Mitoxantrone treatment in a patient with multiple sclerosis and pattern III lesions

@article{Grter2018MitoxantroneTI,
  title={Mitoxantrone treatment in a patient with multiple sclerosis and pattern III lesions},
  author={Thomas Gr{\"u}ter and Imke Metz and Anna Gahlen and Janina Kneiphof and Lidia Stork and Wolfgang Br{\"u}ck and Ralf Gold and Ingo Kleiter},
  journal={Clinical and Experimental Neuroimmunology},
  year={2018},
  volume={9}
}
Brain biopsies of multiple sclerosis patients identified three intraindividually stable lesion patterns. Apart from beneficial effects of plasma exchange in patients with type II lesions, little is known about how multiple sclerosis lesion histology could guide therapeutic decisions. 
2 Citations
Gene Therapy Approaches in an Autoimmune Demyelinating Disease: Multiple Sclerosis.
TLDR
In this review, 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's not far that the gene Therapy approaches would start in human subjects ensuring the highest levels of safety and efficacy.
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References

SHOWING 1-8 OF 8 REFERENCES
Relation between humoral pathological changes in multiple sclerosis and response to therapeutic plasma exchange
TLDR
Patients with multiple sclerosis with pattern II pathology are more likely to respond favourably to TPE than are patients with patterns I or III, and patients with several patterns of demyelination are equally likely to improve after TPE.
Differences in the Reponses to Apheresis Therapy of Patients With 3 Histopathologically Classified Immunopathological Patterns of Multiple Sclerosis
TLDR
Evidence is provided that the response to apheresis treatment is associated with immunopathological patterns, and patients with both patterns 1 and 2 improved clinically after apheresi treatment, but pattern 2 patients who showed signs of a humoral immune response benefited most.
Heterogeneity of multiple sclerosis lesions: Implications for the pathogenesis of demyelination
TLDR
At a given time point of the disease, the patterns of demyelination were heterogeneous between patients, but were homogenous within multiple active lesions from the same patient, suggesting that MS may be a disease with heterogeneous pathogenetic mechanisms.
Preferential Loss of Myelin‐Associated Glycoprotein Reflects Hypoxia‐Like White Matter Damage in Stroke and Inflammatory Brain Diseases
TLDR
Brain white matter lesions presenting with MAG loss and apoptotic-like oligodendrocyte destruction, irrespective of their primary disease cause, revealed a prominent nuclear expression of hypoxia inducible factor-1α in various cell types, including oligodendedrocytes.
Autoreactive CD8+ T cells in multiple sclerosis: a new target for therapy?
TLDR
The arguments for a possible role for CD8(+) T cells, a lymphocyte subset that has long been underrated in multiple sclerosis and should now be considered in new therapeutic approaches, are outlined.
Demyelination and neurodegeneration in multiple sclerosis: The role of hypoxia
TLDR
Initial tissue injury occurs already within the first hours and days after lipopolysaccharide (LPS) injection, which paves the way for focal demyelination occurring, at the earliest, 5 to 7 days later, and provides evidence that the mechanistic explanation is incomplete and falls short to explain some specific features of such lesions.
Mitoxantrone exerts both cytotoxic and immunoregulatory effects on activated microglial cells
TLDR
It is found that MX induced microglial cell death in a dose-dependent manner, and the cell death was mainly from late apoptosis and necrosis, which represents an important mechanism underlying the therapeutic effect of this drug on MS patients.
Roles of Activated Microglia in Hypoxia Induced Neuroinflammation in the Developing Brain and the Retina
TLDR
Because AMCs play a pivotal role in hypoxic injuries in the developing brain affecting both neurons and oligodendrocytes, a fuller understanding of the underlying molecular mechanisms of microglial activation under such conditions would be desirable for designing a novel therapeutic strategy for management of hypoxic damage.