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[PMID]:27774721
[Au] Autor:Puetz VB; Parker D; Kohn N; Dahmen B; Verma R; Konrad K
[Ad] Endereço:Division of Psychology and Language Sciences, University College London, London, United Kingdom.
[Ti] Título:Altered brain network integrity after childhood maltreatment: A structural connectomic DTI-study.
[So] Source:Hum Brain Mapp;38(2):855-868, 2017 02.
[Is] ISSN:1097-0193
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Childhood maltreatment is associated with alterations in neural architecture that potentially put these children at increased risk for psychopathology. Alterations in white matter (WM) tracts have been reported, however no study to date has investigated WM connectivity in brain networks in maltreated children to quantify global and local abnormalities through graph theoretical analyses of DTI data. We aimed for a multilevel investigation examining the DTI-based structural connectome and its associations with basal cortisol levels of 25 children with documented maltreatment experiences before age 3, and 24 matched controls (age: 10.6 ± 1.75 years). On the global and lobar level, maltreated children showed significant reductions in global connectivity strength, local connectivity and increased path length, suggesting deviations from the small-world network architecture previously associated with psychopathology. Reductions in global connectivity were associated with placement instability, attenuated cortisol secretion and higher levels of internalizing and externalizing behaviours. Regional measures revealed lower connectivity strength especially in regions within the ventromedial prefrontal cortex (vMPFC) in maltreated children. These findings show that childhood maltreatment is associated with systemic global neurodevelopmental alterations in WM networks next to regional alterations in areas involved in the regulation of affect. These alterations in WM organization could underlie global functional deficits and multi-symptom patterns frequently observed in children with maltreatment experiences. Hum Brain Mapp 38:855-868, 2017. © 2016 Wiley Periodicals, Inc.
[Mh] Termos MeSH primário: Encéfalo/diagnóstico por imagem
Maus-Tratos Infantis
Imagem de Tensor de Difusão
Transtornos Mentais/diagnóstico por imagem
Vias Neurais/diagnóstico por imagem
Substância Branca/diagnóstico por imagem
[Mh] Termos MeSH secundário: Adolescente
Mapeamento Encefálico
Criança
Maus-Tratos Infantis/psicologia
Feminino
Seres Humanos
Processamento de Imagem Assistida por Computador
Imagem por Ressonância Magnética
Masculino
Transtornos Mentais/etiologia
Modelos Neurológicos
Fibras Nervosas Mielinizadas/fisiologia
Escalas de Graduação Psiquiátrica
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180217
[Lr] Data última revisão:
180217
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE
[do] DOI:10.1002/hbm.23423


  2 / 11834 MEDLINE  
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[PMID]:27775478
[Au] Autor:Bahrami N; Sharma D; Rosenthal S; Davenport EM; Urban JE; Wagner B; Jung Y; Vaughan CG; Gioia GA; Stitzel JD; Whitlow CT; Maldjian JA
[Ad] Endereço:From the Advanced Neuroscience Imaging Research (ANSIR) Laboratory (N.B., D.S., E.M.D., Y.J., C.T.W., J.A.M.), Wake Forest School of Medicine (S.R.), Department of Radiology-Neuroradiology (Y.J., C.T.W.), Department of Biomedical Engineering (N.B., J.E.U., Y.J., J.D.S., C.T.W.), Department of Family
[Ti] Título:Subconcussive Head Impact Exposure and White Matter Tract Changes over a Single Season of Youth Football.
[So] Source:Radiology;281(3):919-926, 2016 Dec.
