The DOI matches its Crossref record, with a small difference in title or year; 36 of the 38 references it cites were found in a registry or an index.
Accelerated Plaque Accumulation, Associative Learning Deficits, and Up-regulation of α7 Nicotinic Receptor Protein in Transgenic Mice Co-expressing Mutant Human Presenilin 1 and Amyloid Precursor Proteins
Open accessAbstract
Familial Alzheimer's disease-associated mutations in presenilin 1 or 2 or amyloid precursor protein result in elevated beta-amyloid, beta-amyloid accumulation, and plaque formation in the brains of affected individuals. By crossing presenilin 1 transgenic mice carrying the A246E mutation with plaque-producing amyloid precursor protein K670N/M671L transgenic mice (Tg2576), we show that co-expression of both mutant transgenes results in acceleration of amyloid accumulation and associative learning deficits. At 5 months of age with no detectable plaque pathology, amyloid precursor protein transgenic animals are impaired in contextual fear learning following two pairings of conditioned and unconditioned stimuli but appear normal following a more robust five-pairing training. At 9 months of age when beta-amyloid deposition is evident, these mice are impaired following both two-pairing and five-pairing protocols. Mice carrying both transgenes are impaired in contextual fear conditioning at either age. All transgenic animal groups performed as well as controls in cued fear conditioning, indicating that the contextual fear learning deficits are hippocampus-specific. The associative learning impairments are coincident with elevated alpha 7 nicotinic acetylcholine receptor protein in the dentate gyrus. These findings provide two robust and rapid assays for beta-amyloid-associated effects that can be performed on young animals: impaired contextual fear learning and up-regulation of alpha 7 nicotinic receptors.
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“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 [56]
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“Fear in Tg2576 mice is a common observation made in this genotype (Dineley et al., 2002).”
From Arbovirus infection increases the risk for the development of neurodegenerative disease pathology in the murine model (2024) · cites this paper as Dineley et al., 2002
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“Tg2576 mice exhibit elevated Aβ from 2 months old onward, plaques after 6 months old, and cognitive deficits beginning at 5 months old [32,33,34].”
From VEEV TC-83 Triggers Dysregulation of the Tryptophan–Kynurenine Pathway in the Central Nervous System That Correlates with Cognitive Impairment in Tg2576 Mice (2024) · cites this paper as [33]
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2 of the 38 references couldn’t be matched to a known paper.
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Items 201–213 of 213
Nicotinic Acetylcholine Receptors in Alzheimer’s and Parkinson’s Disease
Dineley, K. T. (2014) · The Receptors · doi:10.1007/978-1-4939-1167-7_19
Self-citationNeural Stem Cells in Alzheimer's Disease
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Mechanisms of Memory Deficits in Mouse Models of Alzheimer's Disease
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Self-citationBindingDB Entry 50038292: Allosteric modulators of the alpha7 nicotinic acetylcholine receptor.
BindingDB (2012) · UC San Diego · doi:10.7270/q2ws8v3b
Metadata
- Authors
- Dineley, K. T., Xia, X., Bui, D., Sweatt, J. D., & Zheng, H.
- Affiliations
- Baylor College of Medicine (US)
- Corresponding author
- Dineley, Kelly T.
- Sweatt, J. David
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2002-06
- Volume
- 277
- Issue
- 25
- Pages
- 22768-22780
- ISSN
- 0021-9258 (ISSN-L)
- OpenAlex
- W1999234381
- Cited by
- 212
- References
- 38
- Citations by year
- 2026: 1 · 2025: 4 · 2024: 3 · 2023: 2 · 2022: 1 · 2021: 3 · 2020: 6 · 2019: 9 · 2018: 9 · 2017: 10 · 2016: 9 · 2015: 8 · 2014: 10 · 2013: 7 · 2012: 15
- FWCI
- 7.19
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- Alzheimer's Association
- National Alliance for Research on Schizophrenia and Depression
- National Institutes of Health
- National Institute on Aging
- National Institute of Mental Health
- National Institute of Neurological Disorders and Stroke
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nicotinic Acetylcholine Receptors Study
- Keywords
- familial Alzheimer's disease, presenilin 1, amyloid precursor protein, Tg2576 mice, amyloid-beta deposition, amyloid plaques, contextual fear conditioning, alpha7 nicotinic acetylcholine receptor, dentate gyrus, hippocampus, transgenic mice
- MeSH terms
- Age Factors, Animals, Behavior, Animal, Fear, Hippocampus, Immunohistochemistry, Learning, Membrane Proteins, Mice, Transgenic, Mutation, Protein Binding, Receptors, Nicotinic, Shock, Time Factors, Immunoblotting, Up-Regulation, Amyloid beta-Protein Precursor, Transgenes, Mice, Presenilin-1, alpha7 Nicotinic Acetylcholine Receptor
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