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Fulltext Extraction, Analytical and Advanced Methods for Detection of Allura Red AC (E129) in Food and Beverages Products

Rovina K, Siddiquee S, Shaarani SM

Front Microbiol, 2016;7:798.
PMID: 27303385 DOI: 10.3389/fmicb.2016.00798

Allura Red AC (E129) is an azo dye that widely used in drinks, juices, bakery, meat, and sweets products. High consumption of Allura Red has claimed an adverse effects of human health including allergies, food intolerance, cancer, multiple sclerosis, attention deficit hyperactivity disorder, brain damage, nausea, cardiac disease and asthma due to the reaction of aromatic azo compounds (R = R' = aromatic). Several countries have banned and strictly controlled the uses of Allura Red in food and beverage products. This review paper is critically summarized on the available analytical and advanced methods for determination of Allura Red and also concisely discussed on the acceptable daily intake, toxicology and extraction methods.

Matched MeSH terms: Multiple Sclerosis
Fulltext The impact of physical exercise on the fatigue symptoms in patients with multiple sclerosis: a systematic review and meta-analysis

Razazian N, Kazeminia M, Moayedi H, Daneshkhah A, Shohaimi S, Mohammadi M, et al.

BMC Neurol, 2020 Mar 13;20(1):93.
PMID: 32169035 DOI: 10.1186/s12883-020-01654-y

BACKGROUND: Despite many benefits of the physical activity on physical and mental health of patients with Multiple Sclerosis (MS), the activity level in these patients is still very limited, and they continue to suffer from impairment in functioning ability. The main aim of this study is thus to closely examine exercise's effect on fatigue of patients with MS worldwide, with particular interest on Iran based on a comprehensive systematic review and meta-analysis.
METHODS: The studies used in this systematic review were selected from the articles published from 1996 to 2019, in national and international databases including SID, Magiran, Iranmedex, Irandoc, Google Scholar, Cochrane, Embase, ScienceDirect, Scopus, PubMed and Web of Science (ISI). These databases were thoroughly searched, and the relevant ones were selected based on some plausible keywords to the aim of this study. Heterogeneity index between studies was determined using Cochran's test and I2. Due to heterogeneity in studies, the random effects model was used to estimate standardized mean difference.
RESULTS: From the systematic review, a meta-analysis was performed on 31 articles which were fulfilled the inclusion criteria. The sample including of 714 subjects was selected from the intervention group, and almost the same sample size of 720 individuals were selected in the control group. Based on the results derived from this meta-analysis, the standardized mean difference between the intervention group before and after the intervention was respectively estimated to be 23.8 ± 6.2 and 16.9 ± 3.2, which indicates that the physical exercise reduces fatigue in patients with MS.
CONCLUSION: The results of this study extracted from a detailed meta-analysis reveal and confirm that physical exercise significantly reduces fatigue in patients with MS. As a results, a regular exercise program is strongly recommended to be part of a rehabilitation program for these patients.

Matched MeSH terms: Multiple Sclerosis/complications; Multiple Sclerosis/rehabilitation*
The past, present and future of imaging in multiple sclerosis

Ramli N, Rahmat K, Azmi K, Chong HT

J Clin Neurosci, 2010 Apr;17(4):422-7.
PMID: 20167498 DOI: 10.1016/j.jocn.2009.09.014

Despite technological advances in imaging, multiple sclerosis (MS) remains a clinical diagnosis that is supported, but not replaced, by laboratory or imaging findings. However, imaging is essential in the current diagnostic criteria of MS, for prediction of the likelihood of MS for patients with clinically isolated syndromes, correlation with lesion pathology and assessment of treatment outcome. This article gives an overview of imaging in MS with particular emphasis on the role of MRI in various diagnostic imaging criteria. Novel imaging for MS using 3 Tesla field strengths, magnetization transfer imaging, diffusion tensor imaging, magnetic resonance spectroscopy and cell-specific contrast will be reviewed.

Matched MeSH terms: Multiple Sclerosis/pathology*
Fulltext Brown-Séquard Syndrome as a First Presentation of Multiple Sclerosis

Ralot TK, Singh R, Bafna C, Rajesh S, Singh S

Malays J Med Sci, 2017 Aug;24(4):106-110.
PMID: 28951696 DOI: 10.21315/mjms2017.24.4.13

A female patient aged 48 years presented with sub-acute onset of weakness in right upper and lower limb over the past one month and numbness over left side of body below neck level. Multiple sclerosis (MS) presenting as Brown-Séquard syndrome is very rare. We present a case of hemicord myelitis which presented as Brown-Séquard syndrome as a first manifestation, which was later diagnosed as MS during subsequent relapses.