[Is] ISSN:1527-1315
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Purpose To examine the effects of subconcussive impacts resulting from a single season of youth (age range, 8-13 years) football on changes in specific white matter (WM) tracts as detected with diffusion-tensor imaging in the absence of clinically diagnosed concussions. Materials and Methods Head impact data were recorded by using the Head Impact Telemetry system and quantified as the combined-probability risk-weighted cumulative exposure (RWE ). Twenty-five male participants were evaluated for seasonal fractional anisotropy (FA) changes in specific WM tracts: the inferior fronto-occipital fasciculus (IFOF), inferior longitudinal fasciculus, and superior longitudinal fasciculus (SLF). Fiber tracts were segmented into a central core and two fiber terminals. The relationship between seasonal FA change in the whole fiber, central core, and the fiber terminals with RWE was also investigated. Linear regression analysis was conducted to determine the association between RWE and change in fiber tract FA during the season. Results There were statistically significant linear relationships between RWE and decreased FA in the whole (R = 0.433; P = .003), core (R = 0.3649; P = .007), and terminals (R = 0.5666; P < .001) of left IFOF. A trend toward statistical significance (P = .08) in right SLF was observed. A statistically significant correlation between decrease in FA of the right SLF terminal and RWE was also observed (R = 0.2893; P = .028). Conclusion This study found a statistically significant relationship between head impact exposure and change of FA fractional anisotropy value of whole, core, and terminals of left IFOF and right SLF's terminals where WM and gray matter intersect, in the absence of a clinically diagnosed concussion. RSNA, 2016.
[Mh] Termos MeSH primário: Concussão Encefálica/patologia
Futebol Americano/lesões
Traumatismos Cranianos Fechados/patologia
Substância Branca/patologia
[Mh] Termos MeSH secundário: Adolescente
Criança
Imagem de Tensor de Difusão
Lobo Frontal/patologia
Seres Humanos
Masculino
Fibras Nervosas Mielinizadas/patologia
Vias Neurais/patologia
Lobo Occipital/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171201
[Lr] Data última revisão:
171201
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


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[PMID]:29046438
[Au] Autor:Almeida RG; Lyons DA
[Ad] Endereço:Centre for Discovery Brain Sciences, rgalmeid@staffmail.ed.ac.uk david.lyons@ed.ac.uk.
[Ti] Título:On Myelinated Axon Plasticity and Neuronal Circuit Formation and Function.
[So] Source:J Neurosci;37(42):10023-10034, 2017 Oct 18.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Studies of activity-driven nervous system plasticity have primarily focused on the gray matter. However, MRI-based imaging studies have shown that white matter, primarily composed of myelinated axons, can also be dynamically regulated by activity of the healthy brain. Myelination in the CNS is an ongoing process that starts around birth and continues throughout life. Myelin in the CNS is generated by oligodendrocytes and recent evidence has shown that many aspects of oligodendrocyte development and myelination can be modulated by extrinsic signals including neuronal activity. Because modulation of myelin can, in turn, affect several aspects of conduction, the concept has emerged that activity-regulated myelination represents an important form of nervous system plasticity. Here we review our increasing understanding of how neuronal activity regulates oligodendrocytes and myelinated axons , with a focus on the timing of relevant processes. We highlight the observations that neuronal activity can rapidly tune axonal diameter, promote re-entry of oligodendrocyte progenitor cells into the cell cycle, or drive their direct differentiation into oligodendrocytes. We suggest that activity-regulated myelin formation and remodeling that significantly change axonal conduction properties are most likely to occur over timescales of days to weeks. Finally, we propose that precise fine-tuning of conduction along already-myelinated axons may also be mediated by alterations to the axon itself. We conclude that future studies need to analyze activity-driven adaptations to both axons and their myelin sheaths to fully understand how myelinated axon plasticity contributes to neuronal circuit formation and function.
[Mh] Termos MeSH primário: Axônios/fisiologia
Encéfalo/fisiologia
Bainha de Mielina/fisiologia
Fibras Nervosas Mielinizadas/fisiologia
Rede Nervosa/fisiologia
Plasticidade Neuronal/fisiologia
[Mh] Termos MeSH secundário: Animais
Encéfalo/citologia
Diferenciação Celular/fisiologia
Seres Humanos
Rede Nervosa/citologia
Neurogênese/fisiologia
Oligodendroglia/fisiologia
Substância Branca/citologia
Substância Branca/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171027
[Lr] Data última revisão:
171027
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171020
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.3185-16.2017


  4 / 11834 MEDLINE  
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[PMID]:28972120
[Au] Autor:Melo-Carrillo A; Strassman AM; Nir RR; Schain AJ; Noseda R; Stratton J; Burstein R
[Ad] Endereço:Department of Anesthesia, Critical Care & Pain Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215.
