scholarly journals Intranasal Delivery of A Novel Amnion Cell Secretome Prevents Neuronal Damage and Preserves Function In A Mouse Multiple Sclerosis Model

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Reas S. Khan ◽  
Kimberly Dine ◽  
Bailey Bauman ◽  
Michael Lorentsen ◽  
Lisa Lin ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Neuronal Damage ◽  
Intranasal Delivery ◽  
Amnion Cell ◽  
Multiple Sclerosis Model

scholarly journals Pannexin 1 involvement in bladder dysfunction in a multiple sclerosis model

2013 ◽  
Vol 3 (1) ◽  
Author(s):  
Hiromitsu Negoro ◽  
Sarah E. Lutz ◽  
Louis S. Liou ◽  
Akihiro Kanematsu ◽  
Osamu Ogawa ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Bladder Dysfunction ◽  
Pannexin 1 ◽  
Multiple Sclerosis Model

Therapeutic Effects of Physical Exercise and the Mesenchymal Stem Cell Secretome by Modulating Neuroinflammatory Response in Multiple Sclerosis

2021 ◽  
Vol 16 ◽  
Author(s):  
Lina María González ◽  
Laura Natalia Ospina ◽  
Laura Elena Sperling ◽  
Orlando Chaparro ◽  
Jaison Daniel Cucarián
Keyword(s):  
Multiple Sclerosis ◽  
Stem Cells ◽  
Physical Exercise ◽  
Disease Progression ◽  
Neuronal Damage ◽  
Experimental Studies ◽  
Chronic Inflammatory Disease ◽  
Therapeutic Effects ◽  
Local Inflammatory Response ◽  
Neuroinflammatory Response

Multiple sclerosis (MS) is a neurodegenerative, demyelinating, and chronic inflammatory disease characterized by central nervous system (CNS) lesions that lead to high levels of disability and severe physical and cognitive disturbances. Conventional therapies are not enough to control the neuroinflammatory process in MS and are not able to inhibit ongoing damage to the CNS. Thus, the secretome of mesenchymal stem cells (MSC-S) has been postulated as a potential therapy that could mitigate symptoms and disease progression. We considered that its combination with physical exercise (EX) could induce superior effects and increase the MSC-S effectiveness in this condition. Recent studies have revealed that both EX and MSC-S share similar mechanisms of action that mitigate auto-reactive T cell infiltration, regulate the local inflammatory response, modulate the proinflammatory profile of glial cells, and reduce neuronal damage. Clinical and experimental studies have reported that these treatments in an isolated way also improve myelination, regeneration, promote the release of neurotrophic factors, and increase the recruitment of endogenous stem cells. Together, these effects reduce disease progression and improve patient functionality. Despite these results, the combination of these methods has not yet been studied in MS. In this review, we focus on molecular elements and cellular responses induced by these treatments in a separate way, showing their beneficial effects in the control of symptoms and disease progression in MS, as well as indicating their contribution in clinical fields. In addition, we propose the combined use of EX and MSC-S as a strategy to boost their reparative and immunomodulatory effects in this condition, combining their benefits on synaptogenesis, neurogenesis, remyelination, and neuroinflammatory response. The findings here reported are based on the scientific evidence and our professional experience that will bring significant progress to regenerative medicine to deal with this condition.

Neuronal damage in T1-hypointense multiple sclerosis lesions demonstrated in vivo using proton magnetic resonance spectroscopy

1999 ◽  
Vol 46 (1) ◽  
pp. 79-87 ◽  
Author(s):  
Marianne A. A. Van Walderveen ◽  
Frederik Barkhof ◽  
Petra J. W. Pouwels ◽  
Ronald A. Van Schijndel ◽  
Chris H. Polman ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Magnetic Resonance ◽  
Magnetic Resonance Spectroscopy ◽  
Proton Magnetic Resonance ◽  
Proton Magnetic Resonance Spectroscopy ◽  
Neuronal Damage ◽  
Resonance Spectroscopy

Oligoprotective effect of metformin through the AMPK-dependent on restoration of mitochondrial hemostasis in the cuprizone-induced multiple sclerosis model

2019 ◽  
Vol 50 (3) ◽  
pp. 263-271 ◽  
Author(s):  
Seyed Hossein Hosseini Largani ◽  
Maryam Borhani-Haghighi ◽  
Parichehr Pasbakhsh ◽  
Vahid Pirhajati Mahabadi ◽  
Saied Nekoonam ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Multiple Sclerosis Model

scholarly journals Latent-period stool proteomic assay of multiple sclerosis model indicates protective capacity of host-expressed protease inhibitors

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Carlos G. Gonzalez ◽  
Stephanie K. Tankou ◽  
Laura M. Cox ◽  
Ellen P. Casavant ◽  
Howard L. Weiner ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Latent Period ◽  
Protease Inhibitors ◽  
Protective Capacity ◽  
Multiple Sclerosis Model

