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Multi-metric behavioral comparison of APPsw and P301L models for Alzheimer's Disease: linkage of poorer cognitive performance to tau pathology in forebrain
Abstract
APPsw transgenic mice bearing the "Swedish" amyloid precursor protein (APP) mutation and JNPL3 transgenic mice bearing the P301L (Tau) mutation were compared to control non-transgenic (NT) mice in an extensive behavioral test battery administered between 5 and 8.5 months of age. APP mice were impaired in a variety of cognitive-based tasks prior to overt Abeta plaque development, making involvement of mutant APP overexpression and/or oligomeric Abeta assemblies most likely. Although Tau mice, as a group, were not impaired in any single behavioral measure, a collective assessment of behavioral measures through discriminant function analysis showed that Tau mice were impaired in overall behavioral (cognitive) performance. Moreover, correlation analyses involving Tau mice alone revealed linkage between poorer cognitive performance in all three water maze tasks and the number of neurofibrillary tangle (NFT)-containing neurons in neocortex and hippocampus. These findings indicate that: (1) APP mice show early and extensive cognitive impairment before evident Abeta deposition, and (2) the process or product of NFT formation in Tau mice is sufficient to deleteriously impact cognitive performance.
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“These spatial working memory deficits are generally accepted to be present across the rest of the life span for this model (Hsiao et al., 1996; Westerman et al., 2002; Arendash et al., 2004).”
From Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models (2014) · cites this paper as Arendash et al., 2004
In the citing paper
“In the Tg2576 mouse (Hsiao et al., 1996), the first presentation of cognitive deficits is seen at 5 months of age in spatial working memory (Arendash et al., 2004).”
From Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models (2014) · cites this paper as Arendash et al., 2004
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Metadata
- Authors
- Arendash, G. W., Lewis, J., Leighty, R. E., McGowan, E., Cracchiolo, J. R., Hutton, M., & Garcia, M. F.
- Affiliations
- University of South Florida (US)
- Mayo Clinic (US)
- Corresponding author
- Arendash, Gary W
- Venue
- Brain Research
- Publisher
- Elsevier BV
- Published
- 2004-06
- Volume
- 1012
- Issue
- 1-2
- Pages
- 29-41
- ISSN
- 0006-8993 (ISSN-L)
- OpenAlex
- W2111050644
- Cited by
- 127
- References
- 32
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 6 · 2023: 2 · 2022: 2 · 2021: 3 · 2020: 4 · 2019: 4 · 2018: 2 · 2017: 5 · 2016: 6 · 2015: 8 · 2014: 7 · 2013: 6 · 2012: 9
- FWCI
- 4.59
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Brain Research (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- Alzheimer's disease, P301L tau mutation, cognitive impairment, amyloid precursor protein, amyloid-beta oligomers, neurofibrillary tangles, water maze, hippocampus, neocortex, behavioral phenotypes, discriminant function analysis
- MeSH terms
- Alzheimer Disease, Animals, Behavior, Animal, Cognition Disorders, Female, Mice, Inbred C57BL, Mice, Transgenic, Models, Neurological, Reaction Time, Prosencephalon, Amyloid beta-Protein Precursor, tau Proteins, Point Mutation, Maze Learning, Mice
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