ArticleJournal of molecular neuroscience : MN2014
Evidences for B6C3-Tg (APPswe/PSEN1dE9) double-transgenic mice between 3 and 10 months as an age-related Alzheimer's disease model.
Article in Journal of molecular neuroscience : MN, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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11 citing papers in PubMed.
- Review
- 8-weeks aerobic exercise ameliorates cognitive deficit and mitigates ferroptosis triggered by iron overload in the prefrontal cortex ofFrontiers in neuroscience · 2024Article
- Locomotor Hyperactivity in the Early-Stage Alzheimer's Disease-like Pathology of APP/PS1 Mice: Associated with Impaired Polarization of Astrocyte Aquaporin 4.Aging and disease · 2022Article
- MG53 protein rejuvenates hUC-MSCs and facilitates their therapeutic effects in AD mice by activating Nrf2 signaling pathway.Redox biology · 2022Article
- The Protective Effects of Osteocyte-Derived Extracellular Vesicles Against Alzheimer's Disease Diminished with Aging.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Therapeutic efficacy of novel memantine nitrate MN-08 in animal models of Alzheimer's disease.Aging cell · 2021Article
- Plasmon-Activated Water Reduces Amyloid Burden and Improves Memory in Animals with Alzheimer's Disease.Scientific reports · 2019Article
- Article
- Semi-automatic synthesis and biodistribution of N-(2-BMC medical imaging · 2017Article
- Mitochondrial Sirt3 Expression is Decreased in APP/PS1 Double Transgenic Mouse Model of Alzheimer's Disease.Neurochemical research · 2015Article
- Article
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Authors and funding
11 authors.
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Abstract
Transgenic mouse has shown great advantages in the study of Alzheimer's disease (AD) and drug screening as AD develops rapidly resent years, while more detail information of these transgenic mice and experience of application are needed. To obtain the basic background information of the B6C3-Tg (APPswe/PSEN1dE9) double-transgenic mouse, which was reported with early onset AD, three- to ten-month-old B6C3-Tg AD mice and normal C57BL/6 mice were selected randomly to test the ability of learning memory by Morris water maze, the brain acetylcholinesterase (AChE) activity by AChE kit, and beta amyloid protein level by immunohistochemistry staining. Compared with the control group, the escape latency time of B6C3-Tg AD mice at 9 and 10 months of age is significantly longer (P < 0.05) in Morris maze test, and the activity of brain AChE is higher. β-Amyloid plaques were observed at 3 months of age and developed rapidly. Statistical analysis showed a positive correlation between the area of these plaques and the ages of B6C3-Tg AD mouse (y = 0.0355e(0.5557x), R = 0.9557). The model's behavior is conformed to simulate behaviors of human Alzheimer's disease at the early stage and may provide detail background information a new choice when transgenic mice are needed in the research of AD.
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