disturbance. The patient would become eventually demented and more than 30% patients are suicidal at end stage. As the presentation differs in each individual and most symptoms are rather non-specific, the definitive diagnosis can only be made by postmortem neuropathologic examination. In 2016, the first National Institute of Neurological Disorders and Stroke/National Institute of Biomedical Engineering and Bioengineering (NINDS/NIBIB) consensus meeting defined CTE as a clearly distinct neurodegenerative disease consisting of p-tau aggregates in neurons, astrocytes, and cell processes around small vessels at the depths of the cortical sulci. It is critical to note that the pathognomonic change has only been found in individuals who were exposed to brain trauma, typically multiple episodes. This is important because neuronal and glial tau inclusions are the pathologic hall marker for other major neurodegenerative diseases, including Alzheimer’s disease (AD) and various tauopathies of frontotemporal lobar degeneration (FTLD-tau). Nevertheless, like in AD and primary tauopathies, what triggers the pathological conversion of the physiologically microtubule-associated protein to misfold and aggregate in CTE is still elusive. Related Articles | Metrics

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A time for cocktails and inclusion Shenandoah Robinson, Frances J. Northington, Lauren L. Jantzie 2018, 13 (6):  987-988.  doi: 10.4103/1673-5374.233440 Abstract ( 109 )   PDF (206KB) ( 240 )   Save Perinatal brain injury (PBI) is one of the most important causes of lifelong deficits in cognition, behavior, social interaction and motor skills, as well as epilepsy. PBI encompasses, but is not limited to, hypoxic-ischemic encephalopathy (HIE), intraventricular hemorrhage, periventricular leukomalacia and encephalopathy of prematurity. PBI affects both preterm and term neonates and is a reflection of diverse and complex etiologies and initiating insults,including prenatal genetic and environmental contributions, sentinel obstetrical and perinatal events, and drug exposures. Additionally, consequences of other illnesses and events such as neonatal sepsis, cardiac defects and infantile traumatic brain injury can result in central nervous system (CNS) damage that contributes to PBI. Thus, a large majority of infants who suffer PBI experience a complex blend of CNS insults that impact multiple molecular, cellular, microstructural and ultrastructural pathophysiological mechanisms and result in cumulative deficits. Related Articles | Metrics

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Puerarin protects rat brain against ischemia/ reperfusion injury by suppressing autophagy via the AMPK-mTOR-ULK1 signaling pathwa Jin-Feng Wang, Zhi-Gang Mei, Yang Fu, Song-Bai Yang, Shi-Zhong Zhang, Wei-Feng Huang, Li Xiong, Hua-Jun Zhou, Wei Tao, Zhi-Tao Feng 2018, 13 (6):  989-998.  doi: 10.4103/1673-5374.233441 Abstract ( 231 )   PDF (2719KB) ( 396 )   Save Puerarin suppresses autophagy to alleviate cerebral ischemia/reperfusion injury, and accumulating evidence indicates that the AMPKmTOR signaling pathway regulates the activation of the autophagy pathway through the coordinated phosphorylation of ULK1. In this study, we investigated the mechanisms underlying the neuroprotective effect of puerarin and its role in modulating autophagy via the AMPK-mTOR-ULK1 signaling pathway in the rat middle cerebral artery occlusion model of cerebral ischemia/reperfusion injury. Rats were intraperitoneally injected with puerarin, 50 or 100 mg/kg, daily for 7 days. Then, 30 minutes after the final administration, rats were subjected to transient middle cerebral artery occlusion for 90 minutes. Then, after 24 hours of reperfusion, the Longa score and infarct volume were evaluated in each group. Autophagosome formation was observed by transmission electron microscopy. LC3, Beclin-1 p62,AMPK, mTOR and ULK1 protein expression levels were examined by immunofluorescence and western blot assay. Puerarin substantially reduced the Longa score and infarct volume, and it lessened autophagosome formation in the hippocampal CA1 area following cerebral ischemia/reperfusion injury in a dose-dependent manner. Pretreatment with puerarin (50 or 100 mg/kg) reduced Beclin-1 expression and the LC3-II/LC3-I ratio, as well as p-AMPK and pS317-ULK1 levels. In comparison, it increased p62 expression. Furthermore, puerarin at 100 mg/kg dramatically increased the levels of p-mTOR and pS757-ULK1 in the hippocampus on the ischemic side. Our findings suggest that puerarin alleviates autophagy by activating the APMK-mTOR-ULK1 signaling pathway. Thus, puerarin might have therapeutic potential for treating cerebral ischemia/reperfusion injury. Related Articles | Metrics

