Search results: Found 4

Listing 1 - 4 of 4
Sort by
Myelin-Mediated Inhibition of Axonal Regeneration: Past, Present, and Future

Authors: ---
Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889452064 Year: Pages: 116 DOI: 10.3389/978-2-88945-206-4 Language: English
Publisher: Frontiers Media SA
Subject: Neurology --- Science (General)
Added to DOAB on : 2017-10-13 14:57:01
License:

Loading...
Export citation

Choose an application

Abstract

Pioneering studies conducted in the 1980’s laid the foundation for the hypothesis that axonal regeneration is limited by CNS myelin, and the identification of myelin-associated glycoprotein (MAG), Nogo, and oligodendrocyte myelin glycoprotein (OMgp) as inhibitors of neurite outgrowth firmly established myelin as a key factor in regenerative failure. Mechanistically, it has been shown that MAG, Nogo, and OMgp mediate inhibition by binding to either Nogo receptor (NgR) or paired immunoglobulin receptor B (PirB), and initiating a signaling cascade that culminates in the activation of RhoA.Since the discovery of these proteins, there has been tremendous interest in identifying compounds and molecular mechanisms that are capable of overcoming myelin-mediated inhibition. Many studies have focused on pharmacological antagonism of receptors and signaling intermediates, while others have sought to identify and enhance endogenous pro-regenerative pathways. The most notable example of the latter is the conditioning lesion effect, which led to the discovery of cyclic AMP’s ability to overcome inhibition by MAG and myelin. Many of the agents tested in these studies have been shown to promote axonal regeneration in vivo, and this research topic allows researchers to share information about new treatments that have been developed in both academia and industry. As we look toward the future, it is becoming increasingly clear that reversal of myelin-mediated inhibition alone will not be sufficient to produce functional recovery from spinal cord injury, and that other factors, such as astroglial scarring, the expression of chondroitin sulfate proteoglycans, neuronal cell death, and lack of neurotrophic support, must also be taken into consideration. Combinatorial approaches therefore hold a great deal of promise, and we hope to initiate a dialogue on how stem cell transplantation, chondroitinase ABC, gene therapy, growth-promoting agents, and other methods can be combined to optimize functional recovery. We introduce this topic in honor of the life and work of Dr. Marie T. Filbin (1955-2014). Through these articles, we highlight past achievements in the field, novel findings, unanswered questions and innovative ideas that we hope will lead to new advances in axonal regeneration.

The ventricular-subventricular zone: a source of oligodendrocytes in the adult brain

Authors: --- ---
Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889192687 Year: Pages: 104 DOI: 10.3389/978-2-88919-268-7 Language: English
Publisher: Frontiers Media SA
Subject: Neurology --- Science (General)
Added to DOAB on : 2015-12-03 13:02:24
License:

Loading...
Export citation

Choose an application

Abstract

Demyelinating diseases are characterized by an extensive loss of oligodendrocytes and myelin sheaths from axolemma, which commonly result in disability in young adults. To date, there is no effective treatment against these neurological disorders. In the adult brain, there are neural stem cells (NSCs) that reside within a niche denominated ventricular-subventricular zone (V-SVZ) in the lateral wall of the cerebral ventricles. NSCs give rise to neurons and oligodendrocytes that help preserve cellular homeostasis. Growing evidence indicates that V-SVZ progenitor cells may represent an endogenous source of oligodendrocytes that can be useful to treat demyelinating diseases. This e-Book collected the most recent evidence regarding the mechanisms that modulate the proliferation, migration, quiescence, cell-fate choices and survival of oligodendrocyte precursors generated in the V-SVZ. Herein, we compiled information about the role of Sonic hedgehog, NMDA receptors, ErbB proteins, hemopressin, erythropoietin, osmolarity and microglia in the oligodendrocyte production. Some chapters also describe the role of oligodendrocyte precursors in the preservation of cellular homeostasis, aging and white matter repair. All these information is presented as novel research findings, short communications, and review articles, which were written by experts in the field of oligodendrocyte generation, myelin production and white matter re-myelination.