Wrong cytokine backed in multiple-sclerosis model

2003 ◽  
Vol 2 (4) ◽  
pp. 203 ◽  
Author(s):  
Jane Bradbury
Keyword(s):  
Multiple Sclerosis ◽  
Multiple Sclerosis Model

Changes and variability of proton density and T1 relaxation times in early multiple sclerosis: MRI markers of neuronal damage in the cerebral cortex

2015 ◽  
Vol 26 (8) ◽  
pp. 2578-2586 ◽  
Author(s):  
René-Maxime Gracien ◽  
Sarah C. Reitz ◽  
Stephanie Michelle Hof ◽  
Vinzenz Fleischer ◽  
Hilga Zimmermann ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Cerebral Cortex ◽  
Neuronal Damage ◽  
Relaxation Times ◽  
Proton Density ◽  
T1 Relaxation

scholarly journals A metabolic perspective on CSF-mediated neurodegeneration in multiple sclerosis

Brain ◽  
2019 ◽  
Vol 142 (9) ◽  
pp. 2756-2774 ◽  
Author(s):  
Maureen Wentling ◽  
Carlos Lopez-Gomez ◽  
Hye-Jin Park ◽  
Mario Amatruda ◽  
Achilles Ntranos ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Neuronal Damage ◽  
Morphological Changes ◽  
Progressive Multiple Sclerosis ◽  
Functional Screening ◽  
Disease Course ◽  
Post Translational Modification ◽  
Neurodegenerative Process ◽  
Relapsing Remitting ◽  
Multiple Sclerosis Patients

Abstract Multiple sclerosis is an autoimmune demyelinating disorder of the CNS, characterized by inflammatory lesions and an underlying neurodegenerative process, which is more prominent in patients with progressive disease course. It has been proposed that mitochondrial dysfunction underlies neuronal damage, the precise mechanism by which this occurs remains uncertain. To investigate potential mechanisms of neurodegeneration, we conducted a functional screening of mitochondria in neurons exposed to the CSF of multiple sclerosis patients with a relapsing remitting (n = 15) or a progressive (secondary, n = 15 or primary, n = 14) disease course. Live-imaging of CSF-treated neurons, using a fluorescent mitochondrial tracer, identified mitochondrial elongation as a unique effect induced by the CSF from progressive patients. These morphological changes were associated with decreased activity of mitochondrial complexes I, III and IV and correlated with axonal damage. The effect of CSF treatment on the morphology of mitochondria was characterized by phosphorylation of serine 637 on the dynamin-related protein DRP1, a post-translational modification responsible for unopposed mitochondrial fusion in response to low glucose conditions. The effect of neuronal treatment with CSF from progressive patients was heat stable, thereby prompting us to conduct an unbiased exploratory lipidomic study that identified specific ceramide species as differentially abundant in the CSF of progressive patients compared to relapsing remitting multiple sclerosis. Treatment of neurons with medium supplemented with ceramides, induced a time-dependent increase of the transcripts levels of specific glucose and lactate transporters, which functionally resulted in progressively increased glucose uptake from the medium. Thus ceramide levels in the CSF of patients with progressive multiple sclerosis not only impaired mitochondrial respiration but also decreased the bioavailability of glucose by increasing its uptake. Importantly the neurotoxic effect of CSF treatment could be rescued by exogenous supplementation with glucose or lactate, presumably to compensate the inefficient fuel utilization. Together these data suggest a condition of ‘virtual hypoglycosis’ induced by the CSF of progressive patients in cultured neurons and suggest a critical temporal window of intervention for the rescue of the metabolic impairment of neuronal bioenergetics underlying neurodegeneration in multiple sclerosis patients.

Neuronal damage and neuroinflammation markers in patients with autoimmune encephalitis and multiple sclerosis

2019 ◽  
Vol 34 (5) ◽  
pp. 1473-1485 ◽  
Author(s):  
V. Fominykh ◽  
L. Brylev ◽  
V. Gaskin ◽  
R. Luzin ◽  
A. Yakovlev ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Neuronal Damage ◽  
Autoimmune Encephalitis

Vitamin D3-mediated resistance to a multiple sclerosis model disease depends on myeloid cell 1,25-dihydroxyvitamin D3 synthesis and correlates with increased CD4+ T cell CTLA-4 expression

2020 ◽  
Vol 338 ◽  
pp. 577105 ◽  
Author(s):  
Justin A. Spanier ◽  
Faye E. Nashold ◽  
Corwin D. Nelson ◽  
Corinne E. Praska ◽  
Colleen E. Hayes
Keyword(s):  
Multiple Sclerosis ◽  
T Cell ◽  
Vitamin D3 ◽  
Myeloid Cell ◽  
Cd4 T Cell ◽  
Dihydroxyvitamin D3 ◽  
1,25 Dihydroxyvitamin D3 ◽  
Multiple Sclerosis Model
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