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The intra-neuroendoscopic technique: a new method for rapid removal of acute severe intraventricular hematoma Bo Du, Ai-Jun Shan, Yu-Juan Zhang, Jin Wang, Kai-Wen Peng, Xian-Liang Zhong, Yu-Ping Peng 2018, 13 (6):  999-1006.  doi: 10.4103/1673-5374.233442 Abstract ( 185 )   PDF (1314KB) ( 255 )   Save The mortality rate of acute severe intraventricular hematoma is extremely high, and the rate of disability in survivors is high. Intraventricular hematoma has always been a difficult problem for clinical treatment. Although minimally invasive endoscopic hematoma evacuation is widely used to treat this disease, the technique still has room for improvement. Equipment for the intra-neuroendoscopic technique (INET) consists of two of our patented inventions: a transparent sheath (Patent No. ZL 200820046232.0) and a hematoma aspirator (Patent No. ZL 201520248717.8). This study explored the safety and efficacy of INET by comparing it with extraventricular drainage in combination with urokinase thrombolytic therapy. This trial recruited 65 patients with severe intraventricular hemorrhage, including 35 (19 men and 16 women, aged 53.2 ± 8.7 years) in the INET group and 30 (17 men and 13 women, aged 51.5 ± 7.9 years) in the control group (extraventricular drainage plus urokinase thrombolytic therapy). Our results showed that compared with the control group, the INET group exhibited lower intraventricular hemorrhage volumes, shorter intensive care-unit monitoring and ventricular drainage-tube placement times, and fewer incidences of intracranial infection, secondary bleeding, and mortality. Thus, the prognosis of survivors had improved remarkably. These findings indicate that INET is a safe and efficient new method for treating severe intraventricular hematoma. This trial was registered with ClinicalTrials.gov (NCT02515903). Related Articles | Metrics

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Enhancement of matrix metalloproteinases 2 and 9 accompanied with neurogenesis following collagen glycosaminoglycan matrix implantation after surgical brain injury Wei-Cherng Hsu, Chun-Hsien Yu, Woon-Man Kung, Kuo-Feng Huang 2018, 13 (6):  1007-1012.  doi: 10.4103/1673-5374.233443 Abstract ( 123 )   PDF (3271KB) ( 224 )   Save Surgical brain injury may result in irreversible neurological deficits. Our previous report showed that partial regeneration of a traumatic brain lesion is achieved by implantation of collagen glycosaminoglycan (CGM). Matrix metalloproteinases (MMPs) may play an important role in neurogenesis but there is currently a lack of studies displaying the relationship between the stimulation of MMPs and neurogenesis after collagen glycosaminoglycan implantation following surgical brain trauma. The present study was carried out to further examine the expression of MMP2 and MMP9 after implantation of collagen glycosaminoglycan (CGM) following surgical brain trauma. Using the animal model of surgically induced brain lesion,we implanted CGM into the surgical trauma. Rats were thus divided into three groups: (1) sham operation group: craniotomy only; (2) lesion (L) group: craniotomy + surgical trauma lesion; (3) lesion + CGM (L +CGM) group: CGM implanted following craniotomy and surgical trauma lesion. Cells positive for SOX2 (marker of proliferating neural progenitor cells) and matrix metalloproteinases (MMP2 and MMP9) in the lesion boundary zone were assayed and analyzed by immunofluorescence and ELISA commercial kits,respectively. Our results demonstrated that following implantation of CGM after surgical brain trauma,significant increases in MMP2+/SOX2+ cells and MMP9+/SOX2+ cells were seen within the lesion boundary zone in the L + CGM group. Tissue protein concentrations of MMP2 and MMP9 also increased after CGM scaffold implantation. These findings suggest that implantation of a CGM scaffold alone after surgical brain trauma can enhance the expression of MMP2 and MMP9 accompanied by neurogenesis. Related Articles | Metrics