Induction of Central Nervous System Disease by the Adaptive Immune Response

Authors: ---
Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889453474 Year: Pages: 141 DOI: 10.3389/978-2-88945-347-4 Language: English
Publisher: Frontiers Media SA
Subject: Medicine (General) --- Allergy and Immunology --- Neurology
Added to DOAB on : 2018-02-27 16:16:45
License:

Loading...
Export citation

Choose an application

Abstract

Over the last years it has become evident that many neurological diseases of the central nervous system (CNS) are induced by a specific adaptive immune response directed against molecules expressed on CNS-resident cells. Well-recognized examples are anti-N-Methyl-D-Aspartate Receptor (NMDAR) encephalitis which is characterized by the presence of antibodies against neuron-expressed NMDAR, or neuromyelitis optica (NMO), induced by antibodies to astrocyte-expressed aquaporin-4. Many more examples exist, and antibodies, and T or/and B cells have increasingly been associated with CNS disease. Often the symptoms of these diseases have not been typically reported to have an immune aetiology. Beside classical neurological symptoms like ataxia, vision disturbance, and motor or sensory symptoms, these can include cognitive disturbances, behavioral abnormalities, or/and epileptic seizures. Although much has been learned regarding the pathophysiology of prototypic examples of these disorders, there are still major gaps in our understanding of their biology. This may be due to the fact that they are rare diseases, and their therapies are still very limited. This research topic includes contributions addressing the analysis of the adaptive immune response driving disease including target antigens, molecular epitope mapping, and factors involved in the disease pathogenesis such as complement activation cascades, genetic and genomic regulation, as well as environmental triggers. Diagnostic criteria and methods, and treatment are also discussed. The overall aim of the volume is to review progress in our pathophysiological understanding of immune-mediated CNS disorders in order to advance diagnostic and therapeutic approaches, and ultimately improve outcomes for patients.

The Molecular and Cellular Basis for Parkinson's Disease

Author:
ISBN: 9783039215485 / 9783039215492 Year: Pages: 230 DOI: 10.3390/books978-3-03921-549-2 Language: eng
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Medicine (General) --- Neurology
Added to DOAB on : 2019-12-09 11:49:15
License:

Loading...
Export citation

Choose an application

Abstract

The focus on dopamine-sensitive motor symptoms, in association with the improvement of motor complications in the heterogeneous disease entity Parkinson's disease, has led to a certain standstill in research. This Special Issue provides new concepts and new ideas on the pathogenesis, genetics, and clinical maintenance of Parkinson's disease and related disorders. Not only new experimental findings, but also clinical outcomes, case series, and research on alternative, non-pharmacological therapies are included. The objective is to bridge the currently increasing gap between experimental and clinical research on Parkinson's disease and related disorders.

Keywords

epigenetics --- Parkinson’s disease --- brain --- DNA methylation --- Parkinson’s disease --- fatty acid ?-oxidation --- long-chain acylcarnitine --- Parkinson’s disease --- fatty acyls --- glycerolipids --- glycerophospholipids --- sphingolipids --- sterol lipids --- lipoproteins --- ?-synuclein-mediated pathology --- disease-modifying effects --- neuroprotection --- autophagy --- cysteinyl-dopamine --- hypochlorite --- oxidative stress --- Parkinson’s disease --- redox cycling --- Parkinson’s disease --- brain iron --- motor dysfunction --- neurometabolites --- magnetic resonance imaging --- magnetic resonance spectroscopy --- GABA --- spectroscopy --- Parkinson’s disease --- neuroinflammation --- alpha-Synuclein --- immunotherapy --- mesenchymal stem cells --- secretome --- exosomes --- Parkinson’s disease --- microRNAs --- Parkinson disease --- multiprofessional therapy --- inpatient treatment --- multimodal complex treatment --- caffeic acid --- chlorogenic acid --- rotenone --- Parkinson’s disease --- neuroprotection --- dopaminergic neuron --- myenteric plexus --- enteric glial cell --- metallothionein --- Parkinson’s disease --- microbiota --- molecular mimicry --- microbiome --- alpha-synuclein --- curli --- gut-brain axis --- neurodegeneration --- glucocerebrosidase --- Parkinson’s disease --- Gaucher’s disease --- Lewy Body Dementia --- REM sleep behavior disorders --- [123I]FP-CIT-SPECT --- DAT --- nigral cells --- Parkinson’s disease --- parkinsonisms --- cell line --- differentiation --- HOG --- immature oligodendrocyte --- Krabbe’s disease --- oligodendrocyte --- mature oligodendrocyte --- MO3.13 --- myelin --- multiple sclerosis --- schizophrenia --- SH-SY5Y

Listing 1 - 4 of 4
Sort by
Narrow your search