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https://www.readbyqxmd.com/read/28322741/evidence-of-k-homeostasis-disruption-in-cellular-dysfunction-triggered-by-7-ketocholesterol-24s-hydroxycholesterol-and-tetracosanoic-acid-c24-0-in-158n-murine-oligodendrocytes
#1
Maryem Bezine, Meryam Debbabi, Thomas Nury, Rym Ben-Khalifa, Mohammad Samadi, Mustapha Cherkaoui-Malki, Anne Vejux, Jérôme de Sèze, Thibault Moreau, Mohamed El-Ayeb, Gérard Lizard
Imbalance in the homeostasis of K(+) ions has been reported to contribute to the pathogenesis of neurodegenerative diseases. 7-ketocholesterol (7KC), 24S-hydroxycholesterol (24S-OHC), and tetracosanoic acid (C24:0), often found at increased levels in patients with Alzheimer's disease, Multiple Sclerosis and X-ALD, are able to trigger numerous nerve cell dysfunctions. We therefore studied the impact of 7KC, 24S-OHC, and C24:0 on 158N murine oligodendrocytes, and determined their impact on K(+) homeostasis. The effects of 7KC, 24S-OHC and C24:0 on lipid membrane organization and membrane potential were examined with merocyanine 540 (MC540) and bis-(1,3-diethylthiobarbituric acid) trimethine oxonol (DiSBAC2(3)), respectively...
March 17, 2017: Chemistry and Physics of Lipids
https://www.readbyqxmd.com/read/28322157/diabetes-related-neurological-implications-and-pharmacogenomics
#2
Rojas Carranza Camilo Andrés, Bustos Cruz Rosa Helena, Pino Pinzón Carmen Juliana, Ariza Marquez Yeimy Viviana, Gómez Bello Rosa Margarita, Cañadas Garre Marisa
Diabetes mellitus (DM) is the most commonly occurring cause of neuropathy around the world and is beginning to grow in countries where there is a risk of obesity. DM Type II, (T2DM) is a common age-related disease and is a major health concern, particularly in developed countries in Europe where the population is aging. T2DM is a chronic disease which is characterised by hyperglycemia, hyperinsulinemia and insulin resistance, together with the body's inability to use glucose as energy. Such metabolic disorder produces a chronic inflammatory state, as well as changes in lipid metabolism leading to hypertriglyceridemia, thereby producing chronic deterioration of the organs and premature morbidity and mortality...
March 17, 2017: Current Pharmaceutical Design
https://www.readbyqxmd.com/read/28276944/imaging-and-spectroscopic-approaches-to-probe-brain-energy-metabolism-dysregulation-in-neurodegenerative-diseases
#3
Gilles Bonvento, Julien Valette, Julien Flament, Fanny Mochel, Emmanuel Brouillet
Changes in energy metabolism are generally considered to play an important role in neurodegenerative diseases such as Alzheimer's, Parkinson's, and Huntington's diseases. Whether these changes are causal or simply a part of self-defense mechanisms is a matter of debate. Furthermore, energy defects have often been discussed solely in the context of their probable neuronal origin without considering the cellular heterogeneity of the brain. Recent data point towards the existence of a tri-cellular compartmentation of brain energy metabolism between neurons, astrocytes, and oligodendrocytes, each cell type having a distinctive metabolic profile...
January 1, 2017: Journal of Cerebral Blood Flow and Metabolism
https://www.readbyqxmd.com/read/28269202/colony-size-effect-on-neural-differentiation-of-embryonic-stem-cells-microprinted-on-stromal-cells
#4
Ramila Joshi, James Buchanan, Hossein Tavana
Controlling cellular microenvironment to induce neural differentiation of embryonic stem cells (ESCs) remains a major challenge. We address this need by introducing a micro-engineered co-culture system that resembles embryonic development in terms of direct intercellular interactions and induces neural differentiation of ESCs. A polymeric aqueous two-phase system (ATPS)-mediated robotic microprinting technology allows precise localization of mouse ESCs (mESCs) over a layer of supporting stromal cells. mESCs proliferate over a 2-week culture period into a single colony of defined size...