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Catgut implantation at acupoints increases the expression of glutamate aspartate transporter and glial glutamate transporter-1 in the brain of rats with spasticity after stroke Rui-Qing Li, Ming-Yue Wan, Jing Shi, Hui-Ling Wang, Fei-Lai Liu, Cheng-Mei Liu, Jin Huang, Ren-Chao Liu, Le Ma, Xiao-Dong Feng 2018, 13 (6):  1013-1018.  doi: 10.4103/1673-5374.233444 Abstract ( 128 )   PDF (549KB) ( 226 )   Save Catgut implantation at acupoints has been shown to alleviate spasticity after stroke in rats. However, the underlying mechanisms are poorly understood. In this study, we used the rat middle cerebral artery occlusion model of stroke. Three days after surgery, absorbable surgical catgut sutures were implanted at Dazhui (GV14), Jizhong (GV6), Houhui, Guanyuan (CV4) and Zhongwan (CV12). The Zea Longa score was used to assess neurological function. The Modified Ashworth Scale was used to evaluate muscle tension. The 2,3,5-triphenyl-tetrazolium chloride assay was used to measure infarct volume. Immunohistochemical staining was performed for glutamate aspartate transporter (GLAST) and glial glutamate transporter-1 (GLT-1) expression. Western blot assay was used to analyze the expression of GLAST and GLT-1. Reverse transcription and polymerase chain reaction were carried out to assess the expression of GLAST and GLT-1 mRNAs. After catgut implantation at the acupoints, neurological function was substantially improved, muscle tension was decreased, and infarct volume was reduced in rats with spasticity after stroke. Furthermore, the expression of GLAST and GLT-1 mRNAs was increased on the injured (left) side. Our findings demonstrate that catgut implantation at acupoints alleviates spasticity after stroke, likely by increasing the expression of GLAST and GLT-1. Related Articles | Metrics

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Synaptic aging disrupts synaptic morphology and function in cerebellar Purkinje cells Wen-Juan Fan, Ming-Chao Yan, Lai Wang, Yi-Zheng Sun, Jin-Bo Deng, Jie-Xin Deng 2018, 13 (6):  1019-1025.  doi: 10.4103/1673-5374.233445 Abstract ( 262 )   PDF (3663KB) ( 333 )   Save Synapses are key structures in neural networks, and are involved in learning and memory in the central nervous system. Investigating synaptogenesis and synaptic aging is important in understanding neural development and neural degeneration in diseases such as Alzheimer disease and Parkinson’s disease. Our previous study found that synaptogenesis and synaptic maturation were harmonized with brain development and maturation. However, synaptic damage and loss in the aging cerebellum are not well understood. This study was designed to investigate the occurrence of synaptic aging in the cerebellum by observing the ultrastructural changes of dendritic spines and synapses in cerebellar Purkinje cells of aging mice. Immunocytochemistry, DiI diolistic assays, and transmission electron microscopy were used to visualize the morphological characteristics of synaptic buttons, dendritic spines and synapses of Purkinje cells in mice at various ages.With synaptic aging in the cerebellum, dendritic spines and synaptic buttons were lost, and the synaptic ultrastructure was altered, including a reduction in the number of synaptic vesicles and mitochondria in presynaptic termini and smaller thin specialized zones in pre- and post-synaptic membranes. These findings confirm that synaptic morphology and function is disrupted in aging synapses, which may be an important pathological cause of neurodegenerative diseases. Related Articles | Metrics

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Quantitative evaluation of extrinsic factors influencing electrical excitability in neuronal networks: Voltage Threshold Measurement Method (VTMM) Shuai An, Yong-Fang Zhao, Xiao-Ying Lü, Zhi-Gong Wang 2018, 13 (6):  1026-1035.  doi: 10.4103/1673-5374.233446 Abstract ( 148 )   PDF (1656KB) ( 244 )   Save The electrical excitability of neural networks is influenced by different environmental factors. Effective and simple methods are required to objectively and quantitatively evaluate the influence of such factors, including variations in temperature and pharmaceutical dosage. The aim of this paper was to introduce ‘the voltage threshold measurement method’, which is a new method using microelectrode arrays that can quantitatively evaluate the influence of different factors on the electrical excitability of neural networks. We sought to verify the feasibility and efficacy of the method by studying the effects of acetylcholine, ethanol, and temperature on hippocampal neuronal networks and hippocampal brain slices. First, we determined the voltage of the stimulation pulse signal that elicited action potentials in the two types of neural networks under normal conditions. Second, we obtained the voltage thresholds for the two types of neural networks under different concentrations of acetylcholine, ethanol, and different temperatures. Finally, we obtained the relationship between voltage threshold and the three influential factors. Our results indicated that the normal voltage thresholds of the hippocampal neuronal network and hippocampal slice preparation were 56 and 31 mV, respectively. The voltage thresholds of the two types of neural networks were inversely proportional to acetylcholine concentration, and had an exponential dependency on ethanol concentration. The curves of the voltage threshold and the temperature of the medium for the two types of neural networks were U-shaped. The hippocampal neuronal network and hippocampal slice preparations lost their excitability when the temperature of the medium decreased below 34 and 33°C or increased above 42 and 43°C, respectively. These results demonstrate that the voltage threshold measurement method is effective and simple for examining the performance/excitability of neuronal networks. Related Articles | Metrics

