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Multiple sclerosis molecular mechanism

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https://www.readbyqxmd.com/read/28334918/adaptive-human-immunity-drives-remyelination-in-a-mouse-model-of-demyelination
#1
Mohamed El Behi, Charles Sanson, Corinne Bachelin, Léna Guillot-Noël, Jennifer Fransson, Bruno Stankoff, Elisabeth Maillart, Nadège Sarrazin, Vincent Guillemot, Hervé Abdi, Isabelle Cournu-Rebeix, Bertrand Fontaine, Violetta Zujovic
One major challenge in multiple sclerosis is to understand the cellular and molecular mechanisms leading to disease severity progression. The recently demonstrated correlation between disease severity and remyelination emphasizes the importance of identifying factors leading to a favourable outcome. Why remyelination fails or succeeds in multiple sclerosis patients remains largely unknown, mainly because remyelination has never been studied within a humanized pathological context that would recapitulate major events in plaque formation such as infiltration of inflammatory cells...
February 22, 2017: Brain: a Journal of Neurology
https://www.readbyqxmd.com/read/28330499/a-novel-multi-network-approach-reveals-tissue-specific-cellular-modulators-of-fibrosis-in-systemic-sclerosis
#2
Jaclyn N Taroni, Casey S Greene, Viktor Martyanov, Tammara A Wood, Romy B Christmann, Harrison W Farber, Robert A Lafyatis, Christopher P Denton, Monique E Hinchcliff, Patricia A Pioli, J Matthew Mahoney, Michael L Whitfield
BACKGROUND: Systemic sclerosis (SSc) is a multi-organ autoimmune disease characterized by skin fibrosis. Internal organ involvement is heterogeneous. It is unknown whether disease mechanisms are common across all involved affected tissues or if each manifestation has a distinct underlying pathology. METHODS: We used consensus clustering to compare gene expression profiles of biopsies from four SSc-affected tissues (skin, lung, esophagus, and peripheral blood) from patients with SSc, and the related conditions pulmonary fibrosis (PF) and pulmonary arterial hypertension, and derived a consensus disease-associate signature across all tissues...
March 23, 2017: Genome Medicine
https://www.readbyqxmd.com/read/28319253/heat-shock-protein-expression-in-cerebral-x-linked-adrenoleukodystrophy-reveals-astrocyte-stress-prior-to-myelin-loss
#3
Anna Lena Görtz, Laura A N Peferoen, Wouter H Gerritsen, Johannes M van Noort, Marianna Bugiani, Sandra Amor
AIMS: X-linked adrenoleukodystrophy (X-ALD) is a genetic white matter disorder in which demyelination occurs due to accumulation of very long chain fatty acids. Inflammation in the brain white matter is a hallmark of the pathology of cerebral X-ALD, but the underlying pathogenic mechanisms are still largely unknown. In other inflammatory demyelinating disorders such as multiple sclerosis, the expression of heat shock proteins (HSPs) in combination with interferon-γ (IFN-γ) has been suggested to play a prominent role in the initiation of demyelination and inflammation...
March 20, 2017: Neuropathology and Applied Neurobiology
https://www.readbyqxmd.com/read/28303450/dr%C3%AE-1-mog-35-55-treatment-reduces-lesion-volumes-and-improves-neurological-deficits-after-traumatic-brain-injury
#4
Liu Yang, Zhijia Liu, Honglei Ren, Lei Zhang, Siman Gao, Li Ren, Zhi Chai, Roberto Meza-Romero, Gil Benedek, Arthur A Vandenbark, Halina Offner, Minshu Li
Traumatic brain injury (TBI) results in severe neurological impairments without effective treatments. Inflammation appears to be an important contributor to key pathogenic events such as secondary brain injury following TBI and therefore serves as a promising target for novel therapies. We have recently demonstrated the ability of a molecular construct comprised of the human leukocyte antigen (HLA)-DRα1 domain linked covalently to mouse (m)MOG-35-55 peptide (DRα1-MOG-35-55 construct) to reduce CNS inflammation and tissue injury in animal models of multiple sclerosis and ischemic stroke...
March 16, 2017: Metabolic Brain Disease
https://www.readbyqxmd.com/read/28302146/relationship-of-acute-axonal-damage-wallerian-degeneration-and-clinical-disability-in-multiple-sclerosis
#5
Shailender Singh, Tobias Dallenga, Anne Winkler, Shanu Roemer, Brigitte Maruschak, Heike Siebert, Wolfgang Brück, Christine Stadelmann
BACKGROUND: Axonal damage and loss substantially contribute to the incremental accumulation of clinical disability in progressive multiple sclerosis. Here, we assessed the amount of Wallerian degeneration in brain tissue of multiple sclerosis patients in relation to demyelinating lesion activity and asked whether a transient blockade of Wallerian degeneration decreases axonal loss and clinical disability in a mouse model of inflammatory demyelination. METHODS: Wallerian degeneration and acute axonal damage were determined immunohistochemically in the periplaque white matter of multiple sclerosis patients with early actively demyelinating lesions, chronic active lesions, and inactive lesions...
