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NO synthase 2 (NOS2) deletion promotes multiple pathologies in a mouse model of Alzheimer's disease.

Publication ,  Journal Article
Colton, CA; Vitek, MP; Wink, DA; Xu, Q; Cantillana, V; Previti, ML; Van Nostrand, WE; Weinberg, JB; Dawson, H
Published in: Proc Natl Acad Sci U S A
August 22, 2006

Alzheimer's disease is characterized by two primary pathological features: amyloid plaques and neurofibrillary tangles. The interconnection between amyloid and tau aggregates is of intense interest, but mouse models have yet to reveal a direct interrelationship. We now show that NO may be a key factor that connects amyloid and tau pathologies. Genetic removal of NO synthase 2 in mice expressing mutated amyloid precursor protein results in pathological hyperphosphorylation of mouse tau, its redistribution to the somatodendritic compartment in cortical and hippocampal neurons, and aggregate formation. Lack of NO synthase 2 in the amyloid precursor protein Swedish mutant mouse increased insoluble beta-amyloid peptide levels, neuronal degeneration, caspase-3 activation, and tau cleavage, suggesting that NO acts at a junction point between beta-amyloid peptides, caspase activation, and tau aggregation.

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Published In

Proc Natl Acad Sci U S A

DOI

ISSN

0027-8424

Publication Date

August 22, 2006

Volume

103

Issue

34

Start / End Page

12867 / 12872

Location

United States

Related Subject Headings

  • tau Proteins
  • Phosphorylation
  • Nitric Oxide Synthase Type II
  • Mice, Knockout
  • Mice
  • Gene Deletion
  • Disease Models, Animal
  • Caspases
  • Caspase 3
  • Brain
 

Citation

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Colton, C. A., Vitek, M. P., Wink, D. A., Xu, Q., Cantillana, V., Previti, M. L., … Dawson, H. (2006). NO synthase 2 (NOS2) deletion promotes multiple pathologies in a mouse model of Alzheimer's disease. Proc Natl Acad Sci U S A, 103(34), 12867–12872. https://doi.org/10.1073/pnas.0601075103
Colton, C. A., M. P. Vitek, D. A. Wink, Q. Xu, V. Cantillana, M. L. Previti, W. E. Van Nostrand, J. B. Weinberg, and H. Dawson. “NO synthase 2 (NOS2) deletion promotes multiple pathologies in a mouse model of Alzheimer's disease.Proc Natl Acad Sci U S A 103, no. 34 (August 22, 2006): 12867–72. https://doi.org/10.1073/pnas.0601075103.
Colton CA, Vitek MP, Wink DA, Xu Q, Cantillana V, Previti ML, et al. NO synthase 2 (NOS2) deletion promotes multiple pathologies in a mouse model of Alzheimer's disease. Proc Natl Acad Sci U S A. 2006 Aug 22;103(34):12867–72.
Colton, C. A., et al. “NO synthase 2 (NOS2) deletion promotes multiple pathologies in a mouse model of Alzheimer's disease.Proc Natl Acad Sci U S A, vol. 103, no. 34, Aug. 2006, pp. 12867–72. Pubmed, doi:10.1073/pnas.0601075103.
Colton CA, Vitek MP, Wink DA, Xu Q, Cantillana V, Previti ML, Van Nostrand WE, Weinberg JB, Dawson H. NO synthase 2 (NOS2) deletion promotes multiple pathologies in a mouse model of Alzheimer's disease. Proc Natl Acad Sci U S A. 2006 Aug 22;103(34):12867–12872.
Journal cover image

Published In

Proc Natl Acad Sci U S A

DOI

ISSN

0027-8424

Publication Date

August 22, 2006

Volume

103

Issue

34

Start / End Page

12867 / 12872

Location

United States

Related Subject Headings

  • tau Proteins
  • Phosphorylation
  • Nitric Oxide Synthase Type II
  • Mice, Knockout
  • Mice
  • Gene Deletion
  • Disease Models, Animal
  • Caspases
  • Caspase 3
  • Brain