Matched MeSH terms: Multiple Sclerosis
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
Fulltext From the Molecular Mechanism to Pre-clinical Results: Anti-epileptic Effects of Fingolimod

Paudel YN, Angelopoulou E, Piperi C, Gnatkovsky V, Othman I, Shaikh MF

Curr Neuropharmacol, 2020;18(11):1126-1137.
PMID: 32310049 DOI: 10.2174/1570159X18666200420125017

Epilepsy is a devastating neurological condition characterized by long-term tendency to generate unprovoked seizures, affecting around 1-2 % of the population worldwide. Epilepsy is a serious health concern which often associates with other neurobehavioral comorbidities that further worsen disease conditions. Despite tremendous research, the mainstream anti-epileptic drugs (AEDs) exert only symptomatic relief leading to 30% of untreatable patients. This reflects the complexity of the disease pathogenesis and urges the precise understanding of underlying mechanisms in order to explore novel therapeutic strategies that might alter the disease progression as well as minimize the epilepsy-associated comorbidities. Unfortunately, the development of novel AEDs might be a difficult process engaging huge funds, tremendous scientific efforts and stringent regulatory compliance with a possible chance of end-stage drug failure. Hence, an alternate strategy is drug repurposing, where anti-epileptic effects are elicited from drugs that are already used to treat non-epileptic disorders. Herein, we provide evidence of the anti-epileptic effects of Fingolimod (FTY720), a modulator of sphingosine-1-phosphate (S1P) receptor, USFDA approved already for Relapsing-Remitting Multiple Sclerosis (RRMS). Emerging experimental findings suggest that Fingolimod treatment exerts disease-modifying anti-epileptic effects based on its anti-neuroinflammatory properties, potent neuroprotection, anti-gliotic effects, myelin protection, reduction of mTOR signaling pathway and activation of microglia and astrocytes. We further discuss the underlying molecular crosstalk associated with the anti-epileptic effects of Fingolimod and provide evidence for repurposing Fingolimod to overcome the limitations of current AEDs.

Matched MeSH terms: Multiple Sclerosis; Multiple Sclerosis, Relapsing-Remitting
High mobility group box 1 (HMGB1) protein in Multiple Sclerosis (MS): Mechanisms and therapeutic potential

Paudel YN, Angelopoulou E, C BK, Piperi C, Othman I

Life Sci, 2019 Dec 01;238:116924.
PMID: 31606383 DOI: 10.1016/j.lfs.2019.116924

Multiple sclerosis (MS) is an autoimmune chronic inflammatory disease with distinctive features of focal demyelination, axonal loss, activation of glial cells, and immune cells infiltration. The precise molecular mechanism underlying the disease progression remains enigmatic despite of the rapid progression on experimental and clinical MS research. The focus of MS therapy relies on the repression of the pathogenic autoimmune response without compromising an adaptive immune response. High mobility group box-1 (HMGB1) protein is a ubiquitous nuclear protein driving pro-inflammatory responses as well as targeting innate immune signaling that initiates and mediates autoimmunity as well as sterile injury. A considerable amount of experimental and human studies suggests the contribution of HMGB1 in the pathogenesis of MS/experimental autoimmune encephalitis (EAE). In this regard, HMGB1 protein has gained increased attention, as an emerging possible therapeutic target against MS. This is more strengthened by the promising therapeutic outcome demonstrated by HMGB1 neutralizing agents in the experimental EAE model. Herein, we attempt to shed more light on the molecular crosstalk of HMGB1 protein in the pathogenesis of MS/EAE suggesting that HMGB1 blockade could impede the pro-inflammatory loop that drives MS autoimmunity.

Matched MeSH terms: Multiple Sclerosis/drug therapy*; Multiple Sclerosis/metabolism; Multiple Sclerosis/pathology
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
Fulltext Longitudinally Extensive Transverse Myelitis in Highly Active Relapsing-remitting Multiple Sclerosis

Ng CF, Remli R, Tan HJ

Neurol India, 2021 11 9;69(5):1412-1413.
PMID: 34747827 DOI: 10.4103/0028-3886.329533

Transverse myelitis in multiple sclerosis is typically a short cord lesion with patchy distribution. Rarely, longitudinally extensive transverse myelitis can be seen in those with highly active disease or frequent relapses. The recognition of this uncommon phenotype in multiple sclerosis is important as the treatment is largely different from other demyelinating diseases. We describe a patient with highly active relapsing-remitting multiple sclerosis on interferon beta-1a who developed LETM after multiple relapses.