March 17, 2017: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/28286738/tsc2-rheb-signaling-mediates-erk-dependent-regulation-of-mtorc1-activity-in-c2c12-myoblasts
#6
Mitsunori Miyazaki, Tohru Takemasa
The enhanced rate of protein synthesis in skeletal muscle cells results in a net increase in total protein content that leads to skeletal muscle growth/hypertrophy. The mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK)-dependent regulation of the activity of mechanistic target of rapamycin (mTOR) and subsequent protein synthesis has been suggested as a regulatory mechanism; however, the exact molecular processes underlying such a regulation are poorly defined. The purpose of this study was to investigate regulatory mechanisms involved in the MEK/ERK-dependent pathway leading to mTORC1 activation in skeletal muscle cells...
March 2017: FEBS Open Bio
https://www.readbyqxmd.com/read/28277827/progress-and-prospects-for-the-use-and-the-understanding-of-the-mode-of-action-of-autologous-hematopoietic-stem-cell-transplantation-in-the-treatment-of-multiple-sclerosis
#7
Fredrika Collins, Majid Kazmi, Paolo A Muraro
A substantial proportion of patients with multiple sclerosis (MS) do not respond to pharmacological treatments and no currently approved therapy has been convincingly demonstrated to prevent or stop disease progression. With MS widely believed to be an auto-immune disease, immunoablative therapy followed by autologous haematopoietic stem cell transplantation (I/AHSCT) is being investigated as an alternative therapeutic option. Areas covered: With the results of phase III comparative trials only a few years away, this article reviews animal and clinical trials of I/AHSCT in the treatment of MS and discusses possible immunological mechanisms behind its action...
March 20, 2017: Expert Review of Clinical Immunology
https://www.readbyqxmd.com/read/28261198/a-fas-hi-lymphoproliferative-phenotype-reveals-non-apoptotic-fas-signaling-in-htlv-1-associated-neuroinflammation
#8
Soraya Maria Menezes, Fabio E Leal, Tim Dierckx, Ricardo Khouri, Daniele Decanine, Gilvaneia Silva-Santos, Saul V Schnitman, Ramon Kruschewsky, Giovanni López, Carolina Alvarez, Michael Talledo, Eduardo Gotuzzo, Douglas F Nixon, Jurgen Vercauteren, David Brassat, Roland Liblau, Anne Mieke Vandamme, Bernardo Galvão-Castro, Johan Van Weyenbergh
Human T-cell lymphotropic virus (HTLV)-1 was the first human retrovirus to be associated to cancer, namely adult T-cell leukemia (ATL), but its pathogenesis remains enigmatic, since only a minority of infected individuals develops either ATL or the neuroinflammatory disorder HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). A functional FAS -670 polymorphism in an interferon (IFN)-regulated STAT1-binding site has been associated to both ATL and HAM/TSP susceptibility. Fas(hi) T stem cell memory (Tscm) cells have been identified as the hierarchical apex of ATL, but have not been investigated in HAM/TSP...
2017: Frontiers in Immunology
https://www.readbyqxmd.com/read/28253983/micrornas-aging-cellular-senescence-and-alzheimer-s-disease
#9
P H Reddy, J Williams, F Smith, J S Bhatti, S Kumar, M Vijayan, R Kandimalla, C S Kuruva, R Wang, M Manczak, X Yin, A P Reddy
Aging is a normal process of living being. It has been reported that multiple cellular changes, including oxidative damage/mitochondrial dysfunction, telomere shortening, inflammation, may accelerate the aging process, leading to cellular senescence. These cellular changes induce age-related human diseases, including Alzheimer's, Parkinson's, multiple sclerosis, amyotrophic lateral sclerosis, cardiovascular, cancer, and skin diseases. Changes in somatic and germ-line DNA and epigenetics are reported to play large roles in accelerating the onset of human diseases...
2017: Progress in Molecular Biology and Translational Science
https://www.readbyqxmd.com/read/28251676/the-balance-between-cathepsin-c-and-cystatin-f-controls-remyelination-in-the-brain-of-plp1-overexpressing-mouse-a-chronic-demyelinating-disease-model
#10
Takahiro Shimizu, Wilaiwan Wisessmith, Jiayi Li, Manabu Abe, Kenji Sakimura, Banthit Chetsawang, Yoshinori Sahara, Koujiro Tohyama, Kenji F Tanaka, Kazuhiro Ikenaka
In demyelinating diseases such as multiple sclerosis (MS), an imbalance between the demyelination and remyelination rates underlies the degenerative processes. Microglial activation is observed in demyelinating lesions; however, the molecular mechanism responsible for the homeostatic/environmental change remains elusive. We previously found that cystatin F (CysF), a cysteine protease inhibitor, is selectively expressed in microglia only in actively demyelinating/remyelinating lesions but ceases expression in chronic lesions, suggesting its role in remyelination...
