The occult aftermath of boxing

The repeated head trauma experienced by boxers can lead to the development of dementia pugilistica (DP)--punch drunk syndrome. The neuropathology of DP in a classic report by Corsellis et al describes the presence of numerous neurofibrillary tangles in the absence of plaques, in contrast to the prof...

Full description

Saved in:
Bibliographic Details
Published in:Journal of neurology, neurosurgery and psychiatry neurosurgery and psychiatry, 1990-05, Vol.53 (5), p.373-378
Main Authors: Roberts, G W, Allsop, D, Bruton, C
Format: Article
Language:English
Subjects:
Adult
Aged
Aged, 80 and over
Alzheimer Disease - pathology
Amyloid - analysis
Amyloid beta-Peptides
Biological and medical sciences
Boxing - injuries
Brain - pathology
Brain Concussion - pathology
Brain Damage, Chronic - pathology
Dementia - pathology
Follow-Up Studies
Humans
Immunoenzyme Techniques
Injuries of the nervous system and the skull. Diseases due to physical agents
Male
Medical sciences
Middle Aged
Neurofibrils - ultrastructure
Traumas. Diseases due to physical agents
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:The repeated head trauma experienced by boxers can lead to the development of dementia pugilistica (DP)--punch drunk syndrome. The neuropathology of DP in a classic report by Corsellis et al describes the presence of numerous neurofibrillary tangles in the absence of plaques, in contrast to the profusion of tangles and plaques seen in Alzheimer's disease (AD). The DP cases used in that report were re-investigated with immunocytochemical methods and an antibody raised to the beta-protein present in AD plaques. We found that all DP cases with substantial tangle formation showed evidence of extensive beta-protein immunoreactive deposits (plaques). These diffuse "plaques" were not visible with Congo-red or standard silver stains. The degree of beta-protein deposition was comparable to that seen in AD. Our data indicate that the present neuropathological description of DP (tangles but no plaques) should be altered to acknowledge the presence of substantial beta-protein deposition (plaques). The molecular markers present in the plaques and tangles of DP are the same as those in AD. Similarities in clinical symptoms, distribution of pathology and neurochemical deficits also exist. Epidemiological studies have shown that head injury is a risk factor in AD. It is probable that DP and AD share common pathogenic mechanisms leading to tangle and plaque formation.
ISSN:0022-3050
1468-330X
DOI:10.1136/jnnp.53.5.373