β-amyloid plaques induce neuritic dystrophy of nitric oxide-producing neurons in a transgenic mouse model of Alzheimer's disease

Joseph Quinn, Forrest Davis, William Woodward, Felix Eckenstein

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

A causative role for nitric oxide has been postulated in a number of neurodegenerative diseases. Using histochemical and immunohistochemical methods, we examined the effect of β-amyloid plaques on nitric oxide-producing cells in transgenic mice which overexpress a mutant human amyloid precursor protein (APP). In 14 month old animals, nitric oxide synthase (NOS)positive dystrophic neurites were observed frequently in the cerebral cortex and hippocampus of all of 16 plaque bearing transgenic animals and in none of 16 wild-type animals. Double labeling of NOS and β-amyloid revealed that 90% of β-amyloid plaques were associated with NOS-containing dystrophic neurites. In 7-month old animals, β-amyloid plaques were very rare, but those present were frequently associated with NOS-positive neuritic dystrophy. We conclude that β-amyloid plaques induce neuritic dystrophy in cortical neurons containing NOS in this model of AD, and hypothesize that this finding may be relevant to the mechanism of β-amyloid neurotoxicity in human AD.

Original languageEnglish (US)
Pages (from-to)203-212
Number of pages10
JournalExperimental Neurology
Volume168
Issue number2
DOIs
StatePublished - 2001

Fingerprint

Amyloid Plaques
Nitric Oxide Synthase
Transgenic Mice
Alzheimer Disease
Nitric Oxide
Neurons
Neurites
Amyloid
Genetically Modified Animals
Wild Animals
Amyloid beta-Protein Precursor
Neurodegenerative Diseases
Cerebral Cortex
Hippocampus

Keywords

  • Animal
  • Disease models
  • Free radicals
  • Oxidative
  • Stress

ASJC Scopus subject areas

  • Neurology
  • Neuroscience(all)

Cite this

β-amyloid plaques induce neuritic dystrophy of nitric oxide-producing neurons in a transgenic mouse model of Alzheimer's disease. / Quinn, Joseph; Davis, Forrest; Woodward, William; Eckenstein, Felix.

In: Experimental Neurology, Vol. 168, No. 2, 2001, p. 203-212.

Research output: Contribution to journalArticle

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