March 2, 2017: Glia
https://www.readbyqxmd.com/read/28241767/multiple-sclerosis-an-example-of-pathogenic-viral-interaction
#11
REVIEW
Walter Fierz
A hypothesis is formulated on viral interaction between HHV-6A and EBV as a pathogenic mechanism in Multiple Sclerosis (MS). Evidence of molecular and genetic mechanisms suggests a link between HHV-6A infection and EBV activation in the brain of MS patients leading to intrathecal B-cell transformation. Consequent T-cell immune response against the EBV-infected cells is postulated as a pathogenic basis for inflammatory lesion formation in the brain of susceptible individuals. A further link between HHV-6A and EBV involves their induction of expression of the human endogenous retrovirus HERV-K18-encoded superantigen...
February 28, 2017: Virology Journal
https://www.readbyqxmd.com/read/28197174/extremely-low-frequency-electromagnetic-fields-stimulation-modulates-autoimmunity-and-immune-responses-a-possible-immuno-modulatory-therapeutic-effect-in-neurodegenerative-diseases
#12
REVIEW
Fabio Guerriero, Giovanni Ricevuti
Increasing evidence shows that extremely low frequency electromagnetic fields (ELF-EMFs) stimulation is able to exert a certain action on autoimmunity and immune cells. In the past, the efficacy of pulsed ELF-EMFs in alleviating the symptoms and the progression of multiple sclerosis has been supported through their action on neurotransmission and on the autoimmune mechanisms responsible for demyelination. Regarding the immune system, ELF-EMF exposure contributes to a general activation of macrophages, resulting in changes of autoimmunity and several immunological reactions, such as increased reactive oxygen species-formation, enhanced phagocytic activity and increased production of chemokines...
December 2016: Neural Regeneration Research
https://www.readbyqxmd.com/read/28195200/dynamical-footprint-of-cross-reactivity-in-a-human-autoimmune-t-cell-receptor
#13
Amit Kumar, Francesco Delogu
The present work focuses on the dynamical aspects of cross-reactivity between myelin based protein (MBP) self-peptide and two microbial peptides (UL15, PMM) for Hy.1B11 T-cell receptor (TCR). This same TCR was isolated from a patient suffering from multiple sclerosis (MS). The study aims at highlighting the chemical interactions underlying recognition mechanisms between TCR and the peptides presented by Major Histocompatibility Complex (MHC) proteins, which form a crucial component in adaptive immune response against foreign antigens...
February 14, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28192470/differentiation-of-oligodendrocyte-progenitor-cells-from-dissociated-monolayer-and-feeder-free-cultured-pluripotent-stem-cells
#14
Tomoko Yamashita, Yuki Miyamoto, Yoshio Bando, Takashi Ono, Sakurako Kobayashi, Ayano Doi, Toshihiro Araki, Yosuke Kato, Takayuki Shirakawa, Yutaka Suzuki, Junji Yamauchi, Shigetaka Yoshida, Naoya Sato
Oligodendrocytes myelinate axons and form myelin sheaths in the central nervous system. The development of therapies for demyelinating diseases, including multiple sclerosis and leukodystrophies, is a challenge because the pathogenic mechanisms of disease remain poorly understood. Primate pluripotent stem cell-derived oligodendrocytes are expected to help elucidate the molecular pathogenesis of these diseases. Oligodendrocytes have been successfully differentiated from human pluripotent stem cells. However, it is challenging to prepare large amounts of oligodendrocytes over a short amount of time because of manipulation difficulties under conventional primate pluripotent stem cell culture methods...
2017: PloS One
https://www.readbyqxmd.com/read/28167760/sphingosine-1-phosphate-receptor-modulation-suppresses-pathogenic-astrocyte-activation-and-chronic-progressive-cns-inflammation
#15
Veit Rothhammer, Jessica E Kenison, Emily Tjon, Maisa C Takenaka, Kalil Alves de Lima, Davis M Borucki, Chun-Cheih Chao, Annabel Wilz, Manon Blain, Luke Healy, Jack Antel, Francisco J Quintana
Multiple sclerosis (MS) is an autoimmune inflammatory demyelinating disease of the CNS that causes disability in young adults as a result of the irreversible accumulation of neurological deficits. Although there are potent disease-modifying agents for its initial relapsing-remitting phase, these therapies show limited efficacy in secondary progressive MS (SPMS). Thus, there is an unmet clinical need for the identification of disease mechanisms and potential therapeutic approaches for SPMS. Here, we show that the sphingosine 1-phosphate receptor (S1PR) modulator fingolimod (FTY720) ameliorated chronic progressive experimental autoimmune encephalomyelitis in nonobese diabetic mice, an experimental model that resembles several aspects of SPMS, including neurodegeneration and disease progression driven by the innate immune response in the CNS...
