The DOI matches its Crossref record; 235 of the 239 references it cites were found in a registry or an index.
Transgenic mouse models of alzheimer disease: Developing a better model as a tool for therapeutic interventions.
Open accessAbstract
Alzheimer disease (AD) is the leading cause of dementia among elderly. Currently, no effective treatment is available for AD. Analysis of transgenic mouse models of AD has facilitated our understanding of disease mechanisms and provided valuable tools for evaluating potential therapeutic strategies. In this review, we will discuss the strengths and weaknesses of current mouse models of AD and the contribution towards understanding the pathological mechanisms and developing effective therapies. Keywords: Alzheimer disease, amyloid-beta, tau, transgenic mouse models, dementia, neurodegeneration, amyloid precursor protein (APP), mild cognitive impairment (MCI), synaptic dysfunction, mutations
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“transgenic animal models are an invaluable tool for studying pathogenic mechanisms and testing therapeutics of AD (Kitazawa et al., 2012; Jankowsky and Zheng, 2017; Sasaguri et al., 2017).”
From Age-dependent microstructure alterations in 5xFAD mice by high-resolution diffusion tensor imaging (2022) · cites this paper as Kitazawa et al., 2012
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1 retracted
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Self-citationCorrelative Memory Deficits, Aβ Elevation, and Amyloid Plaques in Transgenic Mice
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Cited by
Sorted by citations
A new era for understanding amyloid structures and disease
Iadanza, M. G., Jackson, M. P., Hewitt, E. W., Ranson, N. A., & Radford, S. E. (2018) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-018-0060-8 · Cited by 1,002
The case for rejecting the amyloid cascade hypothesis
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Transcription factor-mediated differentiation of human iPSCs into neurons
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Systematic phenotyping and characterization of the 5xFAD mouse model of Alzheimer’s disease.
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Glucagon-like peptide-1: a multi-faceted anti-inflammatory agent
Mehdi, S. F., Pusapati, S., Anwar, M. S., Lohana, D., Kumar, P., Nandula, S. A., Nawaz, F. K., Tracey, K., Yang, H., LeRoith, D., et al. (2023) · Frontiers in Immunology · doi:10.3389/fimmu.2023.1148209 · Cited by 317
Metadata
- Authors
- Kitazawa, M., Medeiros, R., & M. LaFerla, F.
- Affiliations
- University of California, Merced (US)
- University of California, Irvine (US)
- Corresponding author
- Kitazawa, Masashi
- Venue
- Current Pharmaceutical Design
- Publisher
- Bentham Science Publishers Ltd.
- Published
- 2012-03-01
- Volume
- 18
- Issue
- 8
- Pages
- 1131-1147
- ISSN
- 1381-6128 (ISSN-L)
- PMC
- PMC4437619
- OpenAlex
- W2095268222
- Cited by
- 178
- References
- 239
- Citations by year
- 2026: 10 · 2025: 8 · 2024: 12 · 2023: 17 · 2022: 13 · 2021: 17 · 2020: 20 · 2019: 18 · 2018: 25 · 2017: 10 · 2016: 8 · 2015: 6 · 2014: 6 · 2013: 7 · 2012: 1
- FWCI
- 0.72
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Current Pharmaceutical Design (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion, cc-by)
- Funders
- National Institute on Aging (R01AG021982)
- 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, transgenic mouse model, amyloid-beta, tau protein, amyloid precursor protein, mild cognitive impairment, synaptic dysfunction, neurodegeneration, dementia, therapeutic interventions, APP mutations
- MeSH terms
- Aged, Alzheimer Disease, Animals, Disease Models, Animal, Humans, Mice, Transgenic, Drug Design, Mice
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