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Cited by 353Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

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Behavioral Changes in Transgenic Mice Expressing Both Amyloid Precursor Protein and Presenilin-1 Mutations: Lack of Association with Amyloid Deposits

Holcomb, Leigh A., Gordon, Marcia N., Jantzen, Paul, Hsiao, Karen, Duff, Karen, Morgan, Dave·1999·Behavior Genetics
DOI 10.1023/a:1021691918517
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Abstract

Mutations in the amyloid precursor protein (mAPP) and in presenilin 1 (mPS1) have both been linked to increased production of the beta-amyloid peptide (A beta). Doubly transgenic mice produced by mating of a parental line carrying the "Swedish" (K670N/M671L) APP mutation with a FAD4 (M146L) mutant presenilin 1 line developed numerous fibrillar A beta deposits by 6 months of age. Prior work demonstrated that mAPP and doubly transgenic (mAPP/mPS1) mice have deficits in Y-maze alternation behavior as early as 3 months of age. Increased activity was also apparent in the mAPP/mPS1 mice at this time point. These changes in Y-maze performance persisted in mAPP/mPS1 mice at 6 and 9 months of age. The mPS1 singly transgenic mice were not impaired on this task at any age. Six- and nine-month-old mice were also tested for spatial navigation behavior in the Morris water maze. In training trials, no differences in escape latency were detected among the four genotypes. In probe trials, no differences were detected in either the time spent in the trained quadrant or the number of platform crossings among the four groups. Histological staining for A beta amyloid deposits indicates that all doubly transgenic mice have amyloid deposits by 6 months of age (roughly 25 mice examined thus far), yet no 3-month-old mice have been found with deposits. A beta immunostaining confirmed that the 9-month-old mice tested behaviorally also have A beta deposits. Thus, doubly transgenic mice exhibited changes…

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  • Increasing Aβ by expressing FAD mutant PS1 together with FAD mutant APP failed to produce substantial enhancements of the behavioral deficits observed in mice overexpressing FAD mutant APP alone.

    “Our findings are also consistent with research showing that increasing Ab by expressing FAD mutant PS1 together with FAD mutant APP failed to produce substantial enhancements of the behavioral deficits observed in mice overexpressing FAD mutant APP alone (56)(57)(58).”

    From Amyloid precursor protein-induced axonopathies are independent of amyloid-β peptides (2008) · cites this paper as [58]

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Metadata

Authors
Holcomb, L. A., Gordon, M. N., Jantzen, P., Hsiao, K., Duff, K., & Morgan, D.
Affiliations
  • University of South Florida (US)
  • University of Minnesota (US)
  • Mayo Clinic in Florida (US)
ORCID
Venue
Behavior Genetics
Publisher
Springer Science and Business Media LLC
Published
1999-05
Volume
29
Issue
3
Pages
177-185
ISSN
  • 0001-8244 (ISSN-L)
  • 1573-3297
DOI
10.1023/a:1021691918517
OpenAlex
W255871888
Cited by
353
References
29
Citations by year
2026: 4 · 2024: 9 · 2023: 7 · 2022: 7 · 2021: 10 · 2020: 10 · 2019: 9 · 2018: 8 · 2017: 10 · 2016: 10 · 2015: 11 · 2014: 16 · 2013: 8 · 2012: 19
FWCI
10.89
Type
journal article
Language
en
Open access
closed
Licence
Locations
  • Behavior Genetics (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5p01ag014633-03)
  • National Institute on Aging (AG 14633)
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 › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
amyloid precursor protein, presenilin 1, APP/PS1 double transgenic mice, beta-amyloid deposits, Alzheimer's disease, spatial memory impairment, spatial navigation, Morris water maze, behavioral deficits, amyloid plaques
MeSH terms
Alzheimer Disease, Amyloidosis, Animals, Behavior, Animal, Female, Male, Membrane Proteins, Mice, Transgenic, Motor Skills, Mutation, Phenotype, Mental Recall, Gene Expression, Amyloid beta-Protein Precursor, Maze Learning, Mice, Presenilin-1

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