August 2016: Conference Proceedings: Annual International Conference of the IEEE Engineering in Medicine and Biology Society
https://www.readbyqxmd.com/read/28256546/promoting-in-vivo-remyelination-with-small-molecules-a-neuroreparative-pharmacological-treatment-for-multiple-sclerosis
#5
Eva María Medina-Rodríguez, Ana Bribián, Amanda Boyd, Valle Palomo, Jesús Pastor, Alfonso Lagares, Carmen Gil, Ana Martínez, Anna Williams, Fernando de Castro
Multiple Sclerosis (MS) is a neurodegenerative disease where immune-driven demyelination occurs with inefficient remyelination, but therapies are limited, especially those to enhance repair. Here, we show that the dual phosphodiesterase (PDE)7- glycogen synthase kinase (GSK)3 inhibitor, VP3.15, a heterocyclic small molecule with good pharmacokinetic properties and safety profile, improves in vivo remyelination in mouse and increases both adult mouse and adult human oligodendrocyte progenitor cell (OPC) differentiation, in addition to its immune regulatory action...
March 3, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28252608/-clinical-guidelines-for-the-use-of-dimethyl-fumarate-in-relapsing-remitting-multiple-sclerosis
#6
V M Alifirova, A N Boiko, Ya V Vlasov, M V Davydovskaya, M N Zakharova, N A Malkova, E V Popova, S A Sivertseva, N N Spirin, N V Khachanova, Т Е Shmidt
Multiple sclerosis is a chronic demyelinating and neurodegenerative disease of the central nervous system, in which autoimmune inflammation and oxidative stress play essential pathogenetic roles. Activation and infiltration of immune cells in brain tissues, lipid peroxidation products, mitochondrial dysfunction, defective antioxidant protection, and many other pathological factors result in demyelination, axonal injury and death, and apoptosis of oligodendrocytes and neurons, all of which causes constant progression of the disease...
2017: Zhurnal Nevrologii i Psikhiatrii Imeni S.S. Korsakova
https://www.readbyqxmd.com/read/28227432/colony-size-effect-on-neural-differentiation-of-embryonic-stem-cells-microprinted-on-stromal-cells
#7
Ramila Joshi, James Buchanan, Hossein Tavana, Ramila Joshi, James Buchanan, Hossein Tavana, Ramila Joshi, James Buchanan, Hossein Tavana
Controlling cellular microenvironment to induce neural differentiation of embryonic stem cells (ESCs) remains a major challenge. We address this need by introducing a micro-engineered co-culture system that resembles embryonic development in terms of direct intercellular interactions and induces neural differentiation of ESCs. A polymeric aqueous two-phase system (ATPS)-mediated robotic microprinting technology allows precise localization of mouse ESCs (mESCs) over a layer of supporting stromal cells. mESCs proliferate over a 2-week culture period into a single colony of defined size...
August 2016: Conference Proceedings: Annual International Conference of the IEEE Engineering in Medicine and Biology Society
https://www.readbyqxmd.com/read/28213969/highly-efficient-neural-conversion-of-human-pluripotent-stem-cells-in-adherent-and-animal-free-conditions
#8
Dunja Lukovic, Andrea Diez Lloret, Petra Stojkovic, Daniel Rodríguez-Martínez, Maria Amparo Perez Arago, Francisco Javier Rodriguez-Jimenez, Patricia González-Rodríguez, José López-Barneo, Eva Sykova, Pavla Jendelova, Jelena Kostic, Victoria Moreno-Manzano, Miodrag Stojkovic, Shomi S Bhattacharya, Slaven Erceg
Neural differentiation of human embryonic stem cells (hESCs) and induced pluripotent stem cells (hiPSCs) can produce a valuable and robust source of human neural cell subtypes, holding great promise for the study of neurogenesis and development, and for treating neurological diseases. However, current hESCs and hiPSCs neural differentiation protocols require either animal factors or embryoid body formation, which decreases efficiency and yield, and strongly limits medical applications. Here we develop a simple, animal-free protocol for neural conversion of both hESCs and hiPSCs in adherent culture conditions...
