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Cited by 225Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

The DOI matches its Crossref record; 43 of the 43 references it cites were found in a registry or an index.

Cognitive correlates of Aβ deposition in male and female mice bearing amyloid precursor protein and presenilin-1 mutant transgenes

Howlett, David R, Richardson, Jill C, Austin, Angela, Parsons, Andrew A, Bate, Simon T, Davies, D.Ceri, Gonzalez, M.Isabel·2004·Brain Research
DOI 10.1016/j.brainres.2004.05.029
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Abstract

Several transgenic mouse models of Alzheimer's disease (AD) have been developed that exhibit beta-amyloid (Abeta) neuropathology and behavioural deficits. However, not all studies have investigated the relationship between the development of cognitive impairment and neuropathology. Therefore, temporal changes in cognition were investigated in male and female double-mutant APPswexPS1.M146V (TASTPM) transgenic mice using an object recognition test and correlated with the development of cerebral Abeta neuropathology. Both male and female TASTPM mice exhibited similar significant cognitive impairment at 6, 8 and 10 months of age in the object recognition test, compared to wild-type littermates. There was no such cognitive impairment at 3 or 4 months of age. Quantitative immunohistochemistry using a battery of Abeta antibodies demonstrated that cerebral Abeta deposition was first apparent in 3-month-old mice, and it increased with age. The early appearance of cerebral Abeta deposits in the double-transgenic TASTPM mice supports the evidence that mutations in the PS1 gene accelerate Abeta deposition. The cerebral Abeta load was greater in female than in male TASTPM mice at all ages investigated. In the electron microscope, mature Abeta plaques comprising a fibrillar core surrounded by degenerating neurites and reactive glia were first observed in the cortex of TASTPM mice at 6 months of age, the same age at which cognitive impairment became apparent. These results suggest that the cognitive impairment in TASTPM mice is related to the disruption of neural connectivity and not simply Abeta deposition, which first occurs 3 months earlier.

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  1. Moechars, 1995, Molecular and behavioral characterization of transgenic mice expressing mutant app in the brain, Behav. Genet., 25, 280

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Metadata

Authors
Howlett, D. R., Richardson, J. C., Austin, A., Parsons, A. A., Bate, S. T., Davies, D. C., & Gonzalez, M. I.
Affiliations
  • GlaxoSmithKline (United Kingdom) (GB)
  • St George's Hospital (GB)
Corresponding author
Howlett, David R
ORCID
Venue
Brain Research
Publisher
Elsevier BV
Published
2004-08
Volume
1017
Issue
1-2
Pages
130-136
ISSN
0006-8993 (ISSN-L)
DOI
10.1016/j.brainres.2004.05.029
OpenAlex
W2048622057
Cited by
212
References
41
Citations by year
2026: 2 · 2025: 1 · 2024: 21 · 2023: 8 · 2022: 7 · 2021: 10 · 2020: 12 · 2019: 6 · 2018: 17 · 2017: 5 · 2016: 6 · 2015: 13 · 2014: 6 · 2013: 14 · 2012: 15
FWCI
3.91
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
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 › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
Alzheimer's disease, amyloid-beta deposition, presenilin 1 mutations, amyloid precursor protein mutations, cognitive impairment, object recognition, sex differences, amyloid plaques, neuronal connectivity
MeSH terms
Age Factors, Alzheimer Disease, Analysis of Variance, Animals, Behavior, Animal, Cerebral Cortex, Disease Models, Animal, Female, Immunohistochemistry, Male, Membrane Proteins, Mice, Transgenic, Microscopy, Electron, Mutation, Neuropsychological Tests, Sex Characteristics, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Mice, Presenilin-1, Plaque, Amyloid

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