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https://www.readbyqxmd.com/read/28447605/traumatic-spinal-cord-injury
#1
REVIEW
Christopher S Ahuja, Jefferson R Wilson, Satoshi Nori, Mark R N Kotter, Claudia Druschel, Armin Curt, Michael G Fehlings
Traumatic spinal cord injury (SCI) has devastating consequences for the physical, social and vocational well-being of patients. The demographic of SCIs is shifting such that an increasing proportion of older individuals are being affected. Pathophysiologically, the initial mechanical trauma (the primary injury) permeabilizes neurons and glia and initiates a secondary injury cascade that leads to progressive cell death and spinal cord damage over the subsequent weeks. Over time, the lesion remodels and is composed of cystic cavitations and a glial scar, both of which potently inhibit regeneration...
April 27, 2017: Nature Reviews. Disease Primers
https://www.readbyqxmd.com/read/28445478/delayed-histochemical-alterations-within-the-neurovascular-unit-due-to-transient-focal-cerebral-ischemia-and-experimental-treatment-with-neurotrophic-factors
#2
Dominik Michalski, Roman Pitsch, Deepu R Pillai, Bianca Mages, Susanne Aleithe, Jens Grosche, Henrik Martens, Felix Schlachetzki, Wolfgang Härtig
Current stroke therapy is focused on recanalizing strategies, but neuroprotective co-treatments are still lacking. Modern concepts of the ischemia-affected neurovascular unit (NVU) and surrounding penumbra emphasize the complexity during the transition from initial damaging to regenerative processes. While early treatment with neurotrophic factors was shown to result in lesion size reduction and blood-brain barrier (BBB) stabilization, cellular consequences from these treatments are poorly understood. This study explored delayed cellular responses not only to ischemic stroke, but also to an early treatment with neurotrophic factors...
2017: PloS One
https://www.readbyqxmd.com/read/28420961/the-role-of-astrocytes-in-neuroprotection-after-brain-stroke-potential-in-cell-therapy
#3
REVIEW
Andrea Becerra-Calixto, Gloria P Cardona-Gómez
Astrocytes are commonly involved in negative responses through their hyperreactivity and glial scar formation in excitotoxic and/or mechanical injuries. But, astrocytes are also specialized glial cells of the nervous system that perform multiple homeostatic functions for the survival and maintenance of the neurovascular unit. Astrocytes have neuroprotective, angiogenic, immunomodulatory, neurogenic, and antioxidant properties and modulate synaptic function. This makes them excellent candidates as a source of neuroprotection and neurorestoration in tissues affected by ischemia/reperfusion, when some of their deregulated genes can be controlled...
2017: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/28396199/hypoxia-response-element-regulated-mmp-9-promotes-neurological-recovery-via-glial-scar-degradation-and-angiogenesis-in-delayed-stroke
#4
Hongxia Cai, Yuanyuan Ma, Lu Jiang, Zhihao Mu, Zhen Jiang, Xiaoyan Chen, Yongting Wang, Guo-Yuan Yang, Zhijun Zhang
Matrix metalloproteinase 9 (MMP-9) plays a beneficial role in the delayed phase of middle cerebral artery occlusion (MCAO). However, the mechanism is obscure. Here, we constructed hypoxia response element (HRE)-regulated MMP-9 to explore its effect on glial scars and neurogenesis in delayed ischemic stroke. Adult male Institute of Cancer Research (ICR) mice underwent MCAO and received a stereotactic injection of lentivirus carrying HRE-MMP-9 or normal saline (NS)/lentivirus-GFP 7 days after ischemia. We found that HRE-MMP-9 improved neurological outcomes, reduced ischemia-induced brain atrophy, and degraded glial scars (p < 0...
April 7, 2017: Molecular Therapy: the Journal of the American Society of Gene Therapy
https://www.readbyqxmd.com/read/28356158/interactions-between-sirt1-and-mapks-regulate-astrocyte-activation-induced-by-brain-injury-in-vitro-and-in-vivo
#5
Dan Li, Nan Liu, Hai-Hua Zhao, Xu Zhang, Hitoshi Kawano, Lu Liu, Liang Zhao, Hong-Peng Li
BACKGROUND: Astrocyte activation is a hallmark of traumatic brain injury resulting in neurological dysfunction or death for an overproduction of inflammatory cytokines and glial scar formation. Both the silent mating type information (Sirt1) expression and mitogen-activated protein kinase (MAPK) signal pathway activation represent a promising therapeutic target for several models of neurodegenerative diseases. We investigated the potential effects of Sirt1 upregulation and MAPK pathway pharmacological inhibition on astrocyte activation in vitro and in vivo...