February 18, 2017: Stem Cells Translational Medicine
https://www.readbyqxmd.com/read/28213437/%C3%AE-synuclein-multiple-system-atrophy-prions
#9
Amanda L Woerman, Joel C Watts, Atsushi Aoyagi, Kurt Giles, Lefkos T Middleton, Stanley B Prusiner
Multiple system atrophy (MSA) is a rapidly progressive neurodegenerative disease arising from the misfolding and accumulation of the protein α-synuclein in oligodendrocytes, where it forms glial cytoplasmic inclusions (GCIs). Several years of studying synthetic α-synuclein fibrils has provided critical insight into the ability of α-synuclein to template endogenous protein misfolding, giving rise to fibrillar structures capable of propagating from cell to cell. However, more recent studies with MSA-derived α-synuclein aggregates have shown that they have a similar ability to undergo template-directed propagation, like PrP prions...
February 17, 2017: Cold Spring Harbor Perspectives in Medicine
https://www.readbyqxmd.com/read/28170189/mesenchymal-stem-cells-yield-transient-improvements-in-motor-function-in-an-infant-rhesus-macaque-with-severe-early-onset-krabbe-disease
#10
Irina A Isakova, Kate C Baker, Jason Dufour, Donald G Phinney
Krabbe disease, or globoid cell leukodystrophy, is a rare disorder caused by deficient galactosylceramidase activity and loss of myelin-forming oligodendrocytes, resulting in progressive demyelination and severely impaired motor function. Disease symptoms in humans appear within 3-6 months of age (early infantile) and manifest as marked irritability, spasticity, and seizures. The disease is often fatal by the second year of life, with few effective treatment options. Herein we evaluated the therapeutic potential of mesenchymal stem cells (MSCs) administered intracranially to a 1-month-old rhesus macaque diagnosed with severe early-onset Krabbe disease that displayed neurologic and behavioral symptoms similar to those of human patients...
January 2017: Stem Cells Translational Medicine
https://www.readbyqxmd.com/read/28158198/cerebral-microbleeds-in-a-neonatal-rat-model
#11
Brianna Carusillo Theriault, Seung Kyoon Woo, Jason K Karimy, Kaspar Keledjian, Jesse A Stokum, Amrita Sarkar, Turhan Coksaygan, Svetlana Ivanova, Volodymyr Gerzanich, J Marc Simard
BACKGROUND: In adult humans, cerebral microbleeds play important roles in neurodegenerative diseases but in neonates, the consequences of cerebral microbleeds are unknown. In rats, a single pro-angiogenic stimulus in utero predisposes to cerebral microbleeds after birth at term, a time when late oligodendrocyte progenitors (pre-oligodendrocytes) dominate in the rat brain. We hypothesized that two independent pro-angiogenic stimuli in utero would be associated with a high likelihood of perinatal microbleeds that would be severely damaging to white matter...
2017: PloS One
https://www.readbyqxmd.com/read/28153739/the-challenge-of-regenerative-therapies-for-the-optic-nerve-in-glaucoma
#12
David J Calkins, Milos Pekny, Melissa L Cooper, Larry Benowitz
This review arose from a discussion of regenerative therapies to treat optic nerve degeneration in glaucoma at the 2015 Lasker/IRRF Initiative on Astrocytes and Glaucomatous Neurodegeneration. In addition to the authors, participants included Jonathan Crowston, Andrew Huberman, Elaine Johnson, Richard Lu, Hemai Phatnami, Rebecca Sappington, and Don Zack. Glaucoma is a neurodegenerative disease of the optic nerve, and is the leading cause of irreversible blindness worldwide. The disease progresses as sensitivity to intraocular pressure (IOP) is conveyed through the optic nerve head to distal retinal ganglion cell (RGC) projections...
