Axonal damage in acute multiple sclerosis lesions.

  title={Axonal damage in acute multiple sclerosis lesions.},
  author={B. Ferguson and Malgosia K. Matyszak and Margaret M. Esiri and V Hugh Perry},
  journal={Brain : a journal of neurology},
  volume={120 ( Pt 3)},
One of the histological hallmarks of early multiple sclerosis lesions is primary demyelination, with myelin destruction and relative sparing of axons. On the other hand, it is widely accepted that axonal loss occurs in, and is responsible for, the permanent disability characterizing the later chronic progressive stage of the disease. In this study, we have used an antibody against amyloid precursor protein, known to be a sensitive marker of axonal damage in a number of other contexts, in… 

Figures from this paper

Acute axonal damage in multiple sclerosis is most extensive in early disease stages and decreases over time.

The results indicate that a putative axon-protective treatment should start as early as possible and include strategies preventing T cell/macrophage-mediated axon destruction and leading to remyelination of axons.

Axonal injury in multiple sclerosis

  • H. Lassmann
  • Biology
    Journal of neurology, neurosurgery, and psychiatry
  • 2003
Ferguson et al showed that massive axonal damage occurs during the stage of active demyelination in fresh lesions, and suggested that massive acute axonal injury occurs during a small time window of about two weeks after onset of MS.

Neurofilament Changes in Multiple Sclerosis

This chapter will discuss axonal changes in multiple sclerosis, specifically alterations in neurofilament phosphorylation states, and potential mechanisms of axonal protection.

Acute axonal injury in multiple sclerosis. Correlation with demyelination and inflammation.

Characterizing the association of axonal injury and histopathological hallmarks of multiple sclerosis such as demyelination, cellular infiltration and expression of inflammatory mediators and quantifying axonal reduction and signs of acute axonal damage in early lesion development of chronic multiple sclerosis found it to be independent of demYelinating activity and inflammation.

Axonal transection in the lesions of multiple sclerosis.

Transected axons are common in the lesions of multiple sclerosis, and axonal transection may be the pathologic correlate of the irreversible neurologic impairment in this disease.

Inflammatory demyelination is not central to the pathogenesis of multiple sclerosis

Previously considered to be caused by an autoimmune process mainly affecting myelin and oligodendrocytes in the white matter, recent data provide evidence that a generalized, diffuse neurodegenerative process plays an important role in the pathogenesis of MS.

Axonal degeneration in the pathogenesis of multiple sclerosis

Axonal Loss in Multiple Sclerosis

Current knowledge regarding the extent, timing, and clinical significance of axonal damage in the pathogenesis of MS is discussed.



Traumatically induced axonal injury: pathogenesis and pathobiological implications.

This work reviews the pathobiology of traumatically induced axonal injury and considers its attendant consequences in terms of Wallerian degeneration and subsequent deafferentation in the context of mild, moderate and severe traumatic brain injury.

Traumatic brain injury in rat produces changes of beta-amyloid precursor protein immunoreactivity.

Traumatic brain injury appears to induce several types of APP changes, including excitoprotective, modulating intracellular Ca2+ responses, and the decreased immunoreactivity noticed in the periphery of the lesion may render the neurones in this region more vulnerable to secondary injury mechanisms.

Studies in multiple sclerosis

Details of the technique of concentration of CSF and paper electrophoresis as used in the laboratory for the past eight years agree with those advocated recently as a standardized method.

The pathological evolution of multiple sclerosis

The ability of this technique to throw new light on the process of plaque formation and evaluation is critically assessed and the role of changing fluid content of the extra cellular spaces of the CNS in influencing interpretation of the more conventional clinical and electrophysiological findings is discussed.

Studies in multiple sclerosis. I.

  • C. Plum
  • Psychology
    Acta psychiatrica et neurologica Scandinavica. Supplementum
  • 1959

Benign and secondary progressive multiplecells and neuroglia cells . In frozen sections APP was detected sclerosis : a preliminary quantitative MRI study

  • J Neurol
  • 1994

Bundles of amyloid precursor protein-immunoreactive Peters G. Multiple sclerosis In: Minckler J, editor. Pathology of axons in human cerebrovascular white matter lesions. Acta the nervous system

  • Neuropathol (Berl)
  • 1968

Precursor of amyloid protein in Alzheimer in permanent disability . disease undergoes fast anterograde axonal transport

    The morbid anatomy of the demyelinative Li GL , Farooque M , Holtz A , Olsson Y . Changes of beta - amyloid precursor protein after compression trauma to the spinal cord : diseases

    • Amer J Med
    • 1952