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Retinoid X receptor α downregulation is required for tail and caudal spinal cord regeneration in the adult newt Sarah E. Walker, Rachel Nottrodt, Lucas Maddalena, Christopher Carter, Gaynor E. Spencer, Robert L. Carlone 2018, 13 (6):  1036-1045.  doi: 10.4103/1673-5374.233447 Abstract ( 131 )   PDF (3155KB) ( 214 )   Save Some adult vertebrate species, such as newts, axolotls and zebrafish, have the ability to regenerate their central nervous system (CNS). However, the factors that establish a permissive CNS environment for correct morphological and functional regeneration in these species are not well understood. Recent evidence supports a role for retinoid signaling in the intrinsic ability of neurons, in these regeneration-competent species, to regrow after CNS injury. Previously, we demonstrated that a specific retinoic acid receptor (RAR) subtype, RARβ, mediates the effects of endogenous retinoic acid (RA) on neuronal growth and guidance in the adult newt CNS after injury. Here, we now examine the expression of the retinoid X receptor RXRα (a potential heterodimeric transcriptional regulator with RARβ), in newt tail and spinal cord regeneration. We show that at 21 days post-amputation (dpa), RXRα is expressed at temporally distinct periods and in non-overlapping spatial domains compared to RARβ. Whereas RARβ protein levels increase, RXRα proteins level decrease by 21 dpa. A selective agonist for RXR, SR11237, prevents both this downregulation of RXRα and upregulation of RARβ and inhibits tail and caudal spinal cord regeneration. Moreover, treatment with a selective antagonist for RARβ, LE135, inhibits regeneration with the same morphological consequences as treatment with SR11237. Interestingly, LE135 treatment also inhibits the normal downregulation of RXRα in tail and spinal cord tissues at 21 dpa. These results reveal a previously unidentified, indirect regulatory feedback loop between these two receptor subtypes in regulating the regeneration of tail and spinal cord tissues in this regeneration-competent newt. Related Articles | Metrics

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Injection of bone marrow mesenchymal stem cells by intravenous or intraperitoneal routes is a viable alternative to spinal cord injury treatment in mice Bruna dos Santos Ramalho, Fernanda Martins de Almeida, Conrado Mendonça Sales, Silmara de Lima, Ana Maria Blanco Martinez 2018, 13 (6):  1046-1053.  doi: 10.4103/1673-5374.233448 Abstract ( 257 )   PDF (4021KB) ( 295 )   Save In spite of advances in surgical care and rehabilitation, the consequences of spinal cord injury (SCI) are still challenging. Several experimental therapeutic strategies have been studied in the SCI field, and recent advances have led to the development of therapies that may act on the inhibitory microenvironment. Assorted lineages of stem cells are considered a good treatment for SCI. This study investigated the effect of systemic transplantation of mesenchymal stem cells (MSCs) in a compressive SCI model. Here we present results of the intraperitoneal route, which has not been used previously for MSC administration after compressive SCI. We used adult female C57BL/6 mice that underwent laminectomy at the T9 level, followed by spinal cord compression for 1 minute with a 30-g vascular clip. The animals were divided into five groups:sham (anesthesia and laminectomy but without compression injury induction), MSC i.p. (intraperitoneal injection of 8 × 105 MSCs in 500 μL of DMEM at 7 days after SCI), MSC i.v. (intravenous injection of 8× 105 MSCs in 500 μL of DMEM at 7 days after SCI), DMEM i.p. (intraperitoneal injection of 500 μL of DMEM at 7 days after SCI), DMEM i.v. (intravenous injection of 500 μL of DMEM at 7 days after SCI). The effects of MSCs transplantation in white matter sparing were analyzed by luxol fast blue staining. The number of preserved fibers was counted in semithin sections stained with toluidine blue and the presence of trophic factors was analyzed by immunohistochemistry. In addition, we analyzed the locomotor performance with Basso Mouse Scale and Global Mobility Test. Our results showed white matter preservation and a larger number of preserved fibers in the MSC groups than in the DMEM groups. Furthermore, the MSC groups had higher levels of trophic factors (brain-derived neurotrophic factor, nerve growth factor,neurotrophin-3 and neurotrophin-4) in the spinal cord and improved locomotor performance. Our results indicate that injection of MSCs by either intraperitoneal or intravenous routes results in beneficial outcomes and can be elected as a choice for SCI treatment. Related Articles | Metrics

