The Experts below are selected from a list of 132 Experts worldwide ranked by ideXlab platform
Regina C. Armstrong - One of the best experts on this subject based on the ideXlab platform.
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pdgf and fgf2 pathways regulate distinct oligodendrocyte lineage responses in Experimental Demyelination with spontaneous remyelination
Neurobiology of Disease, 2005Co-Authors: Joshua C Murtie, Yongxing Zhou, Adam C Vana, Regina C. ArmstrongAbstract:Repair of myelin damage in the adult CNS requires oligodendrocyte progenitor (OP) proliferation and subsequent differentiation into remyelinating oligodendrocytes. Platelet-derived growth factor (PDGF) and fibroblast growth factor-2 (FGF2) have been predicted to act individually and/or cooperatively to generate remyelinating oligodendrocytes. Analysis of PDGF alpha receptor (PDGF alpha R) heterozygous (+/-) mice indicates that PDGF alpha R expression modulates oligodendrocyte density in non-lesioned adult CNS. Analysis of cuprizone Demyelination and recovery in PDGF alpha R+/- mice, FGF2 knockout (-/-) mice, and PDGF alpha R+/- FGF2-/- mice demonstrated that: (1) OP proliferation and oligodendrocyte regeneration is impaired in PDGF alpha R heterozygotes, (2) PDGF alpha R+/- and FGF2-/- deletions do not act cooperatively to impair OP amplification, (3) oligodendrocyte differentiation is more frequent in FGF2-/- mice, and (4) FGF2 deletion in combination with the PDGF alpha R+/- genotype rescues impaired oligodendrocyte regeneration of PDGF alpha R heterozygotes. These findings demonstrate distinct roles for PDGF and FGF2 in vivo in the context of a demyelinating disease with spontaneous remyelination.
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Demyelination increases radial diffusivity in corpus callosum of mouse brain
NeuroImage, 2005Co-Authors: Shengkwei Song, Regina C. Armstrong, Jun E. Yoshino, Shiowjiuan Lin, Shuwei Sun, Anne H CrossAbstract:Myelin damage, as seen in multiple sclerosis (MS) and other demyelinating diseases, impairs axonal conduction and can also be associated with axonal degeneration. Accurate assessments of these conditions may be highly beneficial in evaluating and selecting therapeutic strategies for patient management. Recently, an analytical approach examining diffusion tensor imaging (DTI) derived parameters has been proposed to assess the extent of axonal damage, Demyelination, or both. The current study uses the well-characterized cuprizone model of Experimental Demyelination and remyelination of corpus callosum in mouse brain to evaluate the ability of DTI parameters to detect the progression of myelin degeneration and regeneration. Our results demonstrate that the extent of increased radial diffusivity reflects the severity of Demyelination in corpus callosum of mouse brain affected by cuprizone treatment. Subsequently, radial diffusivity decreases with the progression of remyelination. Furthermore, radial diffusivity changes were specific to the time course of changes in myelin integrity as distinct from axonal injury, which was detected by betaAPP immunostaining and shown to be most extensive prior to Demyelination. Radial diffusivity offers a specific assessment of Demyelination and remyelination, as distinct from acute axonal damage.
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Demyelination increases radial diffusivity in corpus callosum of mouse brain
NeuroImage, 2005Co-Authors: Shengkwei Song, Regina C. Armstrong, Jun E. Yoshino, Anne H Cross, Tuan Q LeAbstract:Abstract Myelin damage, as seen in multiple sclerosis (MS) and other demyelinating diseases, impairs axonal conduction and can also be associated with axonal degeneration. Accurate assessments of these conditions may be highly beneficial in evaluating and selecting therapeutic strategies for patient management. Recently, an analytical approach examining diffusion tensor imaging (DTI) derived parameters has been proposed to assess the extent of axonal damage, Demyelination, or both. The current study uses the well-characterized cuprizone model of Experimental Demyelination and remyelination of corpus callosum in mouse brain to evaluate the ability of DTI parameters to detect the progression of myelin degeneration and regeneration. Our results demonstrate that the extent of increased radial diffusivity reflects the severity of Demyelination in corpus callosum of mouse brain affected by cuprizone treatment. Subsequently, radial diffusivity decreases with the progression of remyelination. Furthermore, radial diffusivity changes were specific to the time course of changes in myelin integrity as distinct from axonal injury, which was detected by βAPP immunostaining and shown to be most extensive prior to Demyelination. Radial diffusivity offers a specific assessment of Demyelination and remyelination, as distinct from acute axonal damage.