March 29, 2017: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/28346426/mrl-proteins-cooperate-with-activated-ras-in-glia-to-drive-distinct-oncogenic-outcomes
#6
E Taylor, N Alqadri, L Dodgson, D Mason, E Lyulcheva, G Messina, D Bennett
The Mig10/RIAM/Lpd (MRL) adapter protein Lpd regulates actin dynamics through interactions with Scar/WAVE and Ena/VASP proteins to promote the formation of cellular protrusions and to stimulate invasive migration. However, the ability of MRL proteins to interact with multiple actin regulators and to promote serum response factor (SRF) signalling has raised the question of whether MRL proteins employ alternative downstream mechanisms to drive oncogenic processes in a context-dependent manner. Here, using a Drosophila model, we show that overexpression of either human Lpd or its Drosophila orthologue Pico can promote growth and invasion of Ras(V12)-induced cell tumours in the brain...
March 27, 2017: Oncogene
https://www.readbyqxmd.com/read/28340583/inflammatory-signature-of-cerebellar-neurodegeneration-during-neonatal-hyperbilirubinemia-in-ugt1-mouse-model
#7
Simone Vodret, Giulia Bortolussi, Jana Jašprová, Libor Vitek, Andrés F Muro
BACKGROUND: Severe hyperbilirubinemia is toxic during central nervous system development. Prolonged and uncontrolled high levels of unconjugated bilirubin lead to bilirubin-induced neurological damage and eventually death by kernicterus. Bilirubin neurotoxicity is characterized by a wide array of neurological deficits, including irreversible abnormalities in motor, sensitive and cognitive functions, due to bilirubin accumulation in the brain. Despite the abundant literature documenting the in vitro and in vivo toxic effects of bilirubin, it is unclear which molecular and cellular events actually characterize bilirubin-induced neurodegeneration in vivo...
March 24, 2017: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/28324953/electrical-resistance-increases-at-the-tissue-electrode-interface-as-an-early-response-to-nucleus-accumbens-deep-brain-stimulation
#8
Rajas P Kale, Abbas Z Kouzani, Julian Berk, Ken Walder, Michael Berk, Susannah J Tye
The therapeutic actions of deep brain stimulation are not fully understood. The early inflammatory response of electrode implantation is associated with symptom relief without electrical stimulation, but is negated by anti-inflammatory drugs. Early excitotoxic necrosis and subsequent glial scarring modulate the conductivity of the tissue-electrode interface, which can provide some detail into the inflammatory response of individual patients. The feasibility of this was demonstrated by measuring resistance values across a bipolar electrode which was unilaterally implanted into the nucleus accumbens of a rat while receiving continuous deep brain stimulation with a portable back-mounted device using clinical parameters (130Hz, 200μA, 90μs) for 3 days...
August 2016: Conference Proceedings: Annual International Conference of the IEEE Engineering in Medicine and Biology Society
https://www.readbyqxmd.com/read/28317912/the-soft-mechanical-signature-of-glial-scars-in-the-central-nervous-system
#9
Emad Moeendarbary, Isabell P Weber, Graham K Sheridan, David E Koser, Sara Soleman, Barbara Haenzi, Elizabeth J Bradbury, James Fawcett, Kristian Franze
Injury to the central nervous system (CNS) alters the molecular and cellular composition of neural tissue and leads to glial scarring, which inhibits the regrowth of damaged axons. Mammalian glial scars supposedly form a chemical and mechanical barrier to neuronal regeneration. While tremendous effort has been devoted to identifying molecular characteristics of the scar, very little is known about its mechanical properties. Here we characterize spatiotemporal changes of the elastic stiffness of the injured rat neocortex and spinal cord at 1...
March 20, 2017: Nature Communications
https://www.readbyqxmd.com/read/28300871/glial-scar-modulation-as-therapeutic-tool-in-spinal-cord-injury-in-animal-models
#10
Jéssica Rodrigues Orlandin, Carlos Eduardo Ambrósio, Valéria Maria Lara
PURPOSE: Spinal Cord injury represents, in veterinary medicine, most of the neurological attendances and may result in permanent disability, death or euthanasia. Due to inflammation resulting from trauma, it originates the glial scar, which is a cell interaction complex system. Its function is to preserve the healthy circuits, however, it creates a physical and molecular barrier that prevents cell migration and restricts the neuroregeneration ability. METHODS: This review aims to present innovations in the scene of treatment of spinal cord injury, approaching cell therapy, administration of enzyme, anti-inflammatory, and other active principles capable of modulating the inflammatory response, resulting in glial scar reduction and subsequent functional improvement of animals...