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Local injection of bone morphogenetic protein 7 promotes neuronal regeneration and motor function recovery after acute spinal cord injury Chen Chen, Guang-Chao Bai, Hong-Liang Jin, Kun Lei, Kuan-Xin Li 2018, 13 (6):  1054-1060.  doi: 10.4103/1673-5374.233449 Abstract ( 120 )   PDF (550KB) ( 221 )   Save After spinal cord injury, the number of glial cells and motor neurons expressing bone morphogenetic protein 7 (BMP7) increases, indicating that upregulation of BMP7 can promote nerve repair. We, therefore, tested whether direct injection of BMP7 into acutely injured rat spinal cord can affect neurological recovery. Allen’s impactor was used to create spinal cord injury at T10. The injury site was then injected with 50 ng BMP7 (BMP7 group) or physiological saline (control group) for 7 consecutive days. Electrophysiological examination showed that the amplitude of N1 in motor evoked potentials (MEP) decreased after spinal cord injury. At 8 weeks post-operation, the amplitude of N1 in the BMP7 group was remarkably higher than that at 1 week post-operation and was higher than that of the control group. Basso, Beattie,Bresnahan scale (BBB) scores, hematoxylin-eosin staining, and western blot assay showed that at 1, 2, 4 and 8 weeks post-operation,BBB scores were increased; Nissl body staining was stronger; the number of Nissl-stained bodies was increased; the number of vacuoles gradually decreased; the number of synapses was increased; and the expression of neuronal marker, neurofilament protein 200, was increased in the hind limbs of the BMP7 group compared with the control group. Western blot assay showed that the expression of GFAP protein in BMP7 group and control group did not change significantly and there was no significant difference between the BMP7 and control groups. These data confirmed that local injection of BMP7 can promote neuronal regeneration after spinal cord injury and promote recovery of motor function in rats. Related Articles | Metrics

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Small-worldness of brain networks after brachial plexus injury: a resting-state functional magnetic resonance imaging study Wei-Wei Wang, Ye-Chen Lu, Wei-Jun Tang, Jun-Hai Zhang, Hua-Ping Sun, Xiao-Yuan Feng, Han-Qiu Liu 2018, 13 (6):  1061-1065.  doi: 10.4103/1673-5374.233450 Abstract ( 160 )   PDF (425KB) ( 302 )   Save Research on brain function after brachial plexus injury focuses on local cortical functional reorganization, and few studies have focused on brain networks after brachial plexus injury. Changes in brain networks may help understanding of brain plasticity at the global level. We hypothesized that topology of the global cerebral resting-state functional network changes after unilateral brachial plexus injury. Thus, in this cross-sectional study, we recruited eight male patients with unilateral brachial plexus injury (right handedness, mean age of 27.9 ± 5.4 years old) and eight male healthy controls (right handedness, mean age of 28.6 ± 3.2). After acquiring and preprocessing resting-state magnetic resonance imaging data, the cerebrum was divided into 90 regions and Pearson’s correlation coefficient calculated between regions.These correlation matrices were then converted into a binary matrix with affixed sparsity values of 0.1–0.46. Under sparsity conditions,both groups satisfied this small-world property. The clustering coefficient was markedly lower, while average shortest path remarkably higher in patients compared with healthy controls. These findings confirm that cerebral functional networks in patients still show smallworld characteristics, which are highly effective in information transmission in the brain, as well as normal controls. Alternatively, varied small-worldness suggests that capacity of information transmission and integration in different brain regions in brachial plexus injury patients is damaged. Related Articles | Metrics