Mohammad Javan - One of the best experts on this subject based on the ideXlab platform.
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dendrosomal nanocurcumin promotes remyelination through induction of oligodendrogenesis in Experimental Demyelination animal model
Journal of Tissue Engineering and Regenerative Medicine, 2020Co-Authors: Mahsa Motavaf, Mohammad Javan, Majid Sadeghizadeh, Sadegh Babashah, Leila ZareAbstract:Multiple sclerosis (MS) is an autoimmune disease, associated with central nervous system (CNS) inflammation, Demyelination, and axonal loss. Myelin, a multilayer membranous that covers nerve fibers, is essential for rapid impulse conduction. Oligodendrocytes that are generated either from CNS-resident oligodendrocyte progenitor cells (OPCs) or subventricular zone-derived neural stem cells (NSCs) are the myelinating cells of the CNS. The adult CNS maintains a certain endogenous potential to repair myelin damage. However, this process often fails as MS progresses. The origin of this failure is not fully understood, but it is likely to relate to progenitors/stem cells' arrestment in a quiescent state, incapable of generating new oligodendrocyte. Current treatments for MS are immunomodulatory or immunosuppressive medications, with little to no effect on myelin restoration. Recent studies have provided proof-of-principle that CNS remyelination can be promoted either via enhancing endogenous remyelination or by transplanting myelinating cells. Curcumin, a natural polyphenolic compound, has been shown to have therapeutic properties in several neurodegenerative diseases. Here, we investigated the effect of a curcumin nanoformulation, dendrosomal nanoparticles (DNC) on oligodendrogenesis and remyelination, both in vitro and in animal model of Demyelination. We indicated that DNC enhanced oligodendrogenesis from NSCs and OPCs, in vitro in dose dependent manner. DNC also induced in vivo remyelination via promotion of oligodendrogenesis. Furthermore, DNC enhanced remyelination capacity of transplanted NSCs through promoting their survival and oligodendrogenesis capacity. Our findings suggest that DNC has significant beneficial effects in demyelinating conditions, either as mono-therapy or as being paired with transplantation approaches.
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fibroblast growth factor 2 enhanced the recruitment of progenitor cells and myelin repair in Experimental Demyelination of rat hippocampal formations
Cell, 2015Co-Authors: Mahdieh Azin, Javad Mirnajafizadeh, Mohammad JavanAbstract:Objective Hippocampal insults have been observed in multiple sclerosis (MS) patients. Fibroblast growth factor-2 (FGF2) induces neurogenesis in the hippocampus and en- hances the proliferation, migration and differentiation of oligodendrocyte progenitor cells (OPCs). In the current study, we have investigated the effect of FGF2 on the processes of gliotoxin induced Demyelination and subsequent remyelination in the hippocampus.
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basic fibroblast growth factor potentiates myelin repair following induction of Experimental Demyelination in adult mouse optic chiasm and nerves
Journal of Molecular Neuroscience, 2012Co-Authors: Samaneh Dehghan, Javad Mirnajafizadeh, Mohammad Javan, Fereshteh Pourabdolhossein, Hossein BaharvandAbstract:Induction of Demyelination in the central nervous system induce the oligodendrocyte progenitors to proliferate, migrate, and differentiate for restoring new myelin sheathes around demyelinated axons. Factors which increase the response of endogenous progenitor cells could be used to improve remyelination. In the current study, the effect of bFGF on lysolecithin-induced Demyelination and remyelination processes in mouse optic chiasm and nerves was investigated. Lysolecithin was injected into the optic chiasm of Balb/C mice. Two groups of animals received doses of bFGF (1 or 5 ng/kg i.p.) just before and every 3 days after lysolecithin injection. Delay and amplitude of visual evoked potential (VEP) waves were recorded as indices of axonal Demyelination at 7th, 13th, and 28th days post-lesion. Myelin basic protein (MBP) and Olig2 gene expressions were studied as indices of myelination and oligodendrocyte precursors’ recruitment into the lesion. Lysolecithin elongated delay of P1 wave and declined the amplitude of P1-N1 wave. Lysolecithin decreased MBP and increased Olig2 expression in different days post-lesion. Lysolecithin-induced changes in VEPs were partially ameliorated by endogenous repair. bFGF reduced the increased delay, increased the reduced amplitude of P1-N1 wave, increased MBP gene expression, and accelerated the increasing pattern of Olig2. bFGF seems to be able to potentiate the endogenous repair mechanisms of myelin. Its effect on Demyelination and remyelination processes seems to be mediated by oligodendrocyte progenitor cells and their differentiation to myelinating cells.