January 30, 2017: Experimental Eye Research
https://www.readbyqxmd.com/read/28153532/fty720-fingolimod-reverses-%C3%AE-synuclein-induced-downregulation-of-brain-derived-neurotrophic-factor-mrna-in-oln-93-oligodendroglial-cells
#13
Ismael Segura-Ulate, Barbara Yang, Javier Vargas-Medrano, Ruth G Perez
Multiple system atrophy (MSA) is a demyelinating neurodegenerative disorder characterized by accumulation of aggregated α-synuclein (aSyn) inside oligodendrocyte precursors, mature oligodendroglia, and neurons. MSA dysfunction is associated with loss of trophic factor production by glial and neuronal cells. Here, we report that recombinant wild type human aSyn uptake by OLN-93, an oligodendroglia cell-line, reduced brain-derived neurotrophic factor (BDNF) expression. Furthermore, OLN-93 cells stably transfected with human wild type or an MSA-associated mutant aSyn, A53E that produces neuronal and glial inclusions, reduced BDNF mRNA to nearly unmeasurable qPCR levels...
January 31, 2017: Neuropharmacology
https://www.readbyqxmd.com/read/28153013/effects-of-dexamethasone-and-meloxicam-on-borrelia-burgdorferi-induced-inflammation-in-glial-and-neuronal-cells-of-the-central-nervous-system
#14
Geeta Ramesh, Alejandra N Martinez, Dale S Martin, Mario T Philipp
BACKGROUND: Lyme neuroborreliosis (LNB), caused by the spirochete Borrelia burgdorferi (Bb), affects both the central and peripheral nervous systems. Previously, we reported that in a model of acute LNB in rhesus monkeys, treatment with the anti-inflammatory drug dexamethasone significantly reduced both pleocytosis and levels of cerebrospinal fluid (CSF) immune mediators that were induced by Bb. Dexamethasone also inhibited the formation of inflammatory, neurodegenerative, and demyelinating lesions in the brain and spinal cord of these animals...
February 2, 2017: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/28127945/in-vivo-conversion-of-astrocytes-to-myelinating-cells-by-mir-302-367-and-valproate-to-enhance-myelin-repair
#15
Maryam Ghasemi-Kasman, Leila Zare, Hossein Baharvand, Mohammad Javan
Enhancement of repair potential for degenerative brain diseases has been a research priority during recent years. Considering recent advancements in the field of direct transdifferentiation, conversion of astrocytes as a prominent component of glial scars to the progenitor cells that contribute to the repair mechanisms seems interesting. Recently, we have reported miR-302/367-mediated in vivo conversion of astrocytes into neuroblasts and neurons. In the current study, we used miR-302/367 and valproate (VPA) to show the possibility of conversion of astrocytes to oligodendrocyte progenitor cells and myelinating cells in a cuprizone (CPZ)-induced model of demyelination...
January 27, 2017: Journal of Tissue Engineering and Regenerative Medicine
https://www.readbyqxmd.com/read/28121007/nanotubes-impregnated-human-olfactory-bulb-neural-stem-cells-promote-neuronal-differentiation-in-trimethyltin-induced-neurodegeneration-rat-model
#16
H E Marei, A A Elnegiry, A Zaghloul, A Althani, N Afifi, A Abd-Elmaksoud, A Farag, S Lashen, S Rezk, Z Shouman, C Cenciarelli, Anwarul Hasan
Neural stem cells (NSCs) are multipotent self-renewing cells that could be used in cellular-based therapy for a wide variety of neurodegenerative diseases including Alzheimer's diseases (AD), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), and multiple sclerosis (MS). Being multipotent in nature, they are practically capable of giving rise to major cell types of the nervous tissue including neurons, astrocytes and oligodendrocytes. This is in marked contrast to neural progenitor cells which are committed to a specific lineage fate...
