1,721,130 research outputs found
Serum levels of anti-myelin antibodies in relapsing-remitting multiple sclerosis patients during different phases of disease activity and immunomodulatory therapy
Full text linkAntibodies against myelin oligodendrocyte antigens have been found in the immunoreactive brain lesions of Multiple Sclerosis (MS) patients. Recently it has been proposed that these antibodies can be used as a prognostic marker in the course of disease. However, the serum levels of these autoantibodies during different phases of disease activity or after an immunomodulatory therapy have been poorly investigated. In this study the serum levels of anti-myelin oligodendrocyte glycoprotein (MOG) (directed against the epitopes 1-26 and 15-40) and anti-myelin basic protein (MBP) antibodies were sequentially measured in the same MS patient either in relapse or remission phases. We found that MS patients in the relapse phase had higher serum anti-MOG (peptides 1-26 and 15-40) and anti-MBP antibody levels than controls. In addition, the levels of anti-MOG 1-26 were also elevated during the relapse as compared with the remission phase but no significant changes were found in the levels of anti-MOG 15-40 of anti-MBP antibodies. We also evaluated the effect of interferon-beta (beta) therapy on anti-myelin antibodies. 1-year of interferon-beta treatment did not induce any changes in the levels of anti-MOG and anti-MBP antibodies. In conclusion, these data indicate that the use of peripheral levels of autoantibodies against MOG and MBP as marker of multiple sclerosis might be complicated by the phase of disease activity and by the epitope of the MOG protein used
Complement-mediated cytotoxicity of antibodies to the GABA(B) receptor
No full textabstract not availabl
Relapsing-remitting autoimmune agrypnia
No full textA woman affected by multiple cranial nerve palsy developed several episodes of total insomnia and respiratory crises resulting from central breathing depression associated with dysautonomic symptoms. Oligoclonal IgG bands were present in her cerebrospinal fluid, and immunohistochemistry showed increased binding of serum and cerebrospinal fluid on gamma-aminobutyric acid-ergic, synapse-rich neuronal cells. Immunosuppressive treatment and plasma exchange were followed by clinical improvement, with restoration of sleep architecture and disappearance of respiratory crises, suggesting autoimmune pathogenesis of the syndrome
Spontaneous recovery from anti-NMDAR encephalitis
No full textEncephalitis associated with antibodies (Abs) to the N-methyl-D-aspartate receptor (NMDAR) can occur in a paraneoplastic or non-paraneoplastic form. We report a young woman with non-paraneoplastic anti-NMDAR encephalitis who experienced spontaneous recovery
Stroke integrated care pathway during COVID-19 pandemic
No full textDear Editor,
We read with a great interest the publication on “Acute stroke management pathway during Coronavirus-19 pandemic” [1] where Baracchini et al. shared their experience in the management of stroke patients in a COVID-19 Hospital. In particular, they underlined how pre-triage, a mobile CT unit for COVID-19 patients, and dedicated COVID-19 areas were effective measures to deal with the COVID-19 emergency. We would like to share our experience on the changes of integrated care pathway (ICP) focused on ischemic stroke patients
Leptin as a marker of multiple sclerosis activity in patients treated with interferon-beta
No full textThe role of leptin was investigated in relapsing-remitting multiple sclerosis (MS). Control and MS patients showed comparable baseline serum leptin levels. During the first year of IFNbeta-1a treatment, leptin significantly decreased since 2 months after starting therapy in 11 patients who had no relapses. A significant decrease in IL12/IL10 ratio was observed in this group of patients only after 1 year of treatment. An increase of leptin was observed before the first clinical exacerbation in 13 relapsing patients. Leptin may play a pathogenic role in MS and can be a useful marker of disease activity and response to therapy
Comprehensive Observational and Longitudinal study on the Outbreak of Stroke-related Spasticity focusing on the Early Onset management with Botulinum NeuroToxin (COLOSSEO-BoNT): protocol for a real-world prospective observational study on upper limb spasticity
Full text linkIntroduction Poststroke spasticity (PSS) affects up to 40% of patients who had a stroke. Botulinum neurotoxin type A (BoNT-A) has been shown to improve spasticity, but the optimal timing of its application remains unclear. While several predictors of upper limb PSS are known, their utility in clinical practice in relation to BoNT-A treatment has yet to be fully elucidated. The COLOSSEO-BoNT study aims to investigate predictors of PSS and the effects of BoNT-A timing on spasticity-related metrics in a real-world setting. Methods and analysis The recruitment will involve approximately 960 patients who have recently experienced an ischaemic stroke (within 10 days, V0) and will follow them up for 24 months. Parameters will be gathered at specific intervals: (V1) 4, (V2) 8, (V3) 12, (V4) 18 months and (V5) 24 months following enrolment. Patients will be monitored throughout their rehabilitation and outpatient clinic journeys and will be compared based on their BoNT-A treatment status - distinguishing between patients receiving treatment at different timings and those who undergo rehabilitation without treatment. Potential predictors will encompass the Fugl-Meyer assessment, the National Institute of Health Stroke Scale (NIHSS), stroke radiological characteristics, performance status, therapies and access to patient care pathways. Outcomes will evaluate muscle stiffness using the modified Ashworth scale and passive range of motion, along with measures of quality of life, pain, and functionality. Ethics and dissemination This study underwent review and approval by the Ethics Committee of the Fondazione Policlinico Universitario Campus Bio-Medico, Rome, Italy. Regardless of the outcome, the findings will be disseminated through publication in peer-reviewed journals and presentations at national and international conferences. Trial registration number NCT05379413
Direct current stimulation modulates LTP and protein expression in rat hippocampus.
No full textIntroduction: Transcranial direct current stimulation (tDCS) can produce
a lasting polarity-specific modulation of cortical excitability in the brain
and it is increasingly used in experimental and clinical settings. A large amount of evidence supports the view that the after-effects of tDCS
are mediated by the interaction with molecular mechanisms of activity-dependent synaptic plasticity. The level of this interaction is unknown.
Some immediate early genes, such as c-fos and zif268, are rapidly induced following neuronal activation and may act as regulators of downstream target genes in coupling short-term events with long-term functional modifications of synaptic function.
Objectives: (1) To assess the effect of DCS on the induction of one of the
most studied NMDA receptor-dependent forms of long-term potentiation
(LTP) of synaptic activity; (2) to shed light on the molecular basis of DCS
after-effects.
Methods: We investigated the effect of anodal and cathodal DCS, applied
to rat brain slices, on LTP induction at CA3-CA1 hippocampal synapses (Shaffer collateral pathway). In the same experimental model, we also
explored by immunohistochemistry the effect of DCS on the expression of c-fos and zif268 proteins in CA and DG regions of the hippocampus.
Results: DCS determined a bidirectional modulation of LTP, that was increased by anodal and reduced by cathodal DCS. Moreover, we found that both polarities of DCS produce a marked and consistent increase in the expression of zif268 in the CA region of the hippocampus, while the same protocols of stimulation produce a less pronounced increase in c-fos expression, that was observed in both the CA and DG regions.
Conclusions: The present data confirm the interaction of DCS with the molecular pathways underlying activity-dependent synaptic plasticity.
The modulation of this processes might become of use in neurological diseases to help enhancing the adaptive and suppress the maladaptive forms of brain plasticity
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