[Ti] Título:Fremanezumab-A Humanized Monoclonal Anti-CGRP Antibody-Inhibits Thinly Myelinated (Aδ) But Not Unmyelinated (C) Meningeal Nociceptors.
[So] Source:J Neurosci;37(44):10587-10596, 2017 Nov 01.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Calcitonin gene-related peptide (CGRP), the most abundant neuropeptide in primary afferent sensory neurons, is strongly implicated in the pathophysiology of migraine headache, but its role in migraine is still equivocal. As a new approach to migraine treatment, humanized anti-CGRP monoclonal antibodies (CGRP-mAbs) were developed to reduce the availability of CGRP, and were found effective in reducing the frequency of chronic and episodic migraine. We recently tested the effect of fremanezumab (TEV-48125), a CGRP-mAb, on the activity of second-order trigeminovascular dorsal horn neurons that receive peripheral input from the cranial dura, and found a selective inhibition of high-threshold but not wide-dynamic range class of neurons. To investigate the basis for this selective inhibitory effect, and further explore the mechanism of action of CGRP-mAbs, we tested the effect of fremanezumab on the cortical spreading depression-evoked activation of mechanosensitive primary afferent meningeal nociceptors that innervate the cranial dura, using single-unit recording in the trigeminal ganglion of anesthetized male rats. Fremanezumab pretreatment selectively inhibited the responsiveness of Aδ neurons, but not C-fiber neurons, as reflected in a decrease in the percentage of neurons that showed activation by cortical spreading depression. These findings identify Aδ meningeal nociceptors as a likely site of action of fremanezumab in the prevention of headache. The selectivity in its peripheral inhibitory action may partly account for fremanezumab's selective inhibition of high-threshold, as a result of a predominant A-δ input to high-threshold neurons, but not wide dynamic-range dorsal horn neurons, and why it may not be effective in all migraine patients. Recently, we reported that humanized CGRP monoclonal antibodies (CGRP-mAbs) prevent activation and sensitization of high-threshold (HT) but not wide-dynamic range trigeminovascular neurons by cortical spreading depression (CSD). In the current paper, we report that CGRP-mAbs prevent the activation of Aδ but not C-type meningeal nociceptors by CSD. This is the first identification of an anti-migraine drug that appears to be selective for Aδ-fibers (peripherally) and HT neurons (centrally). As the main CGRP-mAb site of action appears to be situated outside the brain, we conclude that the initiation of the headache phase of migraine depends on activation of meningeal nociceptors, and that for selected patients, activation of the Aδ-HT pain pathway may be sufficient for the generation of headache perception.
[Mh] Termos MeSH primário: Anticorpos Monoclonais/farmacologia
Peptídeo Relacionado com Gene de Calcitonina/antagonistas & inibidores
Bainha de Mielina/efeitos dos fármacos
Fibras Nervosas Mielinizadas/efeitos dos fármacos
Fibras Nervosas Amielínicas/efeitos dos fármacos
Nociceptores/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Peptídeo Relacionado com Gene de Calcitonina/fisiologia
Seres Humanos
Masculino
Bainha de Mielina/fisiologia
Fibras Nervosas Mielinizadas/fisiologia
Fibras Nervosas Amielínicas/fisiologia
Nociceptores/fisiologia
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (TEV-48125); 83652-28-2 (Calcitonin Gene-Related Peptide)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171117
[Lr] Data última revisão:
171117
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171004
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.2211-17.2017


  5 / 11834 MEDLINE  
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[PMID]:28899915
[Au] Autor:Santiago González DA; Cheli VT; Zamora NN; Lama TN; Spreuer V; Murphy GG; Paez PM
[Ad] Endereço:Hunter James Kelly Research Institute, Department of Pharmacology and Toxicology, Jacobs School of Medicine and Biomedical Sciences, The State University of New York, University at Buffalo, Buffalo, New York 14203, and.
