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Open AccessJournal ArticleDOI

Axonal damage in acute multiple sclerosis lesions.

B. Ferguson, +3 more
- 01 Mar 1997 - 
- Vol. 120, Iss: 3, pp 393-399
TLDR
The results show the expression of amyloid precursor protein in damaged axons within acute multiple sclerosis lesions, and in the active borders of less acute lesions, which may have implications for the design and timing of therapeutic intervention.
Abstract
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 immunocytochemical experiments on paraffin embedded multiple sclerosis lesions of varying ages in order to see at which stage of the disease axonal damage, in addition to demyelination, occurs and may thus contribute to the development of disability in patients. The results show the expression of amyloid precursor protein in damaged axons within acute multiple sclerosis lesions, and in the active borders of less acute lesions. This observation may have implications for the design and timing of therapeutic intervention, one of the most important aims of which must be the reduction of permanent disability.

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Citations
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Journal ArticleDOI

Axonal transection in the lesions of multiple sclerosis.

TL;DR: 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.
Journal ArticleDOI

Biology of Oligodendrocyte and Myelin in the Mammalian Central Nervous System

TL;DR: This review deals with the recent progress related to the origin and differentiation of the oligodendrocytes, their relationships to other neural cells, and functional neuroglial interactions under physiological conditions and in demyelinating diseases.
Journal ArticleDOI

Multiple Sclerosis — The Plaque and Its Pathogenesis

TL;DR: This review focuses on the current knowledge of the pathogenesis of the inflammatory and neurodegenerative elements of the multiple sclerosis plaque.
Journal ArticleDOI

Demyelination increases radial diffusivity in corpus callosum of mouse brain.

TL;DR: In this article, the authors used diffusion tensor imaging (DTI) derived parameters to assess the extent of axonal damage, demyelination and axonal degeneration.
Journal ArticleDOI

Multiple Sclerosis: An Immune or Neurodegenerative Disorder?

TL;DR: Data that support neurodegeneration as the major cause of irreversible neurological disability in MS patients are reviewed and it is questioned whether inflammatory demyelination is primary or secondary in the disease process.
References
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Journal Article

Traumatically induced axonal injury: pathogenesis and pathobiological implications.

TL;DR: 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.
Journal ArticleDOI

The pathological evolution of multiple sclerosis.

TL;DR: 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.
Journal ArticleDOI

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

TL;DR: 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.
Journal ArticleDOI

Alzheimer's amyloid precursor protein accumulates within axonal swellings in human brain lesions.

TL;DR: Results implied that APP accumulated in spheroids regardless of beta protein depositions, because the axonal swellings were not immunolabeled with beta protein.
Journal ArticleDOI

Studies in multiple sclerosis: I. Normal values for paper electrophoresis of serum and cerebrospinal fluid proteins; description of the method with special reference to a practical concentration technique for cerebrospinal fluid protein

J. B. R. Cosgrove, +1 more
- 01 Dec 1965 - 
TL;DR: 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.
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