Targeting remyelination treatment for multiple sclerosis

Nadeem, Maheen

doi:10.5316/wjn.v5.i1.5

Cited by 9 publications

(5 citation statements)

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“… 2012 ; Nadeem et al. 2015 ). CXCL12 binds to their receptor CXCR4 on the surface of oligodendrocyte precursor cells (OPCs) and stimulate its differentiation and maturation (Peng et al.…”

Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: Neuroprotective effects of ellagic acid on cuprizone-induced acute demyelination through limitation of microgliosis, adjustment of CXCL12/IL-17/IL-11 axis and restriction of mature oligodendrocytes apoptosis

Sanadgol

Golab

Tashakkor

et al. 2017

Pharmaceutical Biology

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Context: Ellagic acid (EA) is a natural phenol antioxidant with various therapeutic activities. However, the efficacy of EA has not been examined in neuropathologic conditions.Objective:In vivo neuroprotective effects of EA on cuprizone (cup)-induced demyelination were evaluated.Material and methods: C57BL/6 J mice were fed with chow containing 0.2% cup for 4 weeks to induce oligodendrocytes (OLGs) depletion predominantly in the corpus callosum (CC). EA was administered at different doses (40 or 80 mg/kg body weight/day/i.p.) from the first day of cup diet. Oligodendrocytes apoptosis [TUNEL assay and myelin oligodendrocyte glycoprotein (MOG+)/caspase-3+ cells), gliosis (H&E staining, glial fibrillary acidic protein (GFAP+) and macrophage-3 (Mac-3+) cells) and inflammatory markers (interleukin 17 (IL-17), interleukin 11 (IL-11) and stromal cell-derived factor 1 α (SDF-1α) or CXCL12] during cup intoxication were examined.Results: High dose of EA (EA-80) increased mature oligodendrocytes population (MOG+ cells, p < 0.001), and decreased apoptosis (p < 0.05) compared with the cup mice. Treatment with both EA doses did not show any considerable effects on the expression of CXCL12, but significantly down-regulated the expression of IL-17 and up-regulated the expression of IL-11 in mRNA levels compared with the cup mice. Only treatment with EA-80 significantly decreased the population of active macrophage (MAC-3+ cells, p < 0.001) but not reactive astrocytes (GFAP+ cells) compared with the cup mice.Discussion and conclusion: In this model, EA-80 effectively reduces lesions via reduction of neuroinflammation and toxic effects of cup on mature OLGs. EA is a suitable therapeutic agent for moderate brain damage in neurodegenerative diseases such as multiple sclerosis.

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“… 2012 ; Nadeem et al. 2015 ). CXCL12 binds to their receptor CXCR4 on the surface of oligodendrocyte precursor cells (OPCs) and stimulate its differentiation and maturation (Peng et al.…”

Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: Neuroprotective effects of ellagic acid on cuprizone-induced acute demyelination through limitation of microgliosis, adjustment of CXCL12/IL-17/IL-11 axis and restriction of mature oligodendrocytes apoptosis

Sanadgol

Golab

Tashakkor

et al. 2017

Pharmaceutical Biology

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“…The majority of the hit compounds identified in our screen have known targets, including dopaminergic, adrenergic, and cholinergic receptor signaling, cox, DNA repair, GABA uptake, opioid, P450/cholesterol biosynthesis, and selective estrogen receptor modulators (SERMs) ( Figure 3 C, Table 1 ) that have been identified from previous screens using rodent OPCs. 16 , 17 , 18 We also identified a number of targets and molecules that have been implicated but not well studied in OL biology such as Butyryl cholinesterase 19 , 20 , 21 (Tetraisopropyl pyrophosphoramide), BET bromodomain inhibitors 22 , 23 (I-BET151 and SGC-CBP30), and an NMDA receptor blocker (Ro 25–6981 maleate). 24 , 25 , 26 , 27 Most interestingly, we also identified two potent compounds that have not been previously reported to promote OL maturation or myelination, namely Ro1138452 and SR2211 that target the IP (prostacyclin) receptor pathway and retinoic acid receptor-related orphan receptor γ (RORγ), respectively.…”

Section: Resultsmentioning

confidence: 99%

“…As a validation of our screening platform, several of the compounds we identified, including muscarinic receptor antagonists (benztropine, clemastine and carbetapentane) cytochrome P450 inhibitors (clotrimazole, oxiconazole), SERMs (raloxifene, tamoxifen), dopamine receptor antagonists (fluphenazine), and ROCK inhibitors (ML9, ML7) ( Table 1 ) were recently reported as promoting remyelination of rodent OPCs. 9 , 11 , 16 , 33 , 34 , 35 In addition, inhibition of bromodomain containing proteins has been reported to help improve myelination in a murine system 22 , 23 but its role in the human system has not been examined. Tetraisopropyl pyrophosphoramide, an inhibitor of butyrylcholinesterase (BChE), is another compound of interest that was identified in our screen.…”

