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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

Wilcock, Donna M., Lewis, Matthew R., Van Nostrand, William E., Davis, Judianne, Previti, Mary Lou, Gharkholonarehe, Nastaran, Vitek, Michael P., Colton, Carol A.·2008·The Journal of Neuroscience
DOI 10.1523/jneurosci.5066-07.2008
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Abstract

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 β (Aβ)-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 Aβ. 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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  • The increase in GFAP-expressing cells and impaired cognitive function seen in this AD model are purely attributable to mutant APP as Tg-SwDI mice do not develop neurofibrillary tangles that require mutations in tau.

    “The increase in GFAP-expressing cells and impaired cognitive function seen in this AD model are purely attributable to mutant APP as Tg-SwDI mice do not develop neurofibrillary tangles that require mutations in tau (Wilcock et al., 2008).”

    From Inhibiting USP16 rescues stem cell aging and memory in an Alzheimer’s model (2022) · cites this paper as Wilcock et al., 2008

    The Results report cognitive impairment in APPSwDI mice, and the Introduction says APP-transgenic mice show some cognitive decline without tau pathology. However, the paper does not report an increase in GFAP-expressing cells or establish that the impairment is purely due to mutant APP: the Results find further cognitive decline after NOS2 removal. The Discussion also contradicts the assertion that tangles require tau mutations, describing aggregation of native mouse tau in APPSwDI/NOS2-knockout mice (page numbers unavailable in our copy). (LLM, conf=0.86)

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Metadata

Authors
Wilcock, D. M., Lewis, M. R., Van Nostrand, W. E., Davis, J., Previti, M. L., Gharkholonarehe, N., Vitek, M. P., & Colton, C. A.
Venue
The Journal of Neuroscience
Publisher
Society for Neuroscience
Published
2008-02-13
Volume
28
Issue
7
Pages
1537-1545
ISSN
  • 0270-6474
  • 1529-2401
DOI
10.1523/jneurosci.5066-07.2008
Cited by
162
References
9
Language
en
Licence
creativecommons.org/licenses/by-nc-sa/4.0/ (vor, 182 d)

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