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Progression of amyloid pathology to Alzheimer's disease pathology in an amyloid precursor protein transgenic mouse model by removal of nitric oxide synthase 2.

Publication ,  Journal Article
Wilcock, DM; Lewis, MR; Van Nostrand, WE; Davis, J; Previti, ML; Gharkholonarehe, N; Vitek, MP; Colton, CA
Published in: The Journal of neuroscience : the official journal of the Society for Neuroscience
February 2008

Alzheimer's disease (AD) is characterized by three primary pathologies in the brain: amyloid plaques, neurofibrillary tangles, and neuron loss. Mouse models have been useful for studying components of AD but are limited in their ability to fully recapitulate all pathologies. We crossed the APPSwDI transgenic mouse, which develops amyloid beta (Abeta)-protein deposits only, with a nitric oxide synthase 2 (NOS2) knock-out mouse, which develops no AD-like pathology. APPSwDI/NOS2(-/-) mice displayed impaired spatial memory compared with the APPSwDI mice, yet they have unaltered levels of Abeta. APPSwDI mice do not show tau pathology, whereas APPSwDI/NOS2(-/-) mice displayed extensive tau pathology associated with regions of dense microvascular amyloid deposition. Also, APPSwDI mice do not have any neuron loss, whereas the APPSwDI/NOS2(-/-) mice have significant neuron loss in the hippocampus and subiculum. Neuropeptide Y neurons have been shown to be particularly vulnerable in AD. These neurons appear to be particularly vulnerable in the APPSwDI/NOS2(-/-) mice as we observe a dramatic reduction in the number of NPY neurons in the hippocampus and subiculum. These data show that removal of NOS2 from an APP transgenic mouse results in development of a much greater spectrum of AD-like pathology and behavioral impairments.

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Published In

The Journal of neuroscience : the official journal of the Society for Neuroscience

DOI

EISSN

1529-2401

ISSN

0270-6474

Publication Date

February 2008

Volume

28

Issue

7

Start / End Page

1537 / 1545

Related Subject Headings

  • Nitric Oxide Synthase Type II
  • Neuropeptide Y
  • Neurons
  • Neurology & Neurosurgery
  • Mice, Transgenic
  • Mice
  • Memory Disorders
  • Immunohistochemistry
  • Hippocampus
  • Disease Progression
 

Citation

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ICMJE
MLA
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Wilcock, D. M., Lewis, M. R., Van Nostrand, W. E., Davis, J., Previti, M. L., Gharkholonarehe, N., … Colton, C. A. (2008). Progression of amyloid pathology to Alzheimer's disease pathology in an amyloid precursor protein transgenic mouse model by removal of nitric oxide synthase 2. The Journal of Neuroscience : The Official Journal of the Society for Neuroscience, 28(7), 1537–1545. https://doi.org/10.1523/jneurosci.5066-07.2008
Wilcock, Donna M., Matthew R. Lewis, William E. Van Nostrand, Judianne Davis, Mary Lou Previti, Nastaran Gharkholonarehe, Michael P. Vitek, and Carol A. Colton. “Progression of amyloid pathology to Alzheimer's disease pathology in an amyloid precursor protein transgenic mouse model by removal of nitric oxide synthase 2.The Journal of Neuroscience : The Official Journal of the Society for Neuroscience 28, no. 7 (February 2008): 1537–45. https://doi.org/10.1523/jneurosci.5066-07.2008.
Wilcock DM, Lewis MR, Van Nostrand WE, Davis J, Previti ML, Gharkholonarehe N, et al. Progression of amyloid pathology to Alzheimer's disease pathology in an amyloid precursor protein transgenic mouse model by removal of nitric oxide synthase 2. The Journal of neuroscience : the official journal of the Society for Neuroscience. 2008 Feb;28(7):1537–45.
Wilcock, Donna M., et al. “Progression of amyloid pathology to Alzheimer's disease pathology in an amyloid precursor protein transgenic mouse model by removal of nitric oxide synthase 2.The Journal of Neuroscience : The Official Journal of the Society for Neuroscience, vol. 28, no. 7, Feb. 2008, pp. 1537–45. Epmc, doi:10.1523/jneurosci.5066-07.2008.
Wilcock DM, Lewis MR, Van Nostrand WE, Davis J, Previti ML, Gharkholonarehe N, Vitek MP, Colton CA. Progression of amyloid pathology to Alzheimer's disease pathology in an amyloid precursor protein transgenic mouse model by removal of nitric oxide synthase 2. The Journal of neuroscience : the official journal of the Society for Neuroscience. 2008 Feb;28(7):1537–1545.

Published In

The Journal of neuroscience : the official journal of the Society for Neuroscience

DOI

EISSN

1529-2401

ISSN

0270-6474

Publication Date

February 2008

Volume

28

Issue

7

Start / End Page

1537 / 1545

Related Subject Headings

  • Nitric Oxide Synthase Type II
  • Neuropeptide Y
  • Neurons
  • Neurology & Neurosurgery
  • Mice, Transgenic
  • Mice
  • Memory Disorders
  • Immunohistochemistry
  • Hippocampus
  • Disease Progression