Neuronal cytoskeletal changes are an early consequence of repetitive head injury

@article{Geddes1999NeuronalCC,
  title={Neuronal cytoskeletal changes are an early consequence of repetitive head injury},
  author={Jennian F. Geddes and G. H. Vowles and J. A. R. Nicoll and Tam{\'a}s R{\'e}v{\'e}sz},
  journal={Acta Neuropathologica},
  year={1999},
  volume={98},
  pages={171-178}
}
Abstract While neuropathological studies have established the pathology of dementia pugilistica to be similar to that of Alzheimer’s disease, there is little information about the early histological changes caused by the repetitive trauma that eventually produces dementia pugilistica. We have examined the brains of four young men and a frontal lobectomy specimen from a fifth, age range 23– 28 years, all of whom suffered mild chronic head injury. There were two boxers, a footballer, a mentally… 
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References

SHOWING 1-10 OF 64 REFERENCES
Alzheimer's neurofibrillary changes. A topographic study.
TLDR
Recent observations of neurofibrillary changes in 2 fatal neurologic diseases occurring on the island of Guam, the parkinsonism-dementia complex and the amyotrophic lateral sclerosis syndrome, revealed their quite remarkable numbers and symmetric changes.
Staining of amyloid precursor protein to study axonal damage in mild head injury.
TLDR
Immunostaining with an antibody to amyloid precursor protein, a marker of fast axonal transport, showed multifocal axonal injury in all five patients and all had axonal damage in the fornices, which are important in memory function.
Comparison of the neurofibrillary pathology in Alzheimer’s disease and familial presenile dementia with tangles
TLDR
Results indicate that in the two diseases tau undergoes the same modifications; they confirm that neurofibrillary tangles and neuropil threads like those in AD can exist independently of β-amyloid deposits and that their presence is associated with dementia.
Neurofibrillary tangles, but not Alzheimer‐type pathology, in a young boxer
TLDR
The case of a 23‐year‐old boxer, whose brain showed neurofibrillary tangles in all neocortical areas, but remarkable sparing of medial temporal lobe structures, suggests that the mechanism of tangle formation induced by repetitive head trauma may be different from that in Alzheimer's disease.
Increased numbers of βAPP‐immunoreactive neurones in the entorhinal cortex after head injury
IN a previous publication we hypothesized that Alzheimer's disease (AD) can be induced by the age-related increase in expression of β-amyloid precursor protein (βAPP) in the medial temporal lobe.
Cytoskeletal pathology in familial cerebral amyloid angiopathy (British type) with non-neuritic amyloid plaque formation
TLDR
In FAB severe cytoskeletal pathology is present in areas most affected by amyloid plaque deposits, thus suggesting a localised neurotoxic effect of the poorly characterised amyloidsogenic peptide characteristic of this condition.
The effects of repetitive mild brain injury on cytoskeletal protein and behavior.
TLDR
The behavioral study revealed that after repetitive mild percussion, rats show less efficient habituation to a new environment and it is suggested that the repetition of subthreshold mechanical brain injury may trigger cytoskeletal alteration related to neuronal degeneration.
Chapter 16 Molecular pathology of head trauma: altered βAPP metabolism and the aetiology of Alzheimer's disease
TLDR
Screening of the amyloid precursor protein gene on chromosome 21, which gives rise to the β -amyloid protein found in plaques, has revealed a mutation in some AD families.
Neurofibrillary degeneration in amyotrophic lateral sclerosis/parkinsonism-dementia complex of Guam. Immunochemical characterization of tau proteins.
TLDR
The data suggest that the tau triplet found in amyotrophic lateral sclerosis/parkinsonism-dementia complex of Guam is similar to that observed in Alzheimer's disease, and the regional distribution of tau proteins differs in these disorders.
Stalning af amyloid percursor protein to study axonal damage in mild head Injury
TLDR
Immunostaining with an antibody to amyloid precursor protein, a marker of fast axonal transport, showed multifocal axonal injury in all five patients and all had axonal damage in the fornices, which are important in memory function.
...
1
2
3
4
5
...