Impact of Repetitive Transcranial Magnetic Stimulation on Neurocognition and Oxidative Stress in Relapsing-Remitting Multiple Sclerosis: A Case Report.

Multiple sclerosis (MS) is a neurodegenerative condition whose manifestation and clinical evolution can present themselves in very different ways. Analogously, its treatment has to be personalized and the patient's response may be idiosyncratic. At this moment there is no cure for it, in addition to its clinical course sometimes being torpid, with a poor response to any treatment.

Clinical and Neurochemical Effects of Transcranial Magnetic Stimulation (TMS) in Multiple Sclerosis: A Study Protocol for a Randomized Clinical Trial.

Transcranial Magnetic Stimulation (TMS) is a technique based on the principles of electromagnetic induction. It applies pulses of magnetic radiation that penetrate the brain tissue, and it is a non-invasive, painless, and practically innocuous procedure. Previous studies advocate the therapeutic capacity of TMS in several neurodegenerative and psychiatric processes, both in animal models and in human studies.

Extra-Virgin Olive Oil Modifies the Changes Induced in Non-Nervous Organs and Tissues by Experimental Autoimmune Encephalomyelitis Models.

This study reveals the existence of oxidative stress (reactive oxygen species (ROS)) in non-nervous organs and tissues in multiple sclerosis (MS) by means of a model of experimental autoimmune encephalomyelitis (EAE) in rats. This model reproduces a similar situation to MS, as well as its relationship with intestinal microbiota starting from the changes in bacterial lipopolysaccharide levels (LPS) in the outer wall of the gram-negative bacteria. Finally, the administration of extra-virgin olive oil (EVOO), hydroxytirosol (HT), and oleic acid (OA) exert beneficial effects.

Comparative of transcranial magnetic stimulation and other treatments in experimental autoimmune encephalomyelitis.

The effects of transcranial magnetic stimulation (TMS), natalizumab (nata), dimethyl fumarate (DMF) and dexamethasone (DEX) on clinical score and oxidative stress produced by a single dose of myelin oligodendrocyte glycoprotein (MOG) in tail of Dark Agouti rats was studied. TMS (60Hz and 0.7 mT), nata (5mg/kg), DMF (15mg/kg) and DEX (300μg/kg) was applied for 21 after the administration of MOG (150μg).

Effects of transcranial magnetic stimulation on oxidative stress in experimental autoimmune encephalomyelitis.

Experimental autoimmune encephalomyelitis (EAE) reproduces a multiple sclerosis (MS)-like experimental model. The main objective was to evaluate the effect of extremely low-frequency electromagnetic fields (EL-EMF) application, like a paradigm of transcranial magnetic stimulation (TMS) in the development of EAE. Rats were injected with a single dose of 150 μg of myelin oligodendrocyte glycoprotein (MOG, fragment 35-55) to produce experimental MS.

Transcranial magnetic stimulation modifies astrocytosis, cell density and lipopolysaccharide levels in experimental autoimmune encephalomyelitis.

Aims: Experimental autoimmune encephalomyelitis (EAE) is considered a valid experimental model for multiple sclerosis, a chronic neuroinflammatory condition of the central nervous system. Additionally, some evidence has shown that some microbial products such as the bacterial lipopolysaccharide could lead to the activation of reactive immune cells, triggering neuroinflammation. Several studies have found that transcranial magnetic stimulation (TMS) may exert a neuroprotective effect.

Lipopolysaccharide Binding Protein and Oxidative Stress in a Multiple Sclerosis Model.

Recent findings in experimental autoimmune encephalomyelitis (EAE) suggest that altering certain bacterial populations present in the gut may lead to a proinflammatory condition, that could result in the development of multiple sclerosis (MS). Also, Reactive Oxygen Species seem to be involved in the course of MS. In this study, it has been aimed to relate all these variables starting from an analysis of the lipopolysaccharide (LPS) and LPS-binding protein (LBP) with the determination of parameters related to oxidative stress in the blood, brain and spinal cord.

Elevated melatonin levels in natalizumab-treated female patients with relapsing-remitting multiple sclerosis: relationship to oxidative stress.

Natalizumab is currently the most successful clinical treatment for multiple sclerosis. The use of this drug is associated with the reduction in the number of relapses and a slowing in disease progression, as well as an improvement in signs and symptoms displayed by the patients. To evaluate the effect of natalizumab on melatonin and its relationship with peripheral oxidative damage, we studied the serum melatonin levels in 18 patients with relapsing-remitting multiple sclerosis.

Oxidative stress and inflammation biomarkers in the blood of patients with Huntington's disease.

Objectives: Huntington's disease (HD) is a neurodegenerative disorder for which there is no effective treatment. Oxidative stress and inflammation are known to be involved in HD, but the precise relationship between the two remains unclear. The aim of this study was to analyze oxidative stress and inflammation biomarkers in blood of patients with HD with a view to identifying potential links between them.

Peripheral oxidative stress in relapsing-remitting multiple sclerosis.

Objectives: To evaluate levels of oxidative stress in blood samples in patients with relapsing-remitting MS (RR-MS).

Design And Methods: Peripheral blood samples were collected from 24 RR-MS patients and 15 healthy controls. Levels of the following were measured: carbonylated proteins, 8-hydroxy-2'deoxyguanosine (8OHdG), total glutathione, reduced glutathione (GSH), oxidized glutathione (GSSG), GSH/GSSG ratio, superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GRd), glutathione-S-transferase (GST), myeloperoxidase (MPO), antioxidant gap, total antioxidant capacity (PAO), global oxidative stress (GOS), serum vascular cell adhesion molecule-1 (sVCAM-1) and serum inter-cellular adhesion molecule 1 (sICAM-1).

