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Fulltext Evaluation of neuroprotective effects of alpha-tocopherol in cuprizone-induced demyelination model of multiple sclerosis

Mitra NK, Xuan KY, Teo CC, Xian-Zhuang N, Singh A, Chellian J

Res Pharm Sci, 2020 Dec;15(6):602-611.
PMID: 33828603 DOI: 10.4103/1735-5362.301345

Background and Purpose: Multiple sclerosis (MS) is an autoimmune disorder characterized by demyelination and axonal loss. Quantitative estimation of behavioral, locomotor, and histological changes following the use of alpha-tocopherol (AT) in the animal model of MS have not been reported. The present study was planned to evaluate whether AT can improve sensorimotor dysfunction and reduce demyelination in the cuprizone (CPZ)-induced rat model of MS.
Experimental approach: Female Sprague-Dawley rats (8 weeks) were fed with cuprizone diet for 5 weeks followed by intraperitoneal injections of alpha-tocopherol (100 mg/Kg) or PBS for 2 weeks (groups E1 and E2, n = 8). Group C (n = 8) was fed with normal pellets followed by intraperitoneal doses of PBS. Open-field test and beam walking were carried out on every 10th day. The mean area of demyelination in the corpus callosum was quantified in Luxol® fast blue (LFB) stained histological sections of the forebrain. Qualitative grading for relative changes in the stains of myelinated fibers was also done.
Findings/Results: During withdrawal of CPZ, AT treatment increased the average speed by 22% in group E1, compared to group E2 (P < 0.05). The mean time to walk the beam was reduced in group E1 by 2.6% compared to group E2 (P < 0.05). The rearing frequency was increased in group E1 during week 6-7 compared to that in the period of CPZ treatment. The mean area of demyelination in the corpus callosum showed a 12% reduction in group E1 compared to group E2 (P < 0.05).
Conclusion and implications: Short-term AT therapy showed improvement in motor dysfunction and reduction of demyelination in the animal model of MS.

Matched MeSH terms: Multiple Sclerosis
Fulltext Hormones in experimental autoimmune encephalomyelitis (EAE) animal models

Ghareghani M, Ghanbari A, Eid A, Shaito A, Mohamed W, Mondello S, et al.

Transl Neurosci, 2021 Jan 01;12(1):164-189.
PMID: 34046214 DOI: 10.1515/tnsci-2020-0169

Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system (CNS) in which activated immune cells attack the CNS and cause inflammation and demyelination. While the etiology of MS is still largely unknown, the interaction between hormones and the immune system plays a role in disease progression, but the mechanisms by which this occurs are incompletely understood. Several in vitro and in vivo experimental, but also clinical studies, have addressed the possible role of the endocrine system in susceptibility and severity of autoimmune diseases. Although there are several demyelinating models, experimental autoimmune encephalomyelitis (EAE) is the oldest and most commonly used model for MS in laboratory animals which enables researchers to translate their findings from EAE into human. Evidences imply that there is great heterogeneity in the susceptibility to the induction, the method of induction, and the response to various immunological or pharmacological interventions, which led to conflicting results on the role of specific hormones in the EAE model. In this review, we address the role of endocrine system in EAE model to provide a comprehensive view and a better understanding of the interactions between the endocrine and the immune systems in various models of EAE, to open up a ground for further detailed studies in this field by considering and comparing the results and models used in previous studies.

Matched MeSH terms: Multiple Sclerosis
Fulltext The natural history of optic neuritis in Asian patients: an observational cohort study

Seah, B.H.A., Tow, S.L.C., Ong, K.C.B. Ong, Yang, C.C., Tsai, C.P., Lee, K.H., et al.

