کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
3063907 1580387 2015 8 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Impact of glatiramer acetate on paraclinical markers of neuroprotection in multiple sclerosis: A prospective observational clinical trial
ترجمه فارسی عنوان
اثر گلوتریمر استات بر نشانگرهای پاراکلینیکی محافظت از عصب در مولتیپل اسکلروزیس: یک کارآزمایی بالینی پیشرفته
موضوعات مرتبط
علوم زیستی و بیوفناوری ایمنی شناسی و میکروب شناسی ایمونولوژی
چکیده انگلیسی


• Investigation of GA-treated and therapy-naive MS-patients over 24 months
• Multimodal approach: serum BDNF, FACS, RT-PCR, evoked potentials, and cerebral MRI
• GA transiently increases serum IgG antibody response to MBP.
• GA does not alter BDNF serum or expression levels on peripheral immune cells.
• GA had no influence on neuropsychological, evoked potential and cerebral MRI outcome parameters.

Data from in vitro and animal studies support a neuroprotective role of glatiramer acetate (GA) in multiple sclerosis (MS). We investigated prospectively whether treatment with GA leads to clinical and paraclinical changes associated with neuroprotection in patients with relapsing-remitting (RR) MS. Primary aim of this clinical study was to determine serum BDNF levels in RR-MS patients who were started on GA as compared to patients who remained therapy-naive throughout 24 months. Secondary outcomes included relapses and EDSS, cognition, quality of life, fatigue and depression, BDNF expression levels on peripheral immune cells (FACS, RT-PCR), serum anti-myelin basic peptide (MBP) antibody status, evoked potential and cerebral MRI studies. While GA treatment did not alter serum levels or expression levels on peripheral immune cells of BDNF over time it resulted in a transient increase of serum IgG antibody response to MBP, mainly due to subtype IgG1 (p < 0.05), after 3 months. However, no significant differences were found between GA treated and therapy-naive patients with regard to serum BDNF and intracellular BDNF expression levels, nerve conduction (including median and tibial nerve somatosensory, pattern-shift visual and upper and lower limb motor evoked potentials) or MRI (including volume of hyperintense lesions, volume of hypointense lesions after CE, mean diffusivity and fractional anisotropy) outcome parameters. In conclusion, our findings do not support a major impact of GA treatment on paraclinical markers of neuroprotection in human RR-MS.

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ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Neuroimmunology - Volume 287, 15 October 2015, Pages 98–105
نویسندگان
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