Multiple sclerosis: Lessons from molecular neuropathology

@article{Lassmann2014MultipleSL,
  title={Multiple sclerosis: Lessons from molecular neuropathology},
  author={Hans Lassmann},
  journal={Experimental Neurology},
  year={2014},
  volume={262},
  pages={2-7}
}
  • H. Lassmann
  • Published 1 December 2014
  • Biology, Psychology
  • Experimental Neurology
Chronic Demyelination and Axonal Degeneration in Multiple Sclerosis: Pathogenesis and Therapeutic Implications
TLDR
The development of therapies to restore lost myelin and protect neurons is a promising avenue of investigation for the benefit of patients with MS.
Mechanisms of Neurodegeneration and Axonal Dysfunction in Progressive Multiple Sclerosis
TLDR
The gradual accumulation of disability characteristic of the disease seems to also result from a different set of mechanisms, including in particular immune reactions confined to the Central Nervous System, which could act in combination.
Altered astrocytic function in experimental neuroinflammation and multiple sclerosis
TLDR
This review will address the present knowledge that exists regarding the role of astrocytes in MS and experimental animal models of the disease, and suggest that disease progression and disability are better correlated with the maintenance of a persistent low‐grade inflammation inside the CNS, driven by local glial cells, like astroCytes and microglia.
Neuroprotective therapies for multiple sclerosis and other demyelinating diseases
  • P. Villoslada
  • Biology, Medicine
    Multiple Sclerosis and Demyelinating Disorders
  • 2016
TLDR
Improvement in the understanding of underlying biology, in the design of clinical trials specific for assessing neuroprotection, and new technologies for developing novel therapies for neuroprotection suggest a new avenue for treating MS, Optic Neuritis or Neuromyelitis Optica.
A basic overview of multiple sclerosis immunopathology
TLDR
To limit inflammatory demyelinating processes and delay disease progression, intervention to control inflammation must begin as early as possible.
The link of inflammation and neurodegeneration in progressive multiple sclerosis
TLDR
Current data and recent hypothesis about pathological forces that drive progression of damage in MS, i.e. cumulative cortical demyelination and neurodegeneration as well as diffuse alterations throughout white and grey matter in the brain and spinal cord are summarized.
Newly Identified Deficiencies in the Multiple Sclerosis Central Nervous System and Their Impact on the Remyelination Failure
TLDR
Results have led to a critical reassessment of MS pathogenesis, partly because EGF has little or no role in immunology, and other non-immunological MS abnormalities are reviewed.
Novel mechanism and biomarker of chronic progressive multiple sclerosis
TLDR
The mechanisms proposed in the pathogenesis of SP‐MS are summarized, and a new pathogenic mechanism for neurodegeneration mediated by unique cytotoxic helper T cells is proposed.
Interactions between Axon Cytoskeleton Proteins and Oligodendrocytes during Remyelination
TLDR
Four main factors might be involved in the repair defect in MS: I) astrocytic gliosis, II) axon degeneration, III) and/or OL alterations and finally the coexistence of these parameters with inflammatory cells and molecules in the lesions which renders the clarification of their respective involvement in the persistence of lesions difficult.
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It is proposed that the unequivocal selective early involvement of the astrocyte in MS lesions may have therapeutic relevance and multiple roles for this cell in the evolution of changes encountered in MS depending upon lesion stage and lesion topography.
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TLDR
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