[Ti] Título:Conditional Deletion of the L-Type Calcium Channel Cav1.2 in NG2-Positive Cells Impairs Remyelination in Mice.
[So] Source:J Neurosci;37(42):10038-10051, 2017 Oct 18.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Exploring the molecular mechanisms that drive the maturation of oligodendrocyte progenitor cells (OPCs) during the remyelination process is essential to developing new therapeutic tools to intervene in demyelinating diseases such as multiple sclerosis. To determine whether L-type voltage-gated calcium channels (L-VGCCs) are required for OPC development during remyelination, we generated an inducible conditional knock-out mouse in which the L-VGCC isoform Cav1.2 was deleted in NG2-positive OPCs (Cav1.2 ). Using the cuprizone (CPZ) model of demyelination and mice of either sex, we establish that Cav1.2 deletion in OPCs leads to less efficient remyelination of the adult brain. Specifically, Cav1.2 OPCs mature slower and produce less myelin than control oligodendrocytes during the recovery period after CPZ intoxication. This reduced remyelination was accompanied by an important decline in the number of myelinating oligodendrocytes and in the rate of OPC proliferation. Furthermore, during the remyelination phase of the CPZ model, the corpus callosum of Cav1.2 animals presented a significant decrease in the percentage of myelinated axons and a substantial increase in the mean g-ratio of myelinated axons compared with controls. In addition, in a mouse line in which the Cav1.2 OPCs were identified by a reporter, we establish that Cav1.2 OPCs display a reduced maturational rate through the entire remyelination process. These results suggest that Ca influx mediated by L-VGCCs in oligodendroglial cells is necessary for normal remyelination and is an essential Ca channel for OPC maturation during the remyelination of the adult brain. Ion channels implicated in oligodendrocyte differentiation and maturation may induce positive signals for myelin recovery. Voltage-gated Ca channels (VGCCs) are important for normal myelination by acting at several critical steps during oligodendrocyte progenitor cell (OPC) development. To determine whether voltage Ca entry is involved in oligodendrocyte differentiation and remyelination, we used a conditional knockout mouse for VGCCs in OPCs. Our results indicate that VGCCs can modulate oligodendrocyte maturation in the demyelinated brain and suggest that voltage-gated Ca influx in OPCs is critical for remyelination. These findings could lead to novel approaches for obtaining a better understanding of the factors that control OPC maturation in order to stimulate this pool of progenitors to replace myelin in demyelinating diseases.
[Mh] Termos MeSH primário: Antígenos/biossíntese
Canais de Cálcio Tipo L/deficiência
Deleção de Genes
Bainha de Mielina/metabolismo
Fibras Nervosas Mielinizadas/metabolismo
Proteoglicanas/biossíntese
[Mh] Termos MeSH secundário: Animais
Antígenos/genética
Encéfalo/metabolismo
Encéfalo/patologia
Canais de Cálcio Tipo L/genética
Feminino
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Camundongos Transgênicos
Bainha de Mielina/genética
Fibras Nervosas Mielinizadas/patologia
Oligodendroglia/metabolismo
Oligodendroglia/patologia
Proteoglicanas/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens); 0 (CACNA1C protein, mouse); 0 (Calcium Channels, L-Type); 0 (Proteoglycans); 0 (chondroitin sulfate proteoglycan 4)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170914
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.1787-17.2017


  6 / 11834 MEDLINE  
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[PMID]:28760859
[Au] Autor:Sinclair JL; Fischl MJ; Alexandrova O; Heß M; Grothe B; Leibold C; Kopp-Scheinpflug C
[Ad] Endereço:Division of Neurobiology, Department Biology II, Ludwig-Maximilians-University Munich, 82152 Planegg-Martinsried, Germany.
[Ti] Título:Sound-Evoked Activity Influences Myelination of Brainstem Axons in the Trapezoid Body.
