ArticleJournal of Alzheimer's disease : JAD2020
Generation of Transgenic Cynomolgus Monkeys Overexpressing the Gene for Amyloid-β Precursor Protein.
Article in Journal of Alzheimer's disease : JAD, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 32 citations in OpenAlex.
- Highly efficient and low-mosaicismiScience · 2026Article
- Generation of a rhesus macaque harboring a multivalent reporter for assessing gene editing outcomes.Scientific reports · 2026Article
- Genetically Modified Primate Models for Brain Disorder Research.Neuroscience bulletin · 2026Review
- Modeling Alzheimer's Disease: A Review of Gene-Modified and Induced Animal Models, Complex Cell Culture Models, and Computational Modeling.Brain sciences · 2025Review
- Non-viral generation of transgenic non-human primates via the piggyBac transposon system.Nature communications · 2025Article
- Liver-specific transgenic expression of human NTCP in rhesus macaques confers HBV susceptibility on primary hepatocytes.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Tau and tauopathies across primate species: implications for modeling neurodegenerative disorders.Frontiers in aging neuroscience · 2025Review
- Early blood immune molecular alterations in cynomolgus monkeys with a PSEN1 mutation causing familial Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- A nonhuman primate model with Alzheimer's disease-like pathology induced by hippocampal overexpression of human tau.Alzheimer's research & therapy · 2024Article
- Application and perspective of CRISPR/Cas9 genome editing technology in human diseases modeling and gene therapy.Frontiers in genetics · 2024Review
- Clinical relevance of animal models in aging-related dementia research.Nature aging · 2023Review
- Tropomyosin Isoform Diversity in the Cynomolgus Monkey Heart and Skeletal Muscles Compared to Human Tissues.Biochemistry research international · 2023Article
- XperCT-guided Intra-cisterna Magna Injection of Streptozotocin for Establishing an Alzheimer's Disease Model Using the Cynomolgus Monkey (Experimental neurobiology · 2022Article
- Application of CRISPR/Cas9 System in Establishing Large Animal Models.Frontiers in cell and developmental biology · 2022Review
- Article
- Emerging Electroencephalographic Biomarkers to Improve Preclinical to Clinical Translation in Alzheimer's Disease.Frontiers in aging neuroscience · 2022Review
- Genetically modified large animal models for investigating neurodegenerative diseases.Cell & bioscience · 2021Review
- A Review of the Current Mammalian Models of Alzheimer's Disease and Challenges That Need to Be Overcome.International journal of molecular sciences · 2021Review
- Deconstructing Alzheimer's Disease: How to Bridge the Gap between Experimental Models and the Human Pathology?International journal of molecular sciences · 2021Review
- Aβ Plaques.Free neuropathology · 2020Article
Corrections and comments
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Authors and funding
15 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is the most common cause of dementia and understanding its pathogenesis should lead to improved therapeutic and diagnostic methods. Although several groups have developed transgenic mouse models overexpressing the human amyloid-β precursor protein (APP) gene with AD mutations, with and without presenilin mutations, as well as APP gene knock-in mouse models, these animals display amyloid pathology but do not show neurofibrillary tangles or neuronal loss. This presumably is due to differences between the etiology of the aged-related human disease and the mouse models. Here we report the generation of two transgenic cynomolgus monkeys overexpressing the human gene for APP with Swedish, Artic, and Iberian mutations, and demonstrated expression of gene tagged green fluorescent protein marker in the placenta, amnion, hair follicles, and peripheral blood. We believe that these nonhuman primate models will be very useful to study the pathogenesis of dementia and AD. However, generated Tg monkeys still have some limitations. We employed the CAG promoter, which will promote gene expression in a non-tissue specific manner. Moreover, we used transgenic models but not knock-in models. Thus, the inserted transgene destroys endogenous gene(s) and may affect the phenotype(s). Nevertheless, it will be of great interest to determine whether these Tg monkeys will develop tauopathy and neurodegeneration similar to human AD.
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