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Topics {✒️}

month download article/chapter related subjects tumour necrosis factor–alpha nitric oxide–mediated degeneration intravenous dose–ranging study monoclonal antibody campath–1h macrophage–depletion induced impairment interferon–beta 1b treatment interferon beta–1b treatment ifn–beta 1b treatment serum anti–thyroid antibodies full article pdf monoclonal antibody therapy interferon beta–1a magnetic resonance imaging privacy choices/manage cookies humanised monoclonal antibody campath–1h reduced interferon beta–1b progressive cerebral atrophy campath–1h antibody unrelenting cerebral atrophy established cerebral atrophy experimental autoimmune encephalomyelitis microglial–derived tnfalpha unusually active disease progressive multiple sclerosis humanized monoclonal antibodies toxic inflammatory environment inos–mediated toxicity nmda receptor expression kaplan mr check access instant access autoimmune diseases de waegh sm definite multiple sclerosis multiple sclerosis induces acute axonal damage scope submit manuscript differently affected depending ongoing axonal loss mechanism-based criteria human hematopoietic progenitors diffuse cutaneous scleroderma experimental cns remyelination recommended diagnostic criteria mouse cerebellar neurones neuronal tract degeneration champs study group

Questions {❓}

• Simon JH, Jacobs L, Kinkel RP (2001) Transcallosal bands: a sign of neuronal tract degeneration in early MS?
• Stadelmann C, Kerschensteiner M, Misgeld T, Bruck W, Hohlfeld R, Lassmann H (2002) BDNF and gp145trkB in multiple sclerosis brain lesions: neuroprotective interactions between immune and neuronal cells?
• Verdun E, Isoardo G, Oggero A, Ferrero B, Ghezzi A, Montanari E, Zaffaroni M, Durelli L (2002) Autoantibodies in multiple sclerosis patients before and during IFN–beta 1b treatment: are they correlated with the occurrence of autoimmune diseases?

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         headline:The window of therapeutic opportunity in multiple sclerosis
         description:From 1991–2002, we treated 58 patients with multiple sclerosis (MS) using the humanised monoclonal antibody, Campath–1H, which causes prolonged T lymphocyte depletion. Clinical and surrogate markers of inflammation were suppressed. In both the relapsing–remitting (RR) and secondary progressive (SP) stages of the illness, Campath–1H reduced the annual relapse rate (from 2.2 to 0.19 and from 0.7 to 0.001 respectively; both p < 0.001). Remarkably, MRI scans of patients with SP disease, treated with Campath–1H 7 years previously, showed no new lesion formation. However, despite these effects on inflammation, disability was differently affected depending on the phase of the disease. Patients with SPMS showed sustained accumulation of disability due to uncontrolled progression marked by unrelenting cerebral atrophy, attributable to ongoing axonal loss. The rate of cerebral atrophy was greatest in patients with established cerebral atrophy and highest inflammatory lesion burden before treatment (2.3 versus 0.7 ml/year; p = 0.04). In contrast, patients with RR disease showed an impressive reduction in disability at 6 months after Campath–1H (by a mean of 1.2 EDSS points) perhaps owing to a suppression of on–going inflammation in these patients with unusually active disease. In addition, there was a further significant, albeit smaller, mean improvement in disability up to 36 months after treatment.We speculate that this represents the beneficial effects of early rescue of neurons and axons from a toxic inflammatory environment, and that prevention of demyelination will prevent long–term axonal degeneration. These concepts are currently being tested in a controlled trial comparing Campath–1H and IFN–beta in the treatment of drug–naïve patients with early, active RR MS.
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      headline:The window of therapeutic opportunity in multiple sclerosis
      description:From 1991–2002, we treated 58 patients with multiple sclerosis (MS) using the humanised monoclonal antibody, Campath–1H, which causes prolonged T lymphocyte depletion. Clinical and surrogate markers of inflammation were suppressed. In both the relapsing–remitting (RR) and secondary progressive (SP) stages of the illness, Campath–1H reduced the annual relapse rate (from 2.2 to 0.19 and from 0.7 to 0.001 respectively; both p < 0.001). Remarkably, MRI scans of patients with SP disease, treated with Campath–1H 7 years previously, showed no new lesion formation. However, despite these effects on inflammation, disability was differently affected depending on the phase of the disease. Patients with SPMS showed sustained accumulation of disability due to uncontrolled progression marked by unrelenting cerebral atrophy, attributable to ongoing axonal loss. The rate of cerebral atrophy was greatest in patients with established cerebral atrophy and highest inflammatory lesion burden before treatment (2.3 versus 0.7 ml/year; p = 0.04). In contrast, patients with RR disease showed an impressive reduction in disability at 6 months after Campath–1H (by a mean of 1.2 EDSS points) perhaps owing to a suppression of on–going inflammation in these patients with unusually active disease. In addition, there was a further significant, albeit smaller, mean improvement in disability up to 36 months after treatment.We speculate that this represents the beneficial effects of early rescue of neurons and axons from a toxic inflammatory environment, and that prevention of demyelination will prevent long–term axonal degeneration. These concepts are currently being tested in a controlled trial comparing Campath–1H and IFN–beta in the treatment of drug–naïve patients with early, active RR MS.
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