February 2017: Acta Cirúrgica Brasileira
https://www.readbyqxmd.com/read/28293254/multiple-uses-of-fibrin-sealant-for-nervous-system-treatment-following-injury-and-disease
#11
REVIEW
Natalia Perussi Biscola, Luciana Politti Cartarozzi, Suzana Ulian-Benitez, Roberta Barbizan, Mateus Vidigal Castro, Aline Barroso Spejo, Rui Seabra Ferreira, Benedito Barraviera, Alexandre Leite Rodrigues Oliveira
Lesions to the nervous system often produce hemorrhage and tissue loss that are difficult, if not impossible, to repair. Therefore, scar formation, inflammation and cavitation take place, expanding the lesion epicenter. This significantly worsens the patient conditions and impairment, increasing neuronal loss and glial reaction, which in turn further decreases the chances of a positive outcome. The possibility of using hemostatic substances that also function as a scaffold, such as the fibrin sealant, reduces surgical time and improve postoperative recovery...
2017: Journal of Venomous Animals and Toxins Including Tropical Diseases
https://www.readbyqxmd.com/read/28281545/il-17-induces-reactive-astrocytes-and-up-regulation-of-vascular-endothelial-growth-factor-vegf-through-jak-stat-signaling
#12
Tao You, Yihui Bi, Jun Li, Mingkai Zhang, Xuezhou Chen, Keke Zhang, Jun Li
Spinal cord injury is a grave neurological disability resulting in neuron degeneration and permanent paralysis. The inflammation triggered by the injury would promote the spinal cord lesion in turn. Activated astrocytes during inflammatory response could promote glial scar formation and contribute to the progression of the spinal cord injury. Interleukin 17 (IL-17) was upregulated in inflammatory responses to contusion or compression of the spinal cord. in this study, IL-17 could induce reactive astrocytes which was indicated by a well-known hallmark glial fibrillary acidic protein (GFAP) in vitro and in vivo...
March 10, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28274846/acute-granulocyte-macrophage-colony-stimulating-factor-treatment-modulates-neuroinflammatory-processes-and-promotes-tactile-recovery-after-spinal-cord-injury
#13
Sandie Thomaty, Laurent Pezard, Christian Xerri, Jean-Michel Brezun
Neuroinflammation is known to play a key role in the prognosis of functional recovery after spinal cord injury (SCI). The involvement of microglial and mast cells in early and late stages of inflammation has been receiving increasing attention. This study was aimed at determining the influence of a pro-inflammatory cytokine, the granulocyte macrophage-colony stimulating factor (GM-CSF), on microglia and mast cell activation, glial scar formation and functional recovery following SCI. Rats were randomly injected with saline or GM-CSF one hour after a C4-C5 medio-lateral hemisection...
March 6, 2017: Neuroscience
https://www.readbyqxmd.com/read/28273770/transglutaminase-6-is-an-autoantigen-in-progressive-multiple-sclerosis-and-is-upregulated-in-reactive-astrocytes
#14
Massimiliano Cristofanilli, Daniel Gratch, Benjamin Pagano, Kelsey McDermott, Jessie Huang, Jeffrey Jian, Deneb Bates, Saud A Sadiq
BACKGROUND: Transglutaminase-6 (TGM6), a member of the transglutaminase enzyme family, is found predominantly in central nervous system (CNS) neurons under physiological conditions. It has been proposed as an autoimmune target in cerebral palsy, gluten-sensitive cerebellar ataxia, and schizophrenia. OBJECTIVE: To investigate TGM6 involvement in multiple sclerosis (MS). METHODS: Antibody levels against TGM6 (TGM6-IgG) were measured in the cerebrospinal fluid (CSF) of 62 primary progressive multiple sclerosis (PPMS), 85 secondary progressive multiple sclerosis (SPMS), and 50 relapsing-remitting multiple sclerosis (RRMS) patients and 51 controls...
December 1, 2016: Multiple Sclerosis: Clinical and Laboratory Research
https://www.readbyqxmd.com/read/28262779/ischemic-injury-leads-to-extracellular-matrix-alterations-in-retina-and-optic-nerve
#15
Jacqueline Reinhard, Marina Renner, Susanne Wiemann, Daniel A Shakoor, Gesa Stute, H Burkhard Dick, Andreas Faissner, Stephanie C Joachim
Retinal ischemia occurs in a variety of eye diseases. Restrained blood flow induces retinal damage, which leads to progressive optic nerve degeneration and vision loss. Previous studies indicate that extracellular matrix (ECM) constituents play an important role in complex tissues, such as retina and optic nerve. They have great impact on de- and regeneration processes and represent major candidates of central nervous system glial scar formation. Nevertheless, the importance of the ECM during ischemic retina and optic nerve neurodegeneration is not fully understood yet...