Neurology Asia, 2017;22(4):341-348.
MyJurnal

Optic neuritis, which may be a precursor to multiple sclerosis (MS), is an uncommon disease in
Asian patients. The Asian Collaborative Longitudinal Optic Neuritis Epidemiology (ACLONE) is
an observational cohort study that assessed the risk of recurrent optic neuritis and/or progression
of further neurologic events, either MS or neuromyelitis optica (NMO) in Asian patients with firstever
optic neuritis. Secondary aims were to study the presenting characteristics and visual outcome,
and to identify risk factors for development of either MS or NMO. A total of 112 patients (25 men
and 87 women) aged from 12 to 61 years were recruited from Singapore, Taiwan, South Korea and
Malaysia. Of these, 94 (84%) had unilateral optic neuritis, with the right eye involved in 45 patients
and the left eye in 49 patients and the remaining 18 (16%) had bilateral optic neuritis. Follow up
data was available for 104 patients, and patients were followed for a median duration of 25.9 months.
Of these patients, 6 patients were adjudicated to have reached the primary endpoint (composite of
MS/NMO and optic neuritis): 3 patients with recurrent optic neuritis also subsequently experienced
neurologic symptoms, and 3 patients without recurrent eye involvement had neurologic symptoms.
Only one patient was considered to have prototypical MS, the other 5 were diagnosed with NMO,
all with subsequent antibody confirmation. Optic neuritis in Asian patients has significantly different
presenting characteristics from the classic description. However, in the majority of the patients it is
usually a benign disease, with good visual outcome and no further events.

Matched MeSH terms: Multiple Sclerosis
Fulltext TRPM2 Channel in Microglia as a New Player in Neuroinflammation Associated With a Spectrum of Central Nervous System Pathologies

Malko P, Syed Mortadza SA, McWilliam J, Jiang LH

Front Pharmacol, 2019;10:239.
PMID: 30914955 DOI: 10.3389/fphar.2019.00239

Microglial cells in the central nervous system (CNS) are crucial in maintaining a healthy environment for neurons to function properly. However, aberrant microglial cell activation can lead to excessive generation of neurotoxic proinflammatory mediators and neuroinflammation, which represents a contributing factor in a wide spectrum of CNS pathologies, including ischemic stroke, traumatic brain damage, Alzheimer's disease, Parkinson's disease, multiple sclerosis, psychiatric disorders, autism spectrum disorders, and chronic neuropathic pain. Oxidative stress is a salient and common feature of these conditions and has been strongly implicated in microglial cell activation and neuroinflammation. The transient receptor potential melastatin-related 2 (TRPM2) channel, an oxidative stress-sensitive calcium-permeable cationic channel, is highly expressed in microglial cells. In this review, we examine the recent studies that provide evidence to support an important role for the TRPM2 channel, particularly TRPM2-mediated Ca2+ signaling, in mediating microglial cell activation, generation of proinflammatory mediators and neuroinflammation, which are of relevance to CNS pathologies. These findings lead to a growing interest in the TRPM2 channel, a new player in neuroinflammation, as a novel therapeutic target for CNS diseases.

Matched MeSH terms: Multiple Sclerosis
Fulltext Chronic Inflammatory Diseases at Secondary Sites Ensuing Urogenital or Pulmonary Chlamydia Infections

Cheok YY, Lee CYQ, Cheong HC, Looi CY, Wong WF

Microorganisms, 2020 Jan 17;8(1).
PMID: 31963395 DOI: 10.3390/microorganisms8010127

Chlamydia trachomatis and C. pneumoniae are members of the Chlamydiaceae family of obligate intracellular bacteria. The former causes diseases predominantly at the mucosal epithelial layer of the urogenital or eye, leading to pelvic inflammatory diseases or blindness; while the latter is a major causative agent for pulmonary infection. On top of these well-described diseases at the respective primary infection sites, Chlamydia are notoriously known to migrate and cause pathologies at remote sites of a host. One such example is the sexually acquired reactive arthritis that often occurs at few weeks after genital C. trachomatis infection. C. pneumoniae, on the other hand, has been implicated in an extensive list of chronic inflammatory diseases which include atherosclerosis, multiple sclerosis, Alzheimer's disease, asthma, and primary biliary cirrhosis. This review summarizes the Chlamydia infection associated diseases at the secondary sites of infection, and describes the potential mechanisms involved in the disease migration and pathogenesis.

