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Related Experiment Videos

Amyloid precursor protein in aged nonhuman primates.

L J Martin1, S S Sisodia, E H Koo

  • 1Department of Pathology, University of Heidelberg, Federal Republic of Germany.

Proceedings of the National Academy of Sciences of the United States of America
|February 15, 1991
PubMed
Summary

Neurons may contribute to amyloid plaque formation in Alzheimer disease. This study found amyloid precursor protein (APP) in neurons and around beta/A4 plaques in aged monkeys, supporting a neuronal source for brain amyloid.

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Area of Science:

  • Neuroscience
  • Neuropathology
  • Molecular Biology

Background:

  • Alzheimer disease is characterized by amyloid plaques in the brain.
  • Amyloid is mainly composed of beta/A4 peptide, derived from amyloid precursor protein (APP).
  • Amyloid deposits are found in senile plaques and cerebral blood vessels in aged individuals and primates.

Purpose of the Study:

  • To investigate the distribution of beta/A4 and APP in the cerebral cortices of monkeys of varying ages.
  • To determine if neurons contribute to the amyloid deposits observed in the brain.

Main Methods:

  • Immunohistochemical examination of cerebral cortices from monkeys aged 4 to 41 years.
  • Detection of beta/A4 and APP (outside the beta/A4 domain) using immunoreactivity.

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Main Results:

  • APP immunoreactivity was observed in neuronal cell bodies, dendrites, and axons across all ages.
  • In aged monkeys with senile plaques, prominent APP-positive axons and neurites surrounding beta/A4 plaques were noted.
  • APP-immunoreactive elements were found near beta/A4 deposits within some plaques.

Conclusions:

  • Neuronal APP is present throughout the neuron, from cell body to axon.
  • The presence of APP in neurites within plaques suggests neurons are a source of parenchymal amyloid.
  • These findings support the hypothesis that neurons contribute to amyloid deposition in the brain parenchyma.