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analysis of structural and molecular events associated with adult rat optic chiasm and nerves Demyelination and remyelination possible role for 3rd ventricle proliferating cells
Neuromolecular Medicine, 2011Co-Authors: Sabah Mozafari, Mohammad Amin Sherafat, Motahareh Heibatollahi, Shahram Pourbeiranvand, Taki Tiraihi, Javad Mirnajafizadeh, Mohammad Javan, Abolhasan AhmadianiAbstract:Multiple sclerosis frequently affects the optic apparatus, particularly optic chiasm and nerves. Here, we have reported the structural and molecular characteristics of remyelination in the adult rat optic chiasm and nerves. Moreover, considering the proximity of optic chiasm and 3rd ventricle, we have tried to determine if proliferating cells residing in 3rd ventricle region are able to migrate in response to Experimental Demyelination of the optic chiasm. Following local Demyelination by lysolecithin, remyelination pattern in longitude of optic chiasm and proximal nerves was investigated using myelin staining and marker genes expression. Furthermore, cell tracing was carried out using BrdU labeling of proliferating cells prior to gliotoxin injection. Morphometric analysis revealed that Demyelination was considerable on days 7 and 14 and an incomplete remyelination occurred on day 28 post-lesion. Interestingly, myelin repair was more evident in the caudal part of chiasm, compared to rostral part and proximal optic nerves. Following chiasm and nerve Demyelination, trains of BrdU+ cells were seen near the 3rd ventricle which subsequently moved to lesion site. Nestin was significantly up-regulated in 3rd ventricle surroundings. At the lesion site, Nogo-A gene expression was significantly decreased on days 7 and 14 post lesion, while Olig2, nestin, and GFAP expression was increased on day 7. The changes were then reversed by the time. Myelin repair in optic chiasm seems to be mediated by endogenous progenitors and stem cells. Adult 3rd ventricle proliferating cells may play a role in this context by mobilization into the demyelinated chiasm.
Markus Kipp - One of the best experts on this subject based on the ideXlab platform.
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Lesion Expansion in Experimental Demyelination Animal Models and Multiple Sclerosis Lesions
Molecular Neurobiology, 2015Co-Authors: René Große-veldmann, Birte Becker, Sandra Amor, Paul Van Der Valk, Cordian Beyer, Markus KippAbstract:Gray matter pathology is an important aspect of multiple sclerosis (MS) pathogenesis and disease progression. In a recent study, we were able to demonstrate that the higher myelin content in the white matter parts of the brain is an important variable in the neuroinflammatory response during demyelinating events. Whether higher white matter myelination contributes to lesion development and progression is not known. Here, we compared lesion size of intra-cortical vs. white matter MS lesions. Furthermore, dynamics of lesion development was compared in the cuprizone and lysophosphatidylcholine models. We provide clear evidence that in the human brain, white matter lesions are significantly increased in size as compared to intra-cortical gray matter lesions. In addition, studies using the cuprizone mouse model revealed that the autonomous progression of white matter lesions is more severe compared to that in the gray matter. Focal Demyelination revealed that the application of equal amounts of lysophosphatidylcholine results in more severe Demyelination in the white compared to the gray matter. In summary, lesion progression is most intense in myelin-rich white matter regions, irrespective of the initial lesion trigger mechanism. A better understanding of myelin debris-triggered lesion expansion will pave the way for the development of new protective strategies in the future.
