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alpha-Internexin immunoreactivity reflects variable neuronal vulnerability in Alzheimer's disease and supports the role of the beta-amyloid plaques in inducing neuronal injury.

Abstract
This study investigated the role of alpha-internexin in the neuronal alterations associated with beta-amyloid plaque formation in Alzheimer's disease (AD). Cortical neurons could be defined by their variable content of neurofilament (NF) triplet and alpha-internexin proteins, with a distinct population of supragranular pyramidal cells containing alpha-internexin alone. Both NF triplet and alpha-internexin were localized to reactive axonal structures in physically damaged neurons in experimental trauma models. Similarly, NF triplet and alpha-internexin immunoreactive neurites were localized to plaques densely packed with beta-amyloid fibrils in preclinical AD cases, indicating that certain plaques may cause structural injury or impediment of local axonal transport. However, alpha-internexin, and not NF triplet, ring-like reactive neurites were present in end-stage AD cases, indicating the relatively late involvement of neurons that selectively contain alpha-internexin. These results implicate the expression of specific intermediate filament proteins in a distinct hierarchy of differential neuronal vulnerability to AD.
AuthorsTracey C Dickson, Jyoti A Chuckowree, Meng Inn Chuah, Adrian K West, James C Vickers
JournalNeurobiology of disease (Neurobiol Dis) Vol. 18 Issue 2 Pg. 286-95 (Mar 2005) ISSN: 0969-9961 [Print] United States
PMID15686957 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Amyloid beta-Peptides
  • Carrier Proteins
  • Intermediate Filament Proteins
  • Neurofilament Proteins
  • alpha-internexin
Topics
  • Aged
  • Aged, 80 and over
  • Alzheimer Disease (metabolism, pathology)
  • Amyloid beta-Peptides (metabolism)
  • Animals
  • Brain Injuries (metabolism, pathology)
  • Carrier Proteins (metabolism)
  • Causality
  • Cerebral Cortex (metabolism, pathology)
  • Disease Models, Animal
  • Female
  • Humans
  • Immunohistochemistry
  • Intermediate Filament Proteins
  • Male
  • Middle Aged
  • Nerve Degeneration (metabolism, pathology)
  • Neurites (metabolism, pathology)
  • Neurofilament Proteins (metabolism)
  • Neurons (metabolism, pathology)
  • Plaque, Amyloid (metabolism, pathology)
  • Pyramidal Cells (metabolism, pathology)
  • Rats
  • Rats, Wistar

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