Impaired neurogenesis, neuronal loss, and brain functional deficits in the APPxPS1-Ki mouse model of Alzheimer's disease
Open accessAbstract
Amyloid-β peptide species accumulating in the brain of patients with Alzheimer's disease are assumed to have a neurotoxic action and hence to be key actors in the physiopathology of this neurodegenerative disease. We have studied a new mouse mutant (APPxPS1-Ki) line developing both early-onset brain amyloid-β deposition and, in contrast to most of transgenic models, subsequent neuronal loss. In 6-month-old mice, we observed cell layer atrophies in the hippocampus, together with a dramatic decrease in neurogenesis and a reduced brain blood perfusion as measured in vivo by magnetic resonance imaging. In these mice, neurological impairments and spatial hippocampal dependent memory deficits were also substantiated and worsened with aging. We described here a phenotype of APPxPS1-Ki mice that summarizes several neuroanatomical alterations and functional deficits evocative of the human pathology. Such a transgenic model that displays strong face validity might be highly beneficial to future research on AD physiopathogeny and therapeutics.
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There is a paucity of studies that have applied ASL to mouse models of AD, although cortical hypo-perfusion has been reported in two amyloid models.
“There is a paucity of studies that have applied ASL to mouse models of AD, although cortical hypo-perfusion has been reported in two amyloid models (Faure et al., 2011, Weidensteiner et al., 2009).”
From In vivo imaging of tau pathology using multi-parametric quantitative MRI (2015) · cites this paper as Faure et al., 2011
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- Authors
- Faure, A., Verret, L., Bozon, B., El Tannir El Tayara, N., Ly, M., Kober, F., Dhenain, M., Rampon, C., & Delatour, B.
- Affiliations
- Université Paris-Sud (FR)
- Centre National de la Recherche Scientifique (FR)
- Corresponding author
- Delatour, B.
- Venue
- Neurobiology of Aging
- Publisher
- Elsevier BV
- Published
- 2011-03
- Volume
- 32
- Issue
- 3
- Pages
- 407-418
- ISSN
- 0197-4580 (ISSN-L)
- OpenAlex
- W2037617444
- Cited by
- 112
- References
- 47
- Citations by year
- 2025: 2 · 2024: 2 · 2023: 3 · 2022: 9 · 2021: 6 · 2020: 3 · 2019: 6 · 2018: 11 · 2017: 11 · 2016: 6 · 2015: 11 · 2014: 8 · 2013: 12 · 2012: 6
- FWCI
- 4.86
- Type
- journal article
- Language
- en
- Open access
- green
- hal.science
- Licence
- Locations
- Neurobiology of Aging (publishedVersion)
- PubMed (publishedVersion)
- HAL AMU (submittedVersion)
- HAL (submittedVersion, other-oa)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Alzheimer's disease, amyloid-beta, neurogenesis, neuronal loss, hippocampal atrophy, spatial memory impairment, aging, transgenic mouse model, amyloid-beta toxicity
- MeSH terms
- Age Factors, Aging, Alzheimer Disease, Amyloid, Analysis of Variance, Animals, Anxiety, Brain, Cognition Disorders, Disease Models, Animal, Humans, Magnetic Resonance Imaging, Motor Activity, Movement Disorders, Mutation, Neurologic Examination, Amyloid beta-Protein Precursor, Animals, Genetically Modified, Mice, Presenilin-1, Neurogenesis
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