Neuropathological Characterization of Mutant Amyloid Precursor Protein Yeast Artificial Chromosome Transgenic Mice
Open accessAbstract
Mutations in the amyloid precursor protein (APP) gene result in elevated production and deposition of the 42 amino acid beta-amyloid (Abeta1-42) peptide and early-onset Alzheimer's disease (AD). To accurately examine the effect of the APP FAD mutations in vivo, we introduced yeast artificial chromosomes (YACs) containing the entire genomic copy of human APP harboring FAD mutations into transgenic mice. Our current results demonstrate that mutant APP YAC transgenic mice exhibit many features characteristic of human AD, including regional deposition of Abeta with preferential deposition of Abeta1-42, extensive neuritic abnormalities as evidenced by staining with APP, ubiquitin, neurofilament, and hyperphosphorylated tau antibodies, increased markers of inflammation, and the overlapping deposition of Abeta with apolipoproteins E and J. Our results also suggest that APP YAC transgenic mice possess unique pathological attributes when compared to other transgenic mouse models of AD that may reflect the experimental design of each model.
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The R1.40 transgenic mouse line develops gradual AD-like Aβ pathology, exhibiting both diffuse and fibrillar Aβ deposition beginning at 14-16 months of age in the cortex and 18-20 months of age in the hippocampus.
“The R1.40 transgenic mouse line develops gradual AD-like A pathology, exhibiting both diffuse and fibrillar A deposition beginning at 14 -16 months of age in the cortex and 18 -20 months of age in the hippocampus.36”
From CX3CR1 Deficiency Alters Microglial Activation and Reduces Beta-Amyloid Deposition in Two Alzheimer's Disease Mouse Models (2010) · cites this paper as [36]
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Lee, S., Varvel, N. H., Konerth, M. E., Xu, G., Cardona, A. E., Ransohoff, R. M., & Lamb, B. T. (2010) · The American Journal of Pathology · doi:10.2353/ajpath.2010.100265 · Cited by 539 · see citing works
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- Authors
- Kulnane, L. S., & Lamb, B. T.
- Affiliations
- Case Western Reserve University (US)
- University Hospitals of Cleveland (US)
- ORCID
- Lamb, Bruce T.
- Venue
- Neurobiology of Disease
- Publisher
- Elsevier BV
- Published
- 2001-12
- Volume
- 8
- Issue
- 6
- Pages
- 982-992
- ISSN
- 0969-9961 (ISSN-L)
- OpenAlex
- W2048193733
- Cited by
- 63
- References
- 10
- Citations by year
- 2024: 1 · 2023: 3 · 2021: 1 · 2020: 1 · 2018: 2 · 2017: 2 · 2016: 3 · 2014: 3 · 2013: 2 · 2012: 2
- FWCI
- 1.99
- Type
- journal article
- Language
- en
- Open access
- green
- doaj.org
- Licence
- Locations
- Neurobiology of Disease (publishedVersion)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institutes of Health
- National Institute on Aging (AG14451, AG-08012, P50AG008012)
- National Cancer Institute (CA 43703, P30CA043703)
- Topics
- Health Sciences › Medicine › Physiology › 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, Alzheimer's disease, amyloid-beta deposition, amyloid-beta 42, neuritic plaques, tau hyperphosphorylation, neuroinflammation, apolipoprotein E, clusterin, transgenic mouse model, yeast artificial chromosomes, neuropathology
- MeSH terms
- Aging, Alzheimer Disease, Animals, Apolipoproteins E, Brain, Female, Glycoproteins, Humans, Immunohistochemistry, Male, Membrane Proteins, Mice, Transgenic, Mutation, Neuroglia, Neurons, Peptide Fragments, Sex Characteristics, Amyloid beta-Peptides, Neurites, Amyloid beta-Protein Precursor, Chromosomes, Artificial, Yeast, Gene Targeting, Molecular Chaperones, Clusterin, Mice, Presenilin-1, Plaque, Amyloid
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