ArticleExperimental neurobiology2013
An update of animal models of Alzheimer disease with a reevaluation of plaque depositions.
Article in Experimental neurobiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 97 citations in OpenAlex.
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- Applications of artificial intelligence in drug discovery for neurological diseases.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- Beyond Transgenic Mice: Emerging Models and Translational Strategies in Alzheimer's Disease.International journal of molecular sciences · 2025Review
- Advancement in modeling of Alzheimer's disease: a comprehensive review of preclinical screening platforms.Frontiers in aging neuroscience · 2025Review
- Thy1-ApoE4/C/EBPβ double transgenic mice act as a sporadic model with Alzheimer's disease.Molecular psychiatry · 2024Article
- Prodromic Inflammatory-Oxidative Stress in Peritoneal Leukocytes of Triple-Transgenic Mice for Alzheimer's Disease.International journal of molecular sciences · 2024Article
- Therapeutic Effects of Aβ-Specific Regulatory T Cells in Alzheimer's Disease: A Study in 5xFAD Mice.International journal of molecular sciences · 2024Article
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- Increased central auditory gain in 5xFAD Alzheimer's disease mice as an early biomarker candidate for Alzheimer's disease diagnosis.Frontiers in neuroscience · 2023Article
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- R-carvedilol, a potential new therapy for Alzheimer's disease.Frontiers in pharmacology · 2022Review
- Assessing Sex-Specific Circadian, Metabolic, and Cognitive Phenotypes in the AβPP/PS1 and APPNL-F/NL-F Models of Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2022Article
- Recent advances in drug repurposing using machine learning.Current opinion in chemical biology · 2021Review
- Following spatial Aβ aggregation dynamics in evolving Alzheimer's disease pathology by imaging stable isotope labeling kinetics.Science advances · 2021Article
- Reduction of Amyloid Burden by Proliferated Homeostatic Microglia inInternational journal of molecular sciences · 2021Article
- TNF-α-dependent neuronal necroptosis regulated in Alzheimer's disease by coordination of RIPK1-p62 complex with autophagic UVRAG.Theranostics · 2021Article
- Astrocyte remodeling in the beneficial effects of long-term voluntary exercise in Alzheimer's disease.Journal of neuroinflammation · 2020Article
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- Upregulation of Cisd2 attenuates Alzheimer's-related neuronal loss in mice.The Journal of pathology · 2020Article
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2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Animal models of Alzheimer disease (AD) are used to study the mechanisms underlying AD pathogenesis, genetic interactions with genes of interest, and environmental risk factors that cause sporadic AD as well as to test the therapeutic effects of AD drug-candidates on neuropathology and cognitive function. To attain a comparative view on the AD models developed, representative AD lines were selected and summarized with respect to transgenic constructs and AD-related pathology. In addition, age-dependent plaque deposition data available in the literature for six representative AD models such as Tg2576, PDAPP, TgAPP23, Tg-APPswe/PS1dE9, 3xTg-AD, and 5XFAD mice were reevaluated using a photographic plaque reference scale method that was introduced recently. Tg2576, PDAPP, and TgAPP23 mice, which carry the amyloid precursor protein (APP) transgene, produced initially slow, but progressively accelerated plaque deposition as they aged, resulting in logistic plaque deposition. In contrast, Tg-APPswe/PS1dE9 and 3xTg-AD mice, which carry both APP and PS1 transgenes, developed abruptly accelerated plaque formation from the beginning, resulting in logarithmic plaque deposition. 5XFAD mice, which also carry both the APP and PS1 transgenes, developed a logarithmic deposition beginning at 2 months. This comparative analysis suggests that AD models may be classified into two distinct plaque deposition groups, and that early plaque models such as APPswe/PS1dE9, 3xTg-AD and 5XFAD might be useful to study the biochemical aspects of APP metabolism, whereas late plaque models such as Tg2576, PDAPP, and TgAPP23 might be useful to study more physiological and environmental aspects of AD pathogenesis, which occur on a longer time scale.
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