January 25, 2017: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/28099414/neurotoxic-reactive-astrocytes-are-induced-by-activated-microglia
#17
Shane A Liddelow, Kevin A Guttenplan, Laura E Clarke, Frederick C Bennett, Christopher J Bohlen, Lucas Schirmer, Mariko L Bennett, Alexandra E Münch, Won-Suk Chung, Todd C Peterson, Daniel K Wilton, Arnaud Frouin, Brooke A Napier, Nikhil Panicker, Manoj Kumar, Marion S Buckwalter, David H Rowitch, Valina L Dawson, Ted M Dawson, Beth Stevens, Ben A Barres
Reactive astrocytes are strongly induced by central nervous system (CNS) injury and disease, but their role is poorly understood. Here we show that a subtype of reactive astrocytes, which we termed A1, is induced by classically activated neuroinflammatory microglia. We show that activated microglia induce A1 astrocytes by secreting Il-1α, TNF and C1q, and that these cytokines together are necessary and sufficient to induce A1 astrocytes. A1 astrocytes lose the ability to promote neuronal survival, outgrowth, synaptogenesis and phagocytosis, and induce the death of neurons and oligodendrocytes...
January 26, 2017: Nature
https://www.readbyqxmd.com/read/28093713/timing-of-future-remyelination-therapies-and-their-potential-to-stop-multiple-sclerosis-progression
#18
Burcu Zeydan, Moses Rodriguez, Orhun H Kantarci
Prior to the onset of demyelination in multiple sclerosis (MS), early oligodendrocyte injury, axonal degeneration and astroglial scarring occur. The irreversible progressive phase of MS begins when the axonal loss threshold is reached. Progressive disease onset has the highest impact on a poor prognosis in MS. Conversion to progressive disease is essentially an age-dependent process independent of disease duration and initial disease course. Although prevention of relapses has been the primary approach in the disease management, incomplete recovery from even the first relapse correlates with the long-term neurodegenerative phenotype of progressive MS onset...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/28069797/oligodendrocyte-development-and-cns-myelination-are-unaffected-in-a-mouse-model-of-severe-spinal-muscular-atrophy
#19
Ryan W O'Meara, Sarah E Cummings, Yves De Repentigny, Emily McFall, John-Paul Michalski, Marc-Olivier Deguise, Sabrina Gibeault, Rashmi Kothary
The childhood neurodegenerative disease spinal muscular atrophy (SMA) is caused by loss-of-function mutations or deletions in the Survival Motor Neuron 1 (SMN1) gene resulting in insufficient levels of survival motor neuron (SMN) protein. Classically considered a motor neuron disease, increasing evidence now supports SMA as a multi-system disorder with phenotypes discovered in cortical neuron, astrocyte, and Schwann cell function within the nervous system. In this study, we sought to determine whether Smn was critical for oligodendrocyte (OL) development and central nervous system myelination...
January 9, 2017: Human Molecular Genetics
https://www.readbyqxmd.com/read/28057080/combination-of-alpha-synuclein-immunotherapy-with-anti-inflammatory-treatment-in-a-transgenic-mouse-model-of-multiple-system-atrophy
#20
Elvira Valera, Brian Spencer, Jerel A Fields, Ivy Trinh, Anthony Adame, Michael Mante, Edward Rockenstein, Paula Desplats, Eliezer Masliah
Multiple system atrophy (MSA) is a fatal neurodegenerative disorder characterized by the pathological accumulation of alpha-synuclein (α-syn) in oligodendrocytes. Therapeutic efforts to stop or delay the progression of MSA have yielded suboptimal results in clinical trials, and there are no efficient treatments currently available for MSA patients. We hypothesize that combining therapies targeting different aspects of the disease may lead to better clinical outcomes. To test this hypothesis, we combined the use of a single-chain antibody targeting α-syn modified for improved central nervous system penetration (CD5-D5) with an unconventional anti-inflammatory treatment (lenalidomide) in the myelin basic protein (MBP)-α-syn transgenic mouse model of MSA...
January 5, 2017: Acta Neuropathologica Communications
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