Matched MeSH terms: Multiple Sclerosis
Fulltext Feasibility and toxicity of hematopoietic stem cell transplant in multiple sclerosis

Kuan TLT, Amini F, Seghayat MS

Iran J Basic Med Sci, 2017 Jul;20(7):729-738.
PMID: 28852436 DOI: 10.22038/IJBMS.2017.9000

Multiple sclerosis is a debilitating disease of the central nervous system. It affects people of all ages but is more prevalent among 20-40 year olds. Patients with MS can be presented with potentially any neurological symptom depending on the location of the lesion. A quarter of patients with MS suffer from bilateral lower limb spasticity among other symptoms. These devastating effects can be detrimental to the patient's quality of life. Hematopoietic stem cells (HSCs) have been used as a treatment for MS over the past 2 decades but their safety and efficacy has are undetermined. The objective of this study is to evaluate the feasibility and toxicity of autologous HSCs transplantation in MS. A literature search was done from 1997 to 2016 using different keywords. A total of 9 articles, which met the inclusion and exclusion criteria, were included in this review. The type of conditioning regimen and technique of stem cell mobilization are summarized and compared in this study. All studies reported high-dose immunosuppressive therapy with autologous HSCs transplantation being an effective treatment option for severe cases of multiple sclerosis. Fever, sepsis, and immunosuppression side effects were the most observed adverse effects that were reported in the selected studies. HSCs is a feasible treatment for patients with MS; nevertheless the safety is still a concern due to chemo toxicity.

Matched MeSH terms: Multiple Sclerosis
Gene Therapy Approaches in an Autoimmune Demyelinating Disease: Multiple Sclerosis

Islam MA, Kundu S, Hassan R

Curr Gene Ther, 2020;19(6):376-385.
PMID: 32141417 DOI: 10.2174/1566523220666200306092556

Multiple Sclerosis (MS) is the most common autoimmune demyelinating disease of the Central Nervous System (CNS). It is a multifactorial disease which develops in an immune-mediated way under the influences of both genetic and environmental factors. Demyelination is observed in the brain and spinal cord leading to neuro-axonal damage in patients with MS. Due to the infiltration of different immune cells such as T-cells, B-cells, monocytes and macrophages, focal lesions are observed in MS. Currently available medications treating MS are mainly based on two strategies; i) to ease specific symptoms or ii) to reduce disease progression. However, these medications tend to induce different adverse effects with limited therapeutic efficacy due to the protective function of the blood-brain barrier. Therefore, researchers have been working for the last four decades to discover better solutions by introducing gene therapy approaches in treating MS generally by following three strategies, i) prevention of specific symptoms, ii) halt or reverse disease progression and iii) heal CNS damage by promoting remyelination and axonal repair. In last two decades, there have been some remarkable successes of gene therapy approaches on the experimental mice model of MS - experimental autoimmune encephalomyelitis (EAE) which suggests that it is not far that the gene therapy approaches would start in human subjects ensuring the highest levels of safety and efficacy. In this review, we summarised the gene therapy approaches attempted in different animal models towards treating MS.

Matched MeSH terms: Multiple Sclerosis/genetics*; Multiple Sclerosis/immunology*; Multiple Sclerosis/therapy*
Natalizumab-Related Progressive Multifocal Leukoencephalopathy-Immune Reconstitution Inflammatory Syndrome: A Case Report Highlighting Clinical and MRI Features

Purohit B, Ganewatte E, Kollias SS

Malays J Med Sci, 2016 Sep;23(5):91-95.
PMID: 27904430

Multiple sclerosis (MS) patients treated with natalizumab often face the uncommon but severe complication of developing progressive multifocal leukoencephalopathy (PML). PML may be further complicated by immune reconstitution inflammatory syndrome (IRIS) after the removal of the drug. Since both PML and IRIS are associated with high morbidity and mortality rates, early clinical and radiological diagnosis of these complications is of paramount importance. Here, we report a case of an adult male patient who was diagnosed with PML after receiving natalizumab therapy for 6 years for the treatment of MS. Upon cessation of natalizumab, he presented with a paradoxical worsening of clinical and radiological findings consistent with an inflammatory brain injury due to IRIS. He was treated with high dose corticosteroid therapy followed by a gradual improvement in clinical and imaging findings. This article illustrates the magnetic resonance imaging (MRI) features of natalizumab-associated PML-IRIS, along with a brief overview of its clinical features, complications and management strategies.

Matched MeSH terms: Multiple Sclerosis
Glutamate receptors and transporters as comparative cues to the glutamatergic circuits of the avian and mammalian brain

Islam, M.R., Muzaimi, M., Abdullah, J.M.