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Amyloid-beta-dependent phosphorylation of collapsin response mediator protein-2 dissociates kinesin in Alzheimer’s disease Sara H. Mokhtar, Min Joung Kim, Kylie A. Magee, Pei Mun Aui, Speros Thomas, Maha M. Bakhuraysah, Amani A. Alrehaili1, Jae Young Lee1, David L. Steer, Rachel Kenny, Catriona McLean, Michael F. Azari, Antonis Birpanagos, Ewlina Lipiec, Philip Heraud, Bayden Wood, Steven Petratos 2018, 13 (6):  1066-1080.  doi: 10.4103/1673-5374.233451 Abstract ( 183 )   PDF (6209KB) ( 336 )   Save Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by accumulation of amyloid plaques and neurofibrillary tangles. Prior to the development of these characteristic pathological hallmarks of AD, anterograde axonal transport is impaired. However, the key proteins that initiate these intracellular impairments remain elusive. The collapsin response mediator protein-2 (CRMP-2) plays an integral role in kinesin-1-dependent axonal transport and there is evidence that phosphorylation of CRMP-2 releases kinesin-1. Here, we tested the hypothesis that amyloid-beta (Aβ)-dependent phosphorylation of CRMP-2 disrupts its association with the kinesin-1 (an anterograde axonal motor transport protein) in AD. We found that brain sections and lysates from AD patients demonstrated elevated phosphorylation of CRMP-2 at the T555 site. Additionally, in the transgenic Tg2576 mouse model of familial AD (FAD) that exhibits Aβ accumulation in the brain with age, we found substantial co-localization of pT555CRMP-2 and dystrophic neurites. In SH-SY5Y differentiated neuronal cultures, Aβ-dependent phosphorylation of CRMP-2 at the T555 site was also elevated and this reduced the CRMP-2 association with kinesin-1. The overexpression of an unphosphorylatable form of CRMP-2 in neurons promoted the re-establishment of CRMP-2-kinesin association and axon elongation. These data suggest that Aβ-dependent phosphorylation of CRMP-2 at the T555 site may directly impair anterograde axonal transport protein function, leading to neuronal defects. Related Articles | Metrics

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Astragaloside IV protects RGC-5 cells against oxidative stress Ming Hao, Yu Liu, Ping Chen, Hong Jiang, Hong-Yu Kuang 2018, 13 (6):  1081-1086.  doi: 10.4103/1673-5374.233452 Abstract ( 207 )   PDF (697KB) ( 237 )   Save Astragaloside IV is the main active compound of Astragalus membranaceus. Astragaloside IV has strong anti-oxidative activities and protective effects against progression of peripheral neuropathy. In this study, we determined whether astragaloside IV protects retinal ganglion cells (RGC) from oxidative stress injury using the rat RGC-5 cell line. Hydrogen peroxide (H2O2) was used to induce oxidative stress injury, with the protective effect of astragaloside IV examined. Cell Counting Kit-8 and 4′,6-diamidino-2-phenylindole staining showed that astragaloside IV increased cell survival rate and decreased apoptotic cell number. Flow cytometry showed that astragaloside IV decreased H2O2-induced reactive oxygen species levels. While laser confocal microscopy showed that astragaloside IV inhibited the H2O2-induced decrease of mitochondrial membrane potential. Western blot assay showed that astragaloside IV reduced cytochrome c release induced by H2O2, inhibited Bax and caspase-3 expression, and increased Bcl-2 expression. Altogether, these results indicate that astragaloside IV has potential protective effects against H2O2-induced oxidative stress in retinal ganglion cells. Related Articles | Metrics