February 6, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/28155200/mmp-12-a-promising-therapeutic-target-for-neurological-diseases
#16
REVIEW
Bharath Chelluboina, Koteswara Rao Nalamolu, Jeffrey D Klopfenstein, David M Pinson, David Z Wang, Raghu Vemuganti, Krishna Kumar Veeravalli
The role of matrix metalloproteinase-12 (MMP-12) in the pathogenesis of several inflammatory diseases such as chronic obstructive pulmonary disease, emphysema, and asthma is well established. Several new studies and recent reports from our laboratory and others highlighted the detrimental role of MMP-12 in the pathogenesis of several neurological diseases. In this review, we discuss in detail the pathological role of MMP-12 and the possible underlying molecular mechanisms that contribute to disease pathogenesis in the context of central nervous system diseases such as stroke, spinal cord injury, and multiple sclerosis...
February 2, 2017: Molecular Neurobiology
https://www.readbyqxmd.com/read/28131211/potential-pathophysiological-pathways-that-can-explain-the-positive-effects-of-exercise-on-fatigue-in-multiple-sclerosis-a-scoping-review
#17
REVIEW
Martin Langeskov-Christensen, Etienne J Bisson, Marcia L Finlayson, Ulrik Dalgas
BACKGROUND: Fatigue is one of the most common and most disabling symptoms of multiple sclerosis (MS). It is a multidimensional and complex symptom with multifaceted origins, involving both central and peripheral fatigue mechanisms. Exercise has proven to be safe for people with MS, with cumulating evidence supporting significant reductions in fatigue. However, the potential pathophysiological pathways that can explain the positive effects of exercise on fatigue in MS remain elusive. OBJECTIVES: The objectives were, in PwMS (1) to update the knowledge on the pathophysiology underlying primary and secondary fatigue, and (2) to discuss potential pathophysiological pathways that can explain the positive effects of exercise on MS fatigue...
February 15, 2017: Journal of the Neurological Sciences
https://www.readbyqxmd.com/read/28128996/endogenous-repair-and-development-inspired-therapy-of-neurodegeneration-in-progressive-multiple-sclerosis
#18
Ethan Hollingsworth, Jamil Khouri, Jaime Imitola
In recent years, there has been progress in understanding the etiology and immune mechanisms of multiple sclerosis (MS). However, for most, once the diagnosis is made, significant pathology is already present in the central nervous system (CNS), and in many, this leads to neurodegeneration, which accumulates in disability. Although, the mechanisms of such progression are poorly understood, new data suggest lack of remyelination paired with dysfunction of neurons along with stem and progenitor cells as the basis and recent developmental studies suggest that CNS repair processes share mechanisms with development...
January 27, 2017: Expert Review of Neurotherapeutics
https://www.readbyqxmd.com/read/28121444/whole-proteome-peptide-microarrays-for-profiling-autoantibody-repertoires-within-multiple-sclerosis-and-narcolepsy
#19
Arash Zandian, Björn Forsström, Anna Häggmark-Månberg, Jochen M Schwenk, Mathias Uhlén, Peter Nilsson, Burcu Ayoglu
The underlying molecular mechanisms of autoimmune diseases are poorly understood. To unravel the autoimmune processes across diseases, comprehensive and unbiased analyses of proteins targets recognized by the adaptive immune system are needed. Here we present an approach starting from high-density peptide arrays to characterize autoantibody repertoires and to identify new autoantigens. A set of ten plasma and serum samples from subjects with multiple sclerosis, narcolepsy, and without any disease diagnosis were profiled on a peptide array representing the whole proteome, hosting 2...
February 9, 2017: Journal of Proteome Research
https://www.readbyqxmd.com/read/28120152/copy-number-variations-in-amyotrophic-lateral-sclerosis-piecing-the-mosaic-tiles-together-through-a-systems-biology-approach
#20
REVIEW
Giovanna Morello, Maria Guarnaccia, Antonio Gianmaria Spampinato, Valentina La Cognata, Velia D'Agata, Sebastiano Cavallaro
Amyotrophic lateral sclerosis (ALS) is a devastating and still untreatable motor neuron disease. Despite the molecular mechanisms underlying ALS pathogenesis that are still far from being understood, several studies have suggested the importance of a genetic contribution in both familial and sporadic forms of the disease. In addition to single-nucleotide polymorphisms (SNPs), which account for only a limited number of ALS cases, a consistent number of common and rare copy number variations (CNVs) have been associated to ALS...
January 24, 2017: Molecular Neurobiology
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