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the sphingosine 1 phosphate receptor agonist fty720 is neuroprotective after cuprizone induced cns Demyelination
British Journal of Pharmacology, 2015Co-Authors: Alexander Slowik, Sandra Amor, Cordian Beyer, Tim Clarner, T Schmidt, Markus KippAbstract:Background and Purpose Modulation of the sphingosine 1-phosphate receptor is an approved treatment for relapsing multiple sclerosis because of its anti-inflammatory effect of retaining lymphocytes within the lymph nodes. Here, we evaluated the potential of an agonist at this receptor, FTY720 (fingolimod), to activate the promyelinating pathways within the brain to encourage remyelination and neuroprotection. Experimental Approach In this study, we used the cuprizone model in male C57BL/6 mice and tested the promyelinating and neuroprotective effects of FTY720 after acute and chronic toxin-induced Experimental Demyelination. We used histological, immunohistochemical and gene expression methods. Key Results The midline of the corpus callosum was severely demyelinated after acute and chronic cuprizone-induced Demyelination. Robust endogenous remyelination was evident after acute, but impaired after chronic, Demyelination. FTY720 treatment modestly accelerated myelin recovery after acute but not chronic cuprizone exposure. Markers of gliosis (astrocyte and microglia activation) were not affected by FTY720 treatment. Remarkably, the accumulation of amyloid precursor protein-positive spheroids in axons was less distinct in FTY720-treated animals, indicating that this compound alleviated ongoing axonal damage. Conclusions and Implications We show that even during endogenous remyelination, axonal degeneration continued at a low level, accumulating over time. This continuous neurodegenerative process was ameliorated by FTY720 treatment. FTY720 preserved CNS integrity by direct interaction with brain resident cells, the actions of which are still to be defined.
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myelin debris regulates inflammatory responses in an Experimental Demyelination animal model and multiple sclerosis lesions
Glia, 2012Co-Authors: Tim Clarner, Sandra Amor, Cordian Beyer, Bernd Denecke, Felix Diederichs, Katharina Berger, Paul Van Der Valk, Markus KippAbstract:In multiple sclerosis (MS), gray matter pathology is characterized by less pronounced inflammation when compared with white matter lesions. Although regional differences in the cytoarchitecture may account for these differences, the amount of myelin debris in the cortex during a demyelinating event might also be contributory. To analyze the association between myelin debris levels and inflammatory responses, cortical areas with distinct and sparse myelination were analyzed for micro- and astrogliosis before and after cuprizone-induced Demyelination in mice. In postmortem tissue of MS patients, leucocortical lesions were assessed for the type and level of inflammation in the cortical and white matter regions of the lesion. Furthermore, mice were injected intracerebrally with myelin-enriched debris, and the inflammatory response analyzed in white and grey matter areas. Our studies show that the magnitude of myelin loss positively correlates with microgliosis in the cuprizone model. In MS, the number of MHC class II expressing cells is higher in the white compared with the grey matter part of leucocortical lesions. Finally, direct application of myelin debris into the corpus callosum or cortex of mice induces profound and comparable inflammation in both regions. Our data suggest that myelin debris is an important variable in the inflammatory response during demyelinating events. Whether myelin-driven inflammation affects neuronal integrity remains to be clarified. © 2012 Wiley Periodicals, Inc.