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Efficacy of epalrestat plus α-lipoic acid combination therapy versus monotherapy in patients with diabetic peripheral neuropathy: a meta-analysis of 20 randomized controlled trials Ming Zhao, Jia-Yi Chen, Yu-Dong Chu, Ya-Bin Zhu, Lin Luo, Shi-Zhong Bu 2018, 13 (6):  1087-1095.  doi: 10.4103/1673-5374.233453 Abstract ( 177 )   PDF (1359KB) ( 258 )   Save OBJECTIVE: To evaluate the efficacy of α-lipoic acid (ALA) plus epalrestat combination therapy in the treatment of diabetic peripheral neuropathy (DPN). DATA SOURCES: The electronic databases of PubMed, Medline, Embase, the Cochrane Library, the Chinese National Knowledge Infrastructure, the Wanfang Database and the Chinese Biomedical Database were used to retrieve relevant studies without language restrictions. The search was conducted from the inception of each database to 7 October 2016. The key terms were (diabetic peripheral neuropathy or diabetic neuropathy or DPN) AND (α-lipoic acid or lipoic acid or thioctic acid) AND epalrestat. DATA SELECTION: All of the eligible studies met the following inclusion criteria: (1) Randomized controlled trials that compared efficacy and safety of epalrestat plus ALA combination therapy versus epalrestat or ALA monotherapy in patients with DPN. (2) The minimum duration of treatment was 2 weeks. (3) The  DPN patients were diagnosed using the World Health Organization standardized type 2 diabetes mellitus and DPN criteria. (4) Studies contained at least one measure that could reflect the efficacy of the drug and nerve conduction velocities. Studies in which the control group used epalrestat or ALA combined with other drugs were excluded. Statistical analyses were performed using STATA software for meta-analysis. OUTCOME MEASURES: The primary outcomes were the therapeutic efficacy, median motor nerve conduction velocity (MNCV), median sensory nerve conduction velocity (SNCV), peroneal MNCV and peroneal SNCV. RESULTS: Twenty studies with 1 894 DPN patients were included, including 864 patients in the ALA plus epalrestat group, 473 in the ALA group and 557 in the epalrestat group. The efficacy of ALA plus epalrestat combination therapy was superior to ALA and epalrestat monotherapies (RR = 1.29, 95% CI: 1.21–1.38;RR = 1.43, 95% CI: 1.34–1.54, respectively). ALA plus epalrestat combination therapy also significantly improved median MNCV (WMD = 5.41, 95% CI: 2.07–8.75), median SNCV (WMD = 5.87, 95% CI: 1.52–10.22), peroneal MNCV (WMD = 5.59, 95% CI: 2.70–8.47) and peroneal SNCV (WMD = 4.57, 95% CI: 2.46–6.68). CONCLUSION: ALA plus epalrestat combination therapy was superior to ALA and epalrestat monotherapies for clinical efficacy and nerve conduction velocities in patients with DPN. Related Articles | Metrics

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Myelotomy promotes locomotor recovery in rats subjected to spinal cord injury: a meta-analysis of six randomized controlled trials Chuan Qin, Wen-Hao Zhang, De-Gang Yang, Ming-Liang Yang, Liang-Jie Du, Jian-Jun Li 2018, 13 (6):  1096-1106.  doi: 10.4103/1673-5374.233454 Abstract ( 114 )   PDF (619KB) ( 246 )   Save OBJECTIVE: To investigate the effects of myelotomy on locomotor recovery in rats subjected to spinal cord injury. DATA SOURCES: Electronic databases including PubMed, Science Citation Index, Cochrane Library,China National Knowledge Infrastructure, Chinese Journals Full-text Database, China Biology Medicine disc, and Wanfang Database were searched to retrieve related studies published before September 2017.The MeSH terms (the Medical Subject Headings) such as “myelotomy”, “spinal cord injuries”, “rats”, “randomized controlled trial” and all related entry terms were searched. DATA SELECTION: Randomized controlled trials using myelotomy for the treatment of acute spinal cord injury in rats were included. Basso, Beattie, and Bresnahan scores were adopted as the evaluation method.RevMan Software (version 5.3) was used for data processing. The χ2 and I2 tests were used to assess heterogeneity.Using a random-effects model, a subgroup analysis was conducted to analyze the source of the heterogeneity. OUTCOME MEASURES: Basso, Beattie, and Bresnahan scores were observed 1–6 weeks after spinal cord injury. RESULTS: Six animal trials were included, using a total of 143 lab rats. The included trials were divided into two subgroups by injury degrees (moderate or severe). The pooled results showed that, 1–6 weeks after spinal cord injury, the overall Basso, Beattie, and Bresnahan score was significantly higher in the myelotomy group than in the contusion group (weighted mean difference (WMD) = 0.60; 95% confidence interval(CI): 0.23–0.97; P = 0.001; WMD = 2.10; 95% CI: 1.56–2.64; P < 0.001; WMD = 2.65; 95% CI: 1.73–3.57; P < 0.001; WMD = 1.66; 95% CI: 0.80–2.52; P < 0.001; WMD = 2.09; 95% CI: 0.92–3.26, P < 0.001; WMD = 2.25; 95% CI: 1.06–3.44, P < 0.001). The overall heterogeneity was high (I2 = 85%; I2 = 95%; I2 = 94%; I2 = 88%; I2 = 91%; I2 = 89%). The results in the moderate injury subgroup showed that Basso, Beattie, and Bresnahan scores were significantly higher in the myelotomy group than in the contusion group (WMD = 0.91, 95% CI: 0.52–1.3, P < 0.001; WMD = 2.10; 95% CI: 1.56–2.64, P < 0.001; WMD = 2.65; 95% CI: 1.73–3.57, P < 0.001; WMD = 2.50, 95% CI: 1.72–3.28, P < 0.001; WMD = 3.29, 95% CI: 2.21–4.38, P < 0.001; WMD = 3.27; 95% CI: 2.31–4.23, P < 0.001). The relevant heterogeneity was low. However, there were no significant differences in Basso, Beattie, and Bresnahan scores between the myelotomy and contusion groups in the severe injury subgroup at 2 and 3 weeks after the injury (P = 0.75; P = 0.92). CONCLUSION: To date, this is the first attempt to summarize the potential effect of myelotomy on locomotor recovery in rats with spinal cord injury. Our findings conclude that myelotomy promotes locomotor recovery in rats with spinal cord injury, especially in those with moderate injury. Related Articles | Metrics