[So] Source:J Neurosci;37(34):8239-8255, 2017 Aug 23.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Plasticity of myelination represents a mechanism to tune the flow of information by balancing functional requirements with metabolic and spatial constraints. The auditory system is heavily myelinated and operates at the upper limits of action potential generation frequency and speed observed in the mammalian CNS. This study aimed to characterize the development of myelin within the trapezoid body, a central auditory fiber tract, and determine the influence sensory experience has on this process in mice of both sexes. We find that conduction speed doubles following hearing onset and the ability to support high-frequency firing increases concurrently. Also in this time, the diameter of trapezoid body axons and the thickness of myelin double, reaching mature-like thickness between 25 and 35 d of age. Earplugs were used to induce ∼50 dB elevation in auditory thresholds. If introduced at hearing onset, trapezoid body fibers developed thinner axons and myelin than age-matched controls. If plugged during adulthood, the thickest trapezoid body fibers also showed a decrease in myelin. These data demonstrate the need for sensory activity in both development and maintenance of myelin and have important implications in the study of myelin plasticity and how this could relate to sensorineural hearing loss following peripheral impairment. The auditory system has many mechanisms to maximize the dynamic range of its afferent fibers, which operate at the physiological limit of action potential generation, precision, and speed. In this study we demonstrate for the first time that changes in peripheral activity modifies the thickness of myelin in sensory neurons, not only in development but also in mature animals. The current study suggests that changes in CNS myelination occur as a downstream mechanism following peripheral deficit. Given the required submillisecond temporal precision for binaural auditory processing, reduced myelination might augment sensorineural hearing impairment.
[Mh] Termos MeSH primário: Estimulação Acústica/métodos
Vias Auditivas/fisiologia
Axônios/fisiologia
Potenciais Evocados Auditivos/fisiologia
Fibras Nervosas Mielinizadas/fisiologia
Corpo Trapezoide/fisiologia
[Mh] Termos MeSH secundário: Potenciais de Ação/fisiologia
Animais
Vias Auditivas/citologia
Tronco Encefálico/citologia
Tronco Encefálico/fisiologia
Feminino
Masculino
Camundongos
Camundongos Endogâmicos CBA
Técnicas de Cultura de Órgãos
Som
Corpo Trapezoide/citologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170914
[Lr] Data última revisão:
170914
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170802
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.3728-16.2017


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[PMID]:28751457
[Au] Autor:Feliú A; Bonilla Del Río I; Carrillo-Salinas FJ; Hernández-Torres G; Mestre L; Puente N; Ortega-Gutiérrez S; López-Rodríguez ML; Grandes P; Mecha M; Guaza C
[Ad] Endereço:Functional and Systems Neurobiology Department, Neuroimmunology Group, Instituto Cajal, 28002 Madrid, Spain.
[Ti] Título:2-Arachidonoylglycerol Reduces Proteoglycans and Enhances Remyelination in a Progressive Model of Demyelination.
[So] Source:J Neurosci;37(35):8385-8398, 2017 Aug 30.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The failure to undergo remyelination is a critical impediment to recovery in multiple sclerosis. Chondroitin sulfate proteoglycans (CSPGs) accumulate at demyelinating lesions creating a nonpermissive environment that impairs axon regeneration and remyelination. Here, we reveal a new role for 2-arachidonoylglycerol (2-AG), the major CNS endocannabinoid, in the modulation of CSPGs deposition in a progressive model of multiple sclerosis, the Theiler's murine encephalomyelitis virus-induced demyelinating disease. Treatment with a potent reversible inhibitor of the enzyme monoacylglycerol lipase, which accounts for 85% of the 2-AG degradation in the mouse CNS, modulates neuroinflammation and reduces CSPGs accumulation and astrogliosis around demyelinated lesions in the spinal cord of Theiler's murine encephalomyelitis virus-infected mice. Inhibition of 2-AG hydrolysis augments the number of mature oligodendrocytes and increases MBP, leading to remyelination and functional recovery of mice. Our findings establish a mechanism for 2-AG promotion of remyelination with implications in axonal repair in CNS demyelinating pathologies. The deposition of chondroitin sulfate proteoglycans contributes to the failure in remyelination associated with multiple sclerosis. Here we unveil a new role for 2-arachidonoylglycerol, the major CNS endocannabinoid, in the modulation of chondroitin sulfate proteoglycan accumulation in Theiler's murine encephalomyelitis virus-induced demyelinating disease. The treatment during the chronic phase with a potent reversible inhibitor of the enzyme monoacylglycerol lipase, which accounts for 85% of the 2-arachidonoylglycerol degradation in the mouse CNS, modulates neuroinflammation and reduces chondroitin sulfate proteoglycan deposition around demyelinated lesions in the spinal cord of Theiler's murine encephalomyelitis virus-infected mice. The increased 2-arachidonoylglycerol tone promotes remyelination in a model of progressive multiple sclerosis ameliorating motor dysfunction.