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blbp expression in astrocytes during Experimental Demyelination and in human multiple sclerosis lesions
Brain Behavior and Immunity, 2011Co-Authors: Markus Kipp, Paul Van Der Valk, Tim Clarner, Stefan Gingele, Friederike Pott, Bernd Denecke, Lin Gan, Volker Siffrin, Frauke Zipp, Wolfgang DreherAbstract:Several lines of evidence indicate that remyelination represents one of the most effective mechanisms to achieve axonal protection. For reasons that are not yet understood, this process is often incomplete or fails in multiple sclerosis (MS). Activated astrocytes appear to be able to boost or inhibit endogenous repair processes. A better understanding of remyelination in MS and possible reasons for its failure is needed. Using the well-established toxic Demyelination cuprizone model, we created lesions with either robust or impaired endogenous remyelination capacity. Lesions were analyzed for mRNA expression levels by Affymetrix GeneChip® arrays. One finding was the predominance of immune and stress response factors in the group of genes which were classified as remyelination-supporting factors. We further demonstrate that lesions with impaired remyelination capacity show weak expression of the radial-glia cell marker brain lipid binding protein (BLBP, also called B-FABP or FABP7). The expression of BLBP in activated astrocytes correlates with the presence of oligodendrocyte progenitor cells. BLBP-expressing astrocytes are also detected in Experimental autoimmune encephalomyelitis during the remission phase. Furthermore, highest numbers of BLBP-expressing astrocytes were evident in lesions of early MS, whereas significantly less are present at the rim of (chronic)-active lesions from patients with long disease duration. Transfection experiments show that BLBP regulates growth factor expression in U87 astrocytoma cells. In conclusion, we provide evidence that expression of BLBP in activated astrocytes negatively correlates with disease duration and in parallel with remyelination failure.
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ADAM12 is expressed by astrocytes during Experimental Demyelination.
Brain research, 2010Co-Authors: Fabian Baertling, Cordian Beyer, Maria Kokozidou, Thomas Pufe, Tim Clarner, Reinhard Windoffer, Christoph Jan Wruck, Lars-ove Brandenburg, Markus KippAbstract:Abstract A disintegrin and metalloproteinase (ADAM) 12 represents a member of a large family of similarly structured multi-domain proteins. In the central nervous system (CNS), ADAM12 has been suggested to play a role in brain development, glioblastoma cell proliferation, and in Experimental autoimmune encephalomyelitis. Furthermore, ADAM12 was reported to be almost exclusively expressed by oligodendrocytes and could, therefore, be considered as suitable marker for this cell type. In the present study, we investigated ADAM12 expression in the healthy and pathologically altered murine CNS. As pathological paradigm, we used the cuprizone Demyelination model in which myelin loss during multiple sclerosis is imitated. Besides APC + oligodendrocytes, SMI311 + neurons and GFAP + astrocytes express ADAM12 in the adult mouse brain. ADAM12 expression was further analyzed in vitro . After the induction of Demyelination, we observed that activated astrocytes are the main source of ADAM12 in brain regions affected by oligodendrocyte loss. Exposure of astrocytes in vitro to either lipopolysaccharides (LPS), tumor necrosis factor α (TNFα), glutamate, or hydrogen peroxide revealed a highly stimulus-specific regulation of ADAM12 expression which was not seen in microglial BV2 cells. It appears that LPS- and TNFα-induced ADAM12 expression is mediated via the classic NFκB pathway. In summary, we demonstrated that ADAM12 is not a suitable marker for oligodendrocytes. Our results further suggest that ADAM12 might be implicated in the course of distinct CNS diseases such as demyelinating disorders.
Javad Mirnajafizadeh - One of the best experts on this subject based on the ideXlab platform.
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oct4 transcription factor in conjunction with valproic acid accelerates myelin repair in demyelinated optic chiasm in mice
Neuroscience, 2016Co-Authors: Samaneh Dehghan, Javad Mirnajafizadeh, M Hesaraki, Masoud Soleimani, Yaghoub Fathollahi, Mohamad JavanAbstract:Abstract Multiple sclerosis is a demyelinating disease with severe neurological symptoms due to blockage of signal conduction in affected axons. Spontaneous remyelination via endogenous progenitors is limited and eventually fails. Recent reports showed that forced expression of some transcription factors within the brain converted somatic cells to neural progenitors and neuroblasts. Here, we report the effect of valproic acid (VPA) along with forced expression of Oct4 transcription factor on lysolecithin (LPC)-induced Experimental Demyelination. Mice were gavaged with VPA for one week, and then inducible Oct4 expressing lentiviral particles were injected into the lateral ventricle. After one-week induction of Oct4, LPC was injected into the optic chiasm. Functional remyelination was assessed by visual-evoked potential (VEP) recording. Myelination level was studied using FluoroMyelin staining and immunohistofluorescent (IHF) against proteolipid protein (PLP). IHF was also performed to detect Oct4 and SSEA1 as pluripotency markers and Olig2, Sox10, CNPase and PDGFRα as oligodendrocyte lineage markers. One week after injection of Oct4 expressing vector, pluripotency markers SSEA1 and Oct4 were detected in the rims of the 3rd ventricle. LPC injection caused extensive Demyelination and significantly delayed the latency of VEP wave. Animals pre-treated with VPA + Oct4 expressing vector, showed faster recovery in the VEP latency and enhanced myelination. Immunostaining against oligodendrocyte lineage markers showed an increased number of Sox10+ and myelinating cells. Moreover, transdifferentiation of some Oct4-transfected cells (GFP+ cells) to Olig2+ and CNPase+ cells was confirmed by immunostaining. One-week administration of VPA followed by one-week forced expression of Oct4 enhanced myelination by converting transduced cells to myelinating oligodendrocytes. This finding seems promising for enhancing myelin repair within the adult brains.