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Acupuncture for cerebral palsy: a meta-analysis of randomized controlled trials Ling-Xin Li, Ming-Ming Zhang, Yin Zhang, Jing He 2018, 13 (6):  1107-1117.  doi: 10.4103/1673-5374.233455 Abstract ( 162 )   PDF (417KB) ( 293 )   Save OBJECTIVE: To evaluate the efficacy and safety of acupuncture therapy for children with cerebral palsy. DATA SOURCES: We conducted electronic searches of PUBMED (1950/2017), EMBASE (1974/2017), ScienceDirect (1986/2017), Academic Source Premier (1887/2017), the Cochrane Library (Issue 4, April 2017), Science Citation Index Expanded (1900/2017), China National Knowledge Infrastructure (1915/2017), China Biological Medicine (1990/2017-04), WanFang (1980/2017), VIP (1989/2017), and Chinese Science Citation Database (1989/2017). DATA SELECTION: We included randomized controlled trials that aimed to compare the effect of acupuncture plus rehabilitation training versus rehabilitation training alone. Data about functional motor abilities, daily activity/social participation, effective rate, intellectual development, and adverse effects were included. We used Revman 5.2 software for statistical analysis. OUTCOME MEASURES: The primary outcomes included functional motor abilities, daily activity, and effective rate. The secondary outcomes included intellectual development and adverse effects. RESULTS: Twenty-one studies with a total of 1 718 participants met the inclusion criteria. The effect size of gross motor function (SMD = 0.64, 95% CI: 0.52 to 0.76, P < 0.00001;  I2 = 0%, P = 0.69; in 13 studies with 1 144 patients) and the total effective rate (RR = 1.28, 95% CI: 1.20 to 1.37, P < 0.00001;  I2 = 18%, P = 0.27; in 12 studies with 1 106 patients) suggested that acupuncture plus rehabilitation produced a significant improvement in gross motor function and a high total effective rate. The pooled fine motor function (SMD = 3.48, 95% CI: 2.62 to 4.34, P < 0.00001;  I2 = 64%, P = 0.10; in 2 studies with 193 patients), modified Ashworth scale scores (SMD = –0.31, 95% CI: –0.52 to –0.11, P = 0.003;  I2 = 74%, P = 0.004; in 5 studies with 363 patients) and activities of daily living (SMD = 1.45, 95% CI: 1.20 to 1.71, P < 0.00001; I2 = 78%, P = 0.004; in 4 studies with 313 patients) also indicated improvements in children with cerebral palsy. Publication bias was not observed. Only mild adverse events related to acupuncture were reported. CONCLUSION: Acupuncture plus rehabilitation training improved gross motor function, reduced muscle spasms, and enhanced daily life activities in children with cerebral palsy. However, this conclusion should be interpreted with caution due to the small number of randomized controlled trials available and the small sample sizes. More high-quality and large-scale studies are needed. Related Articles | Metrics

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Injury of thalamocortical connection between the mediodorsal nucleus of the thalamus and the orbitofrontal cortex in a patient with traumatic brain injury Sung Ho Jang, Seong Ho Kim, Sang Seok Yeo 2018, 13 (6):  1118-1120.  doi: 10.4103/1673-5374.233456 Abstract ( 152 )   PDF (429KB) ( 177 )   Save The prefrontal cortex (PFC) is responsible for personality expression and various cognitive functions, including working memory, recognition memory, decision making, attention, and motivation. Anatomical tract-tracing studies have demonstrated that the PFC receives many afferent fibers from the mediodorsal nucleus (MD) of the thalamus through the thalamocortical connection . Related Articles | Metrics