Alzheimer's disease-like neuropathology of gene-targeted APP-SLxPS1mut mice expressing the amyloid precursor protein at endogenous levels
Open accessAbstract
Most transgenic mice used for preclinical evaluation of potential disease-modifying treatments of Alzheimer's disease develop major histopathological features of this disease by several-fold overexpression of the human amyloid precursor protein. We studied the phenotype of three different strains of gene-targeted mice which express the amyloid precursor protein at endogenous levels. Only further crossing with transgenic mice overexpressing mutant human presenilin1 led to the deposition of extracellular amyloid, accompanied by the deposition of apolipoprotein E, an astrocyte and microglia reaction, and the occurrence of dilated cholinergic terminals in the cortex. Features of neurodegeneration, however, were absent. The pattern of plaque development and deposition in these mice was similar to that of amyloid precursor protein overproducing strains if crossed to presenilin1-transgenics. However, plaque development started much later and developed slowly until the age of 18 months but then increased more rapidly.
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To date, Aβ pathologies and cognitive deficits were observed only when two or three familial AD mutations were combined.
“To date, however, Aβ pathologies and cognitive deficits were observed only when two or three familial AD mutations were combined [33–35].”
From Amyloid-β plaque formation and reactive gliosis are required for induction of cognitive deficits in App knock-in mouse models of Alzheimer’s disease (2019) · cites this paper as [34]
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- Authors
- Köhler, C., Ebert, U., Baumann, K., & Schröder, H.
- Affiliations
- University of Cologne (DE)
- Bayer (Germany) (DE)
- Corresponding author
- Köhler, Christoph
- ORCID
- Köhler, Christoph
- Venue
- Neurobiology of Disease
- Publisher
- Elsevier BV
- Published
- 2005-11
- Volume
- 20
- Issue
- 2
- Pages
- 528-540
- ISSN
- 0969-9961 (ISSN-L)
- OpenAlex
- W2044281375
- Cited by
- 37
- References
- 11
- Citations by year
- 2024: 2 · 2021: 1 · 2020: 2 · 2019: 1 · 2018: 1 · 2017: 2 · 2016: 1 · 2015: 3 · 2014: 3 · 2013: 3 · 2012: 2
- FWCI
- 1.19
- 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)
- 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
- Alzheimer's disease, amyloid precursor protein, presenilin 1, gene-targeted mice, amyloid plaques, apolipoprotein E, neurodegeneration, plaque development, transgenic mouse model
- MeSH terms
- Alzheimer Disease, Animals, Apolipoproteins E, Brain, Cathepsin D, Cell Line, Chimera, Cholinergic Fibers, Disease Models, Animal, Female, Gliosis, Humans, Immunohistochemistry, Male, Membrane Proteins, Mice, Mutant Strains, Mice, Transgenic, Phenotype, Amyloid beta-Protein Precursor, Presynaptic Terminals, Gene Targeting, Mice, Presenilin-1, Plaque, Amyloid
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