Orient Neuron Nexus, 2011;2(1):2-9.
MyJurnal

Glutamate is the principal excitatory neurotransmitter in the central nervous system, and plays important roles in both physiological and pathological neuronal processes. Current understanding of the exact mechanisms involved in glutamate-induced neuronal excitotoxicity, in which excessive glutamate causes neuronal dysfunction and degeneration, whether acute or chronic, remain elusive. Conditions, due to acute insults such as ischaemia and traumatic brain injury, and chronic neurodegenerative disorders such as multiple sclerosis and motor neuron disease, suffer from the lack of translational neuroprotection in clinical setting to tackle glutamate excitotoxicity despite steady growth of animal studies that revealed complex cell death pathway interactions. In addition, glutamates are also released by non-neuronal cells including astrocytes and oligodendroglia. Thus, attempts to elucidate this complexity are closely related to our understanding of the glutamatergic circuitry in the brain. Neuronal cells develop a glutamatergic system at glutamatergic synapses that utilise glutamate as an intercellular signaling molecule to characterise the output, input, and termination of this signaling. As to signal input, various kinds of glutamate receptors have been identified and characterized. Na+-dependent glutamate transporters at the plasma membrane are responsible for the signal termination through sequestration of glutamate from the synaptic cleft. The signal output systems comprise vesicular storage and subsequent exocytosis of glutamate by using vesicular glutamate transporters. Similar to the mammalian brain, the regional differences of glutamatergic neurons and glutamate receptor neurons suggest many glutamatergic projections in the avian brain, as supported by recent evidence of glutamate-related genes distribution. Glutamatergic target areas are expected to show high activity of glutamate transporters that remove released glutamate from the synaptic clefts. This review summarises and compares glutamatergic circuits in the avian and mammalian brain, particularly in the olfactory pathway, the paffial organization of glutamatergic neurons and connection with the striatum, hippocampal-septal pathway, visual and auditory pathways, and granule cell-Purkinje cell pathway in the cerebellum. Comparative appreciation of these glutamatergic circuits, particularly with the localisation and/or expression of specific subtypes of glutamate transporters, would provide the morphological basis for physiological and pharmacological designs that supplement existing animal studies of the current proposed mechanisms that underlie glutamate-induced neuronal excitotoxicity.

Matched MeSH terms: Multiple Sclerosis
Fulltext Foot reflexology therapy for non-specific low back pain condition : a protocol for a randomized controlled trial

Nor Dalila Marican, Rozita Hod, Nadiah Wan-Arfah, Azmi Hassan

Int J Public Health Res, 2018;8(1):933-938.
MyJurnal

Introduction Non-specific low back pain is one of the most common physical ailments
affecting millions of people worldwide. This condition constitutes a
significant public health problem and was listed as a prevalent health
complaint in most societies. Even though there are many anecdotal claims
for reflexology in the treatment of various conditions such as a migraine,
arthritis and multiple sclerosis, but very little clinical evidence exists for
reflexology on the management of low back pain per se. This study aims to
evaluate the effects of foot reflexology therapy as an adjunctive treatment to
the Malaysian low back pain standard care in relieving pain and promoting
health-related quality of life among people with non-specific low back pain.
Methods This is a parallel randomized controlled trial with pre and post-treatment
study design. The study setting for the intervention located at Penawar
Reflexology Center, Kuala Terengganu, Malaysia. A total of 100
participants with non-specific low back pain will be allocated to one of two
groups, using a randomization computer program of Research Randomizer.
The control group will receive low back pain standard care, while the
intervention group will receive standard care plus eight sessions of foot
reflexology therapy. The pain intensity and health-related quality of life
scores will be measured using Visual Analogue Scale and Euro-quality of
life scale respectively in both groups. The study was approved by the
Human Research Ethics Committee of University Sultan Zainal Abidin
(UHREC/2016/2/011). The study protocol was registered at
ClinicalTrials.gov, with the ID number of NCT02887430.
Measurements Outcome measures will be undertaken at pre-intervention (week 1), postintervention
(week 6) and follow-up (week 10).
Conclusions This will be the first trial to compare the foot reflexology therapy with
control group among people who medically diagnosed with non-specific low
back pain in Malaysia. The result of this study will contribute to better
management of this population, especially for Malaysia healthcare setting.

Study site: Penawar Reflexology Center, Kuala Terengganu, Malaysia

Matched MeSH terms: Multiple Sclerosis

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