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fibroblast growth factor 2 enhanced the recruitment of progenitor cells and myelin repair in Experimental Demyelination of rat hippocampal formations
Cell, 2015Co-Authors: Mahdieh Azin, Javad Mirnajafizadeh, Mohammad JavanAbstract:Objective Hippocampal insults have been observed in multiple sclerosis (MS) patients. Fibroblast growth factor-2 (FGF2) induces neurogenesis in the hippocampus and en- hances the proliferation, migration and differentiation of oligodendrocyte progenitor cells (OPCs). In the current study, we have investigated the effect of FGF2 on the processes of gliotoxin induced Demyelination and subsequent remyelination in the hippocampus.
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basic fibroblast growth factor potentiates myelin repair following induction of Experimental Demyelination in adult mouse optic chiasm and nerves
Journal of Molecular Neuroscience, 2012Co-Authors: Samaneh Dehghan, Javad Mirnajafizadeh, Mohammad Javan, Fereshteh Pourabdolhossein, Hossein BaharvandAbstract:Induction of Demyelination in the central nervous system induce the oligodendrocyte progenitors to proliferate, migrate, and differentiate for restoring new myelin sheathes around demyelinated axons. Factors which increase the response of endogenous progenitor cells could be used to improve remyelination. In the current study, the effect of bFGF on lysolecithin-induced Demyelination and remyelination processes in mouse optic chiasm and nerves was investigated. Lysolecithin was injected into the optic chiasm of Balb/C mice. Two groups of animals received doses of bFGF (1 or 5 ng/kg i.p.) just before and every 3 days after lysolecithin injection. Delay and amplitude of visual evoked potential (VEP) waves were recorded as indices of axonal Demyelination at 7th, 13th, and 28th days post-lesion. Myelin basic protein (MBP) and Olig2 gene expressions were studied as indices of myelination and oligodendrocyte precursors’ recruitment into the lesion. Lysolecithin elongated delay of P1 wave and declined the amplitude of P1-N1 wave. Lysolecithin decreased MBP and increased Olig2 expression in different days post-lesion. Lysolecithin-induced changes in VEPs were partially ameliorated by endogenous repair. bFGF reduced the increased delay, increased the reduced amplitude of P1-N1 wave, increased MBP gene expression, and accelerated the increasing pattern of Olig2. bFGF seems to be able to potentiate the endogenous repair mechanisms of myelin. Its effect on Demyelination and remyelination processes seems to be mediated by oligodendrocyte progenitor cells and their differentiation to myelinating cells.