[Oxidative stress biomarkers as indicator of chronic inflammatory joint diseases stage].

Objective: To evaluate the participation of oxidative stress (OS) on chronic inflammatory joint disease (CIJD), as well as its possible use as a diagnostic biomarker.

Patients And Methods: The study population comprised 29 patients with CIJD: 18 with rheumatoid arthritis (RA: 13 active/5 inactive); 11 with ankylosing spondylitis (AS: 7 active/4 inactive) and 13 healthy subjects. Activity of the disease was assessed by: RA patients, Disease Activity Score (DAS 28) and AS patients by means of Bath Ankylosing Spondylitis Disease Activity Index (BASDAI).

Infliximab reduces myeloperoxidase concentration in chronic inflammatory joint diseases.

Unlabelled: The present study evaluated the effect of infliximab on the myeloperoxidase (MPO) concentration in chronic inflammatory joint disease. Eighteen patients were divided into active and inactive groups. Erythrocyte sedimentation rate, C-reactive protein, white blood cell counts, MPO concentration, and biomarkers of oxidative stress were measured before and after the infusion of infliximab.

Effect of 17beta-estradiol on olfactory bulbectomy-induced oxidative stress and behavioral changes in rats.

The present study evaluated 17beta-estradiol (17betaE(2)) (2.5 mg/kg sc) effects on bilateral OBX-induced behavioral changes and oxidative stress. OBX in male Wistar rats produced an increase in lipid peroxidation products and a decline in reduced glutathione (GSH) content and glutathione peroxidase (GSH-Px) activity, together with an increase in caspase-3 activity.

Effect of testosterone on oxidative stress and cell damage induced by 3-nitropropionic acid in striatum of ovariectomized rats.

This paper evaluates the effects of testosterone (0.5 mg/kg subcutaneously (s.c.

Protective effect of carvedilol on oxidative stress induced by okadaic acid in N1E-115 cells.

The effect of carvedilol on oxidative and cell damage induced by okadaic acid in N1E-115 cells were studied. The effects of okadaic acid were evaluated as changes in: the quantity of lipid peroxidation products, protein carbonyl groups, reduced glutathione content (GSH), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), catalase and total lactate dehydrogenase (cell LDH). Additionally, a dose of carvedilol (10(-5)M) was added 2h before incubation with okadaic acid (50 nM) and was present until the end of the experiment (2h later added okadaic acid).

17 beta-Estradiol may affect vulnerability of striatum in a 3-nitropropionic acid-induced experimental model of Huntington's disease in ovariectomized rats.

The aim of present study was to clarify the role of female sex hormones in the development and course of neurodegenerative disease in an experimental model of Huntington's disease induced by 3-nitropropionic acid (NPA) (30 mg/kg intraperitoneally (i.p.)/day for 4 days) in ovariectomized rat.

Comparison of melatonin, vitamin E and L-carnitine in the treatment of neuro- and hepatotoxicity induced by thioacetamide.

This study was designed to evaluate and compare the effect of melatonin, vitamin E and L-carnitine on brain and liver oxidative stress and liver damage. Oxidative stress and hepatic failure were produced by a single dose of thioacetamide (TAA) (150 mg kg(-1)) in Wistar rats. A dose of either melatonin (3 mg kg(-1)) vitamin E (20 mg kg(-1) ) or L-carnitine (100 mg kg(-1)) was used.

Hepato- and neurotoxicity induced by thioacetamide: protective effects of melatonin and dimethylsulfoxide.

The effects of melatonin and dimethylsulfoxide (DMSO) on liver and brain oxidative stress, hepatic failure and blood urea nitrogen (BUN) level changes produced by a single dose of thioacetamide (TAA) in Wistar rats were studies. A dose of either melatonin (3 mg kg(-1)day(-1)) or DMSO (2 g kg(-1)day(-1)) was injected for 3 days before and for 2 days after the administration of TAA (150 mg kg(-1) i.p.

Protective effect of melatonin on 3-nitropropionic acid-induced oxidative stress in synaptosomes in an animal model of Huntington's disease.

The effect of melatonin (1 mg/kg BW i.p./day) on the oxidative changes produced by 3-nitropropionic acid (20 mg/kg BW/day for 4 days) in rat striatal and cortical synaptosomes was investigated.

Effect of glucocorticoids on 3-nitropropionic acid-induced oxidative stress in synaptosomes.

The present study with rat striatal and cortical synaptosomes evaluated the effect of dexamethasone (300 microg/kg i.p./day) with and without simultaneous adrenalectomy on the oxidative stress induced by 3-nitropropionic acid (20 mg/kg/day for 4 days).

Protective melatonin effect on oxidative stress induced by okadaic acid into rat brain.

We studied the effect of melatonin on the oxidative changes produced by the intracerebroventricular (i.c.v.

Melatonin effect on renal oxidative stress under constant light exposure.

Recently, numerous studies have shown antioxidant actions of melatonin. Melatonin at both physiological and pharmacological levels stimulates glutathione peroxidase, glutathione reductase and superoxide dismutase activities in the brains of rats and chickens. This study was designed to evaluate the effect of melatonin on nephropathy and oxidative stress under constant light exposure.