Cited by 748Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsDementia and Cognitive Impairment Research

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Characterization of amyloid deposition in the APPswe/PS1dE9 mouse model of Alzheimer disease

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Garcia-Alloza, Monica, Robbins, Elissa M., Zhang-Nunes, Sandy X., Purcell, Susan M., Betensky, Rebecca A., Raju, Susan, Prada, Claudia, Greenberg, Steven M., Bacskai, Brian J., Frosch, Matthew P.·2006·Neurobiology of Disease

DOI 10.1016/j.nbd.2006.08.017

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Abstract

Transgenic mice carrying disease-linked forms of genes associated with Alzheimer disease often demonstrate deposition of the beta-amyloid as senile plaques and cerebral amyloid angiopathy. We have characterized the natural history of beta-amyloid deposition in APPswe/PS1dE9 mice, a particularly aggressive transgenic mouse model generated with mutant transgenes for APP (APPswe: KM594/5NL) and PS1 (dE9: deletion of exon 9). Ex vivo histochemistry showed Abeta deposition by 4 months with a progressive increase in plaque number up to 12 months and a similar increase of Abeta levels. In vivo multiphoton microscopy at weekly intervals showed increasing beta-amyloid deposition as CAA and plaques. Although first appearing at an early age, CAA progressed at a significantly slower rate than in the Tg2576 mice. The consistent and early onset of beta-amyloid accumulation in the APPswe/PS1dE9 model confirms its utility for studies of biochemical and pathological mechanisms underlying beta-amyloid deposition, as well as exploring new therapeutic treatments.

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Background
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Authors: Garcia-Alloza, M., Robbins, E. M., Zhang-Nunes, S. X., Purcell, S. M., Betensky, R. A., Raju, S., Prada, C., Greenberg, S. M., Bacskai, B. J., & Frosch, M. P.
Affiliations: Harvard University (US)
Corresponding author: Frosch, Matthew P.
ORCID: Robbins, Elissa M.
Zhang-Nunes, Sandy X.
Betensky, Rebecca A.
Greenberg, Steven M.
Bacskai, Brian J.
Frosch, Matthew P.
Venue: Neurobiology of Disease
Publisher: Elsevier BV
Published: 2006-12
Volume: 24
Issue: 3
Pages: 516-524
ISSN: 0969-9961 (ISSN-L)
DOI: 10.1016/j.nbd.2006.08.017
OpenAlex: W2005719973
Cited by: 744
References: 46
Citations by year: 2026: 36 · 2025: 28 · 2024: 39 · 2023: 28 · 2022: 41 · 2021: 46 · 2020: 53 · 2019: 43 · 2018: 57 · 2017: 44 · 2016: 45 · 2015: 49 · 2014: 47 · 2013: 51 · 2012: 42
FWCI: 10.38
Type: journal article
Language: en
Open access: green
doaj.org
Licence: cc-by-sa
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Neurobiology of Disease (publishedVersion)
PubMed (publishedVersion)
DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders: Chinese Academy of Agricultural Sciences
National Institutes of Health
National Institute on Aging (R01AG021084, AG021084, R01AG020570, AG 020570)
National Institute of Biomedical Imaging and Bioengineering (EB 000768, R01EB000768)
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › 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: amyloid-beta deposition, APP/PS1 mice, Alzheimer's disease, transgenic mouse model, amyloid plaques, cerebral amyloid angiopathy, multiphoton microscopy, Tg2576 mice
MeSH terms: Age Factors, Alzheimer Disease, Animals, Brain, Disease Models, Animal, Mice, Neurologic Mutants, Mice, Transgenic, Tissue Distribution, Amyloid beta-Protein Precursor, Mice, Plaque, Amyloid

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Characterization of amyloid deposition in the APPswe/PS1dE9 mouse model of Alzheimer disease

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