Matched MeSH terms: Multiple Sclerosis*
Fulltext Clinically definite multiple sclerosis in a young Malay female. A case report

Muthusamy E, Tan CT

Med J Malaysia, 1988 Jun;43(2):170-2.
PMID: 3237134
Matched MeSH terms: Multiple Sclerosis/diagnosis*; Multiple Sclerosis/physiopathology
Autoantibodies to tetraspanins (CD9, CD81 and CD82) in demyelinating diseases

Miyaji K, Paul F, Shahrizaila N, Umapathi T, Yuki N

J Neuroimmunol, 2016 Feb 15;291:78-81.
PMID: 26857499 DOI: 10.1016/j.jneuroim.2015.12.012

Tetraspanin family proteins, CD9, CD81 and CD82 are expressed in the oligodendrocytes and Schwann cells. We investigated autoantibodies to tetraspanin proteins in patients with demyelinating diseases. Sera were collected from 119 multiple sclerosis patients, 19 neuromyelitis optica, 42 acute inflammatory demyelinating polyneuropathy, 23 chronic inflammatory demyelinating polyneuropathy and 13 acute motor axonal neuropathy as well as 55 healthy controls. Few multiple sclerosis and acute inflammatory demyelinating polyneuropathy patients had autoantibodies that were weakly reactive to CD9 or CD81 but the significance is unclear. It is unlikely that these autoantibodies are pathogenic or serve as potential biomarkers in demyelinating diseases.

Matched MeSH terms: Multiple Sclerosis/blood*
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 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 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
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
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*
A previously misdiagnosed cohort of aquaporin 4 antibody-positive neuromyelitis optica spectrum disorder with disease duration of >10 years in multi-ethnic Penang, Malaysia: Clinical features and disease course

Hor JY, Lim TT, Chow HB, Tan K, Cheah CF, Ching YM, et al.

Mult Scler Relat Disord, 2016 Jan;5:89-90.
PMID: 26856950 DOI: 10.1016/j.msard.2015.11.008
Matched MeSH terms: Multiple Sclerosis/diagnosis*; Multiple Sclerosis/immunology*
Fulltext Encephalitis followed by optic neuritis: a case report and review of literature

Hasan S, B Basri H, P Hin L, Stanslas J

Pak J Med Sci, 2013 May;29(3):859-62.
PMID: 24353644

Encephalitis has been included in the causes of optic neuritis, but post encephalitic optic neuritis has been rarely reported. Majority of the cases of optic neuritis are either idiopathic or associated with multiple sclerosis, especially in western countries. This is very important in the Asian population where the incidence and prevalence of multiple sclerosis is not as high as in the Western countries. Although post infectious optic neuritis is more common in children, it can also be found in adults and is usually seen one to three weeks after a symptomatic infective prodrome. Here, we present a case of a 48 year-old-male who developed optic neuritis following viral encephalitis. His first presentation was with severe headache of two weeks duration. Viral encephalitis was diagnosed and treated. The patient presented again three weeks later with right eye pain and other features typical of optic neuritis. Corticosteroid therapy facilitated prompt recovery. Optic neuritis is an uncommon manifestation of encephalitis. It is important that both doctors and patients remain aware of post infectious cause of optic neuritis, which would enable a timely diagnosis and treatment of this reversible cause of vision loss.

Matched MeSH terms: Multiple Sclerosis
Fulltext Feasibility of remotely supervised transcranial direct current stimulation and cognitive remediation: A systematic review

Gough N, Brkan L, Subramaniam P, Chiuccariello L, De Petrillo A, Mulsant BH, et al.

PLoS One, 2020;15(2):e0223029.
PMID: 32092069 DOI: 10.1371/journal.pone.0223029

With technological advancements and an aging population, there is growing interest in delivering interventions at home. Transcranial Direct Current Stimulation (tDCS) and Cognitive Remediation (CR) as well as Cognitive Training (CT) have been widely studied, but mainly in laboratories or hospitals. Thus, the objectives of this review are to examine feasibility and the interventions components to support the domiciliary administration of tDCS and CR. We performed a systematic search of electronic databases, websites and reference lists of included articles from the first date available until October 31, 2018. Articles included had to meet the following criteria: original work published in English using human subjects, majority of tDCS or CR intervention administered remotely. A total of 39 studies were identified (16 tDCS, 23 CR/CT, 5 using both tDCS & CT). Four studies were single case studies and two were multiple case studies. The remaining 33 studies had a range of 9-135 participants. Five tDCS and nine CR/CT studies were double blind randomized controlled trials. Most studies focused on schizophrenia (8/39) and multiple sclerosis (8/39). Literature examined suggests the feasibility of delivering tDCS or CR/CT remotely with the support of information and communication technologies.

Matched MeSH terms: Multiple Sclerosis/therapy
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

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