Section: Discussionmentioning

confidence: 99%

High-throughput screening for myelination promoting compounds using human stem cell-derived oligodendrocyte progenitor cells

Liu¹,

Berlinicke²,

Huang³

et al. 2023

iScience

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“…Multiple sclerosis (MS) is a complex chronic auto-immune inflammatory disease [1,2,3] characterized by repeated demyelination of the central nervous system [4,5,6] Demyelination is a pathophysiological condition including localized destruction of myelin [7,8] Moreover , its pathophysiology involves oligodendrocytes death and axonal degeneration. [8] Lesions or plaques composed of inflammatory and demyelinating cells cross with the correct transmission of nerve impulses and cause neuronal dysfunction mainly autonomic and sensorimotor defects , difficulties in thinking and fatigue.…”

Section: Introductionmentioning

confidence: 99%

Multiple Sclerosis is a Risk Factor for Hyperthyroidism and Interferon Beta Action on Thyroid Hormones via Novel Immuno-neuro-enzymological Mechanisms

Jasim¹

2022

AJPS

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Objective : Multiple sclerosis (MS) is a common neurological disease deeply linked with the immune-inflammatory disorders whereas the term (multiple) mostly refers to the multi-focal zones of Inflammation caused by lymphocytes and macrophages infiltration besides oligodendrocytes death. Accordingly , the dysfunctional immune system able to damage myelin ( a pivotal component of the central nervous system ) which responsible for communication among neurons. The aim of the present study is to innovate a biochemical relationship between MS and thyroid hormones (THs) by highlighting immunological responses and also to examine the action of Interferon beta (IFNβ) drug on thyroid hormone (THs) and thyroid stimulation hormone (TSH). Materials and methods: Sixty (60) Iraqi women in the age ranged (36-43) years were enrolled in the present study, (30) of them were MS patients and the other (30) were healthy. Anyway, the protocol of the study involved four groups: G1 is a healthy control group, G2 involved untreated MS patients, G3 included the MS patients treated with IFNβ for (6) weeks and G4 composed of the same patients treated with IFNβ for (12) weeks. THs (T4 and T3) and TSH levels were determined in sera of all groups. Results: Data of the present study have reported that T4 level was highly significant increase in sera of G2 compared with G1 while it was significant and highly significant decreased in G3 and G4 respectively compared with G2, the difference between G4 and G1 and also between G4 and G3 was significant. T3 level was highly significant increase in sera of G2 compared with G1 but it was highly significant decreased in G3 and G4 compared with G2, the difference between G4 and G1 was non-significant while the difference between G4 and G3 was significant. Conversely, TSH level was highly significant decreased in G2 compared with G1 but it was highly significant increase in G3 and G4 compared with G2, the difference between G4 and G1 and also between G4 and G3 was highly significant. Conclusions : Interestingly , the present study is the first in Iraq reporting that MS may be a key risk factor for hyperthyroidism and also the first suggesting that IFNβ regulates THs biosynthesis via novel immuno-neuro-enzymological mechanisms regarding thyroid peroxidase (TPO) and iodothyronine deiodinase 1 (D1), meanwhile the present study indicates that IFNβ has an indirect antioxidant activity. Moreover, the present study provides a definite clarification for the changed NF kappa B level in MS. Remarkably, the present study reveals that IFNβ is more potent on T3 than T4 while it has less action on TSH.

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Targeting remyelination treatment for multiple sclerosis

Cited by 9 publications

References 0 publications

RETRACTED ARTICLE: Neuroprotective effects of ellagic acid on cuprizone-induced acute demyelination through limitation of microgliosis, adjustment of CXCL12/IL-17/IL-11 axis and restriction of mature oligodendrocytes apoptosis

RETRACTED ARTICLE: Neuroprotective effects of ellagic acid on cuprizone-induced acute demyelination through limitation of microgliosis, adjustment of CXCL12/IL-17/IL-11 axis and restriction of mature oligodendrocytes apoptosis

High-throughput screening for myelination promoting compounds using human stem cell-derived oligodendrocyte progenitor cells

Multiple Sclerosis is a Risk Factor for Hyperthyroidism and Interferon Beta Action on Thyroid Hormones via Novel Immuno-neuro-enzymological Mechanisms

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