[Mh] Termos MeSH primário: Ácidos Araquidônicos/farmacologia
Ácidos Araquidônicos/uso terapêutico
Endocanabinoides/farmacologia
Endocanabinoides/uso terapêutico
Glicerídeos/farmacologia
Glicerídeos/uso terapêutico
Esclerose Múltipla/tratamento farmacológico
Esclerose Múltipla/fisiopatologia
Fibras Nervosas Mielinizadas/efeitos dos fármacos
Fibras Nervosas Mielinizadas/patologia
Proteoglicanas/metabolismo
[Mh] Termos MeSH secundário: Animais
Agonistas de Receptores de Canabinoides/farmacologia
Agonistas de Receptores de Canabinoides/uso terapêutico
Relação Dose-Resposta a Droga
Regulação para Baixo/efeitos dos fármacos
Feminino
Camundongos
Esclerose Múltipla/patologia
Neurogênese/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Arachidonic Acids); 0 (Cannabinoid Receptor Agonists); 0 (Endocannabinoids); 0 (Glycerides); 0 (Proteoglycans); 8D239QDW64 (glyceryl 2-arachidonate)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170925
[Lr] Data última revisão:
170925
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170729
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.2900-16.2017


  8 / 11834 MEDLINE  
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[PMID]:28724828
[Au] Autor:Ozates S; Teke MY
[Ad] Endereço:Department of Ophtalmology, Ankara Ulucanlar Eye Training and Research Hospital, Ankara, Turkey.
[Ti] Título:Ring-shaped myelinated retinal nerve fibers at fovea.
[So] Source:Indian J Ophthalmol;65(7):630-632, 2017 Jul.
[Is] ISSN:1998-3689
[Cp] País de publicação:India
[La] Idioma:eng
[Ab] Resumo:We aim to report an unusual case of myelinated retinal nerve fibers (MRNFs) at fovea. A 39-year-old woman presented with visual impairment and her visual acuity was 20/80 in the right eye. Ophthalmologic examination revealed MRNF lesions at inferior and superior poles of optic disc in the right eye. Furthermore, a ring-shaped MRNF lesion with feathery edges was observed at fovea. MRNF lesions are rarely seen at macula, and to our knowledge, this is the first report of an MRNF lesion at fovea.
[Mh] Termos MeSH primário: Fóvea Central/patologia
Fibras Nervosas Mielinizadas/patologia
Doenças Retinianas/diagnóstico
Células Ganglionares da Retina/patologia
Transtornos da Visão/etiologia
[Mh] Termos MeSH secundário: Adulto
Feminino
Seres Humanos
Doenças Retinianas/complicações
Tomografia de Coerência Óptica
Transtornos da Visão/diagnóstico
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170721
[St] Status:MEDLINE
[do] DOI:10.4103/ijo.IJO_120_17


  9 / 11834 MEDLINE  
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[PMID]:28694334
[Au] Autor:McLane LE; Bourne JN; Evangelou AV; Khandker L; Macklin WB; Wood TL
[Ad] Endereço:Department of Pharmacology, Physiology, and Neuroscience and Cancer Center, New Jersey Medical School, Rutgers University, Newark, New Jersey 07101, and.
[Ti] Título:Loss of Tuberous Sclerosis Complex1 in Adult Oligodendrocyte Progenitor Cells Enhances Axon Remyelination and Increases Myelin Thickness after a Focal Demyelination.