March 6, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28262732/transplantation-of-huc-mscs-seeded-collagen-scaffolds-reduces-scar-formation-and-promotes-functional-recovery-in-canines-with-chronic-spinal-cord-injury
#16
Xing Li, Jun Tan, Zhifeng Xiao, Yannan Zhao, Sufang Han, Dingyang Liu, Wen Yin, Jing Li, Juan Li, Siyi Wanggou, Bing Chen, Caiping Ren, Xingjun Jiang, Jianwu Dai
Spinal cord injury (SCI) can lead to locomotor deficits, and the repair of chronic SCI is considered one of the most challenging clinical problems. Although extensive studies have evaluated treatments for acute SCI in small animals, comparatively fewer studies have been conducted on large-animal SCI in the chronic phase, which is more clinically relevant. Here, we used a collagen-based biomaterial, named the NeuroRegen scaffold, loaded with human umbilical cord-derived mesenchymal stem cells (hUC-MSCs) in a canine chronic SCI model...
March 6, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28254289/a-combination-of-gdnf-and-hucmsc-transplantation-loaded-on-sf-ags-composite-scaffolds-for-spinal-cord-injury-repair
#17
Genlong Jiao, Guofeng Lou, Yunfei Mo, Yongqin Pan, Ziyong Zhang, Rui Guo, Zhizhong Li
Spinal cord injury (SCI) is a severe trauma for which no effective treatment is currently available. In this study, a composited treatment system was prepared using a silk fibroin/alginates/glial cell line-derived neurotrophic factor (SF/AGs/GDNF) scaffold seeded with human umbilical cord mesenchymal stem cells (hUCMSCs) and the combined therapeutic effects of the composite scaffold to repair SCI rats were evaluated. The use of SF as a scaffold material could act as a biomimetic platform allowing neurons to properly accommodate and rebuild the target tissue...
May 1, 2017: Materials Science & Engineering. C, Materials for Biological Applications
https://www.readbyqxmd.com/read/28246640/ultraflexible-nanoelectronic-probes-form-reliable-glial-scar-free-neural-integration
#18
Lan Luan, Xiaoling Wei, Zhengtuo Zhao, Jennifer J Siegel, Ojas Potnis, Catherine A Tuppen, Shengqing Lin, Shams Kazmi, Robert A Fowler, Stewart Holloway, Andrew K Dunn, Raymond A Chitwood, Chong Xie
Implanted brain electrodes construct the only means to electrically interface with individual neurons in vivo, but their recording efficacy and biocompatibility pose limitations on scientific and clinical applications. We showed that nanoelectronic thread (NET) electrodes with subcellular dimensions, ultraflexibility, and cellular surgical footprints form reliable, glial scar-free neural integration. We demonstrated that NET electrodes reliably detected and tracked individual units for months; their impedance, noise level, single-unit recording yield, and the signal amplitude remained stable during long-term implantation...
February 2017: Science Advances
https://www.readbyqxmd.com/read/28226865/electrical-resistance-increases-at-the-tissue-electrode-interface-as-an-early-response-to-nucleus-accumbens-deep-brain-stimulation
#19
Rajas P Kale, Abbas Z Kouzani, Julian Berk, Ken Walder, Michael Berk, Susannah J Tye, Rajas P Kale, Abbas Z Kouzani, Julian Berk, Ken Walder, Michael Berk, Susannah J Tye, Julian Berk, Michael Berk, Susannah J Tye, Abbas Z Kouzani, Rajas P Kale, Ken Walder
The therapeutic actions of deep brain stimulation are not fully understood. The early inflammatory response of electrode implantation is associated with symptom relief without electrical stimulation, but is negated by anti-inflammatory drugs. Early excitotoxic necrosis and subsequent glial scarring modulate the conductivity of the tissue-electrode interface, which can provide some detail into the inflammatory response of individual patients. The feasibility of this was demonstrated by measuring resistance values across a bipolar electrode which was unilaterally implanted into the nucleus accumbens of a rat while receiving continuous deep brain stimulation with a portable back-mounted device using clinical parameters (130Hz, 200μA, 90μs) for 3 days...
August 2016: Conference Proceedings: Annual International Conference of the IEEE Engineering in Medicine and Biology Society
https://www.readbyqxmd.com/read/28223982/mouse-model-of-neurological-complications-resulting-from-encephalitic-alphavirus-infection
#20
Shannon E Ronca, Jeanon Smith, Takaaki Koma, Magda M Miller, Nadezhda Yun, Kelly T Dineley, Slobodan Paessler
Long-term neurological complications, termed sequelae, can result from viral encephalitis, which are not well understood. In human survivors, alphavirus encephalitis can cause severe neurobehavioral changes, in the most extreme cases, a schizophrenic-like syndrome. In the present study, we aimed to adapt an animal model of alphavirus infection survival to study the development of these long-term neurological complications. Upon low-dose infection of wild-type C57B/6 mice, asymptomatic and symptomatic groups were established and compared to mock-infected mice to measure general health and baseline neurological function, including the acoustic startle response and prepulse inhibition paradigm...
2017: Frontiers in Microbiology
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