Alzheimer-type neuropathology in transgenic mice overexpressing V717F β-amyloid precursor protein

Games, Dora; Adams, David; Alessandrini, Ree; Barbour, Robin; Borthelette, Patricia; Blackwell, Catherine; Carr, Tony; Clemens, James; Donaldson, Thomas; Gillespie, Frances; Guido, Terry; Hagopian, Stephanie; Johnson-Wood, Kelly; Khan, Karen; Lee, Mike; Leibowitz, Paul; Lieberburg, Ivan; Little, Sheila; Masliah, Eliezer; McConlogue, Lisa; Montoya-Zavala, Martin; Mucke, Lennart; Paganini, Lisa; Penniman, Elizabeth; Power, Mike; Schenk, Dale; Seubert, Peter; Snyder, Ben; Soriano, Ferdie; Tan, Hua; Vitale, James; Wadsworth, Sam; Wolozin, Ben; Zhao, Jun

doi:10.1038/373523a0

Cited by 2,516Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsDementia and Cognitive Impairment Research

Alzheimer-type neuropathology in transgenic mice overexpressing V717F β-amyloid precursor protein

Games, Dora, Adams, David, Alessandrini, Ree, Barbour, Robin, Borthelette, Patricia, Blackwell, Catherine, Carr, Tony, Clemens, James +26 more·1995·Nature

DOI 10.1038/373523a0

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Abstract

Alzheimer's disease (AD) is the most common cause of progressive intellectual failure in aged humans. AD brains contain numerous amyloid plaques surrounded by dystrophic neurites, and show profound synaptic loss, neurofibrillary tangle formation and gliosis. The amyloid plaques are composed of amyloid beta-peptide (A beta), a 40-42-amino-acid fragment of the beta-amyloid precursor protein (APP). A primary pathogenic role for APP/A beta is suggested by missense mutations in APP that are tightly linked to autosomal dominant forms of AD. A major obstacle to elucidating and treating AD has been the lack of an animal model. Animals transgenic for APP have previously failed to show extensive AD-type neuropathology, but we now report the production of transgenic mice that express high levels of human mutant APP (with valine at residue 717 substituted by phenylalanine) and which progressively develop many of the pathological hallmarks of AD, including numerous extracellular thioflavin S-positive A beta deposits, neuritic plaques, synaptic loss, astrocytosis and microgliosis. These mice support a primary role for APP/A beta in the genesis of AD and could provide a preclinical model for testing therapeutic drugs.

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Mouse models that overexpress APP develop plaques remarkably similar to those observed in AD but do not recapitulate neurofibrillary pathology or widespread neuronal loss.
“Mouse models that overexpress amyloid precursor protein (APP) develop plaques remarkably similar to those observed in AD but do not recapitulate neurofibrillary pathology or widespread neuronal loss (Games et al., 1995;Hsiao et al., 1996;Irizarry et al., 1997a;Urbanc et al., 2002), allowing interpretation of results in the context of amyloid-related pathologies.”
From Dendritic Spine Abnormalities in Amyloid Precursor Protein Transgenic Mice Demonstrated by Gene Transfer and Intravital Multiphoton Microscopy (2005) · cites this paper as Games et al., 1995
APP transgenic mouse models have elevated inflammation markers and gliosis associated with amyloid deposits.
“Similar to AD, APP transgenic mouse models have elevated inflammation markers and gliosis associated with amyloid deposits (Games et al., 1995; Hsiao et al., 1996; Sturchler-Pierrat et al., 1997).”
From Intraneuronal β-Amyloid Aggregates, Neurodegeneration, and Neuron Loss in Transgenic Mice with Five Familial Alzheimer's Disease Mutations: Potential Factors in Amyloid Plaque Formation (2006) · cites this paper as Games et al., 1995
The first successful mouse models reproducing Aβ pathologies overexpressed human APP with either a single Swedish or Indiana mutation.
“The first successful mouse models reproducing Aβ pathologies overexpressed human APP with either a single Swedish [25, 26] or Indiana [27] mutation.”
From Amyloid-β plaque formation and reactive gliosis are required for induction of cognitive deficits in App knock-in mouse models of Alzheimer’s disease (2019) · cites this paper as [27]
Transgenic mouse models successfully recapitulated Aβ plaque formation, increasing support for the amyloid hypothesis.
“These genetic findings led to several transgenic mouse models that successfully recapitulated Aβ plaque formation, increasing support for the hypothesis (Table 1) [23–29].”
From Systems-based proteomics to resolve the biology of Alzheimer’s disease beyond amyloid and tau (2021) · cites this paper as [25]

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A � Deposition Is Associated with Neuropil Changes, but not with Overt Neuronal Loss in the Human Amyloid Precursor Protein V717F (PDAPP) Transgenic Mouse
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Authors: Games, D., Adams, D., Alessandrini, R., Barbour, R., Borthelette, P., Blackwell, C., Carr, T., Clemens, J., Donaldson, T., Gillespie, F., Guido, T., Hagopian, S., Johnson-Wood, K., Khan, K., Lee, M., Leibowitz, P., Lieberburg, I., Little, S., Masliah, E., McConlogue, L., Montoya-Zavala, M., Mucke, L., Paganini, L., Penniman, E., Power, M., Schenk, D., Seubert, P., Snyder, B., Soriano, F., Tan, H., Vitale, J., Wadsworth, S., Wolozin, B., & Zhao, J.
Affiliations: Worcester Polytechnic Institute (US)
University of Massachusetts Chan Medical School (US)
Eli Lilly (United States) (US)
Boston Children's Hospital (US)
University of California San Diego (US)
Scripps Research Institute (US)
ORCID: Blackwell, Catherine
Carr, Tony
Clemens, James
Lee, Mike
Masliah, Eliezer
McConlogue, Lisa
Mucke, Lennart
Tan, Hua
Zhao, Jun
Venue: Nature
Publisher: Springer Science and Business Media LLC
Published: 1995-02
Volume: 373
Issue: 6514
Pages: 523-527
ISSN: 0028-0836 (ISSN-L)
1476-4687
DOI: 10.1038/373523a0
OpenAlex: W2126800086
Cited by: 2,516
References: 28
Citations by year: 2026: 17 · 2025: 34 · 2024: 55 · 2023: 38 · 2022: 42 · 2021: 52 · 2020: 55 · 2019: 42 · 2018: 35 · 2017: 54 · 2016: 69 · 2015: 64 · 2014: 58 · 2013: 75 · 2012: 73
FWCI: 101.17
Type: journal article
Language: en
Open access: closed
Licence: www.springer.com/tdm (tdm)
Locations: Nature (publishedVersion)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords: Alzheimer's disease, amyloid precursor protein, transgenic mice, amyloid-beta, amyloid plaques, neuritic plaques, synaptic loss, astrocyte activation, microglial activation, animal models of Alzheimer's disease, thioflavin S staining
MeSH terms: Alzheimer Disease, Animals, Base Sequence, Brain, Humans, Immunoenzyme Techniques, Mice, Transgenic, Molecular Sequence Data, Mutation, Platelet-Derived Growth Factor, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, DNA Primers, Microscopy, Confocal, Mice

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Alzheimer-type neuropathology in transgenic mice overexpressing V717F β-amyloid precursor protein

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