[So] Source:J Neurosci;37(31):7534-7546, 2017 Aug 02.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Although the mammalian target of rapamycin (mTOR) is an essential regulator of developmental oligodendrocyte differentiation and myelination, oligodendrocyte-specific deletion of tuberous sclerosis complex (TSC), a major upstream inhibitor of mTOR, surprisingly also leads to hypomyelination during CNS development. However, the function of TSC has not been studied in the context of remyelination. Here, we used the inducible Cre-lox system to study the function of TSC in the remyelination of a focal, lysolecithin-demyelinated lesion in adult male mice. Using two different mouse models in which is deleted by Cre expression in oligodendrocyte progenitor cells (OPCs) or in premyelinating oligodendrocytes, we reveal that deletion of affects oligodendroglia differently depending on the stage of the oligodendrocyte lineage. deletion from NG2 OPCs accelerated remyelination. Conversely, deletion from proteolipid protein (PLP)-positive oligodendrocytes slowed remyelination. Contrary to developmental myelination, there were no changes in OPC or oligodendrocyte numbers in either model. Our findings reveal a complex role for TSC in oligodendrocytes during remyelination in which the timing of deletion is a critical determinant of its effect on remyelination. Moreover, our findings suggest that TSC has different functions in developmental myelination and remyelination. Myelin loss in demyelinating disorders such as multiple sclerosis results in disability due to loss of axon conductance and axon damage. Encouragingly, the nervous system is capable of spontaneous remyelination, but this regenerative process often fails. Many chronically demyelinated lesions have oligodendrocyte progenitor cells (OPCs) within their borders. It is thus of great interest to elucidate mechanisms by which we might enhance endogenous remyelination. Here, we provide evidence that deletion of from OPCs, but not differentiating oligodendrocytes, is beneficial to remyelination. This finding contrasts with the loss of oligodendroglia and hypomyelination seen with or deletion in the oligodendrocyte lineage during CNS development and points to important differences in the regulation of developmental myelination and remyelination.
[Mh] Termos MeSH primário: Doenças Desmielinizantes/metabolismo
Doenças Desmielinizantes/patologia
Fibras Nervosas Mielinizadas/patologia
Oligodendroglia/metabolismo
Oligodendroglia/patologia
Células-Tronco/metabolismo
Proteínas Supressoras de Tumor/metabolismo
[Mh] Termos MeSH secundário: Animais
Axônios
Diferenciação Celular/fisiologia
Células Cultivadas
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Bainha de Mielina/metabolismo
Bainha de Mielina/patologia
Fibras Nervosas Mielinizadas/metabolismo
Regeneração Nervosa/fisiologia
Células-Tronco/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Tumor Suppressor Proteins); 0 (tuberous sclerosis complex 1 protein)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170822
[Lr] Data última revisão:
170822
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170712
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.3454-16.2017


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[PMID]:28499058
[Au] Autor:Bypareddy R; Takkar B; Lohchab M; Azad SV; Chawla R
[Ti] Título:Association of Myelinated Retinal Nerve Fibers With Acquired Mulberry Retinal Astrocytoma: Coincidental or Relational?
[So] Source:Ophthalmic Surg Lasers Imaging Retina;48(5):441-442, 2017 May 01.
[Is] ISSN:2325-8179
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Retinal astrocytoma is an important ocular finding for diagnosis of tuberous sclerosis complex and is also an association of neurofibromatosis. The authors present findings of a case of acquired astrocytoma associated with myelinated retinal nerve fibers. The authors also discuss the images and possible cause-effect relationship between them. [Ophthalmic Surg Lasers Imaging Retina. 2017;48:441-442.].
[Mh] Termos MeSH primário: Astrocitoma/diagnóstico
Fibras Nervosas Mielinizadas/patologia
Retina/patologia
Neoplasias da Retina/diagnóstico
[Mh] Termos MeSH secundário: Diagnóstico Diferencial
Feminino
Angiofluoresceinografia
Fundo de Olho
Seres Humanos
Meia-Idade
Tomografia de Coerência Óptica
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170901
[Lr] Data última revisão:
170901
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170513
[St] Status:MEDLINE
[do] DOI:10.3928/23258160-20170428-13



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