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analysis of structural and molecular events associated with adult rat optic chiasm and nerves Demyelination and remyelination possible role for 3rd ventricle proliferating cells
Neuromolecular Medicine, 2011Co-Authors: Sabah Mozafari, Mohammad Amin Sherafat, Motahareh Heibatollahi, Shahram Pourbeiranvand, Taki Tiraihi, Javad Mirnajafizadeh, Mohammad Javan, Abolhasan AhmadianiAbstract:Multiple sclerosis frequently affects the optic apparatus, particularly optic chiasm and nerves. Here, we have reported the structural and molecular characteristics of remyelination in the adult rat optic chiasm and nerves. Moreover, considering the proximity of optic chiasm and 3rd ventricle, we have tried to determine if proliferating cells residing in 3rd ventricle region are able to migrate in response to Experimental Demyelination of the optic chiasm. Following local Demyelination by lysolecithin, remyelination pattern in longitude of optic chiasm and proximal nerves was investigated using myelin staining and marker genes expression. Furthermore, cell tracing was carried out using BrdU labeling of proliferating cells prior to gliotoxin injection. Morphometric analysis revealed that Demyelination was considerable on days 7 and 14 and an incomplete remyelination occurred on day 28 post-lesion. Interestingly, myelin repair was more evident in the caudal part of chiasm, compared to rostral part and proximal optic nerves. Following chiasm and nerve Demyelination, trains of BrdU+ cells were seen near the 3rd ventricle which subsequently moved to lesion site. Nestin was significantly up-regulated in 3rd ventricle surroundings. At the lesion site, Nogo-A gene expression was significantly decreased on days 7 and 14 post lesion, while Olig2, nestin, and GFAP expression was increased on day 7. The changes were then reversed by the time. Myelin repair in optic chiasm seems to be mediated by endogenous progenitors and stem cells. Adult 3rd ventricle proliferating cells may play a role in this context by mobilization into the demyelinated chiasm.
Jun E. Yoshino - One of the best experts on this subject based on the ideXlab platform.
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Demyelination increases radial diffusivity in corpus callosum of mouse brain
NeuroImage, 2005Co-Authors: Shengkwei Song, Regina C. Armstrong, Jun E. Yoshino, Shiowjiuan Lin, Shuwei Sun, Anne H CrossAbstract:Myelin damage, as seen in multiple sclerosis (MS) and other demyelinating diseases, impairs axonal conduction and can also be associated with axonal degeneration. Accurate assessments of these conditions may be highly beneficial in evaluating and selecting therapeutic strategies for patient management. Recently, an analytical approach examining diffusion tensor imaging (DTI) derived parameters has been proposed to assess the extent of axonal damage, Demyelination, or both. The current study uses the well-characterized cuprizone model of Experimental Demyelination and remyelination of corpus callosum in mouse brain to evaluate the ability of DTI parameters to detect the progression of myelin degeneration and regeneration. Our results demonstrate that the extent of increased radial diffusivity reflects the severity of Demyelination in corpus callosum of mouse brain affected by cuprizone treatment. Subsequently, radial diffusivity decreases with the progression of remyelination. Furthermore, radial diffusivity changes were specific to the time course of changes in myelin integrity as distinct from axonal injury, which was detected by betaAPP immunostaining and shown to be most extensive prior to Demyelination. Radial diffusivity offers a specific assessment of Demyelination and remyelination, as distinct from acute axonal damage.
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Demyelination increases radial diffusivity in corpus callosum of mouse brain
NeuroImage, 2005Co-Authors: Shengkwei Song, Regina C. Armstrong, Jun E. Yoshino, Anne H Cross, Tuan Q LeAbstract:Abstract Myelin damage, as seen in multiple sclerosis (MS) and other demyelinating diseases, impairs axonal conduction and can also be associated with axonal degeneration. Accurate assessments of these conditions may be highly beneficial in evaluating and selecting therapeutic strategies for patient management. Recently, an analytical approach examining diffusion tensor imaging (DTI) derived parameters has been proposed to assess the extent of axonal damage, Demyelination, or both. The current study uses the well-characterized cuprizone model of Experimental Demyelination and remyelination of corpus callosum in mouse brain to evaluate the ability of DTI parameters to detect the progression of myelin degeneration and regeneration. Our results demonstrate that the extent of increased radial diffusivity reflects the severity of Demyelination in corpus callosum of mouse brain affected by cuprizone treatment. Subsequently, radial diffusivity decreases with the progression of remyelination. Furthermore, radial diffusivity changes were specific to the time course of changes in myelin integrity as distinct from axonal injury, which was detected by βAPP immunostaining and shown to be most extensive prior to Demyelination. Radial diffusivity offers a specific assessment of Demyelination and remyelination, as distinct from acute axonal damage.
