![]() RIKEN Research 2014.Īlzforum website for webinar and information about animal models of Alzheimer’s disease. New mouse models raise the bar for Alzheimer’s research. New mouse model could revolutionize research in Alzheimer’s disease. Single App knock-in mouse models of Alzheimer’s disease. Saito T, Matsuba Y, Mihira N, Takano J, Nilsson P, Itohara S, Iwata N, Saido TC. Laboratory for Proteolytic Neuroscience, RIKEN Brain Science Instituteĭisease-specific (patient-specific) iPS cellsĪlzheimer’s disease, familial type (iPSCs from FAD patients with mutations in presenilin 1 and presenilin 2 )Īlzheimer’s Disease International (ADI).World Alzheimer Report 2014: Dementia and Risk Reduction. ![]() They are listed on the research models database of the web-based scientific community Alzforum. These mouse strains will stimulate further research identifying the mechanisms and pathways involved in Aβ amyloidosis. The last group of generated mice, App NL-G-F/NL-G-F, mice carry the Swedish mutation, Iberian mutation, and Arctic E693G mutation, which accelerates Aβ aggregation starting at 2 months and memory impairment at 6 months.Īpp NL-F/NL-F and App NL-G-F/NL-G-F mice show typical Aβ pathology, neuroinflammation, and memory impairment, without overexpressing APP or interrupting other mouse genes. App NL-F/NL-F mice, which carry the Swedish and Iberian mutations, show Aβ deposition in the cortex and hippocampus at 6 months and memory impairment at 18 months, whereas App NL/NL mice, which carry only the Swedish mutation, are normal. The Swedish KM670/671NL mutation increases the total amount of Aβ, while the Beyreuther/Iberian I716F mutation increases the ratio of Aβ 42 to Aβ 40. Saido, Takashi Saito, and colleagues at RIKEN Brain Science Institute generated App knock-in mice with the Swedish mutation ( App NL/NL, RBRC06342) Swedish and Iberian mutations ( App NL-F/NL-F, RBRC06343) and Swedish, Iberian, and Arctic mutations ( App NL-G-F/NL-G-F, RBRC06344). Researchers have generated a number of transgenic (Tg) mouse models that overexpress human β amyloid (Aβ) precursor protein (APP) however, these APP-Tg mice showed artificial phenotypes that may have little to do with the human disease. The number of people living with dementia worldwide is estimated at 44 million, and is set to almost double by 2030 if preventive therapies are not found. Importantly, the mice live normally, in contrast to previous APP overexpression-based models which are aggressive and often die of unknown cause(s).Īlzheimer’s disease (AD), which is the major form of dementia, is a syndrome caused by a number of progressive illnesses that affect memory and cognitive capacity. and Takashi Saito, Ph.D.Īpp knock-in mice exhibit AD patient-like Aβ 42-dominant plaque deposition concomitantly with neuroinflammation and memory impairment. Pheno-Pub (JMC phenotype information website)Īpp knock-in mouse strains: new models forĪlzheimer’s disease C57BL/6- App/TcsRbrc (RBRC06342) C57BL/6- App/TcsRbrc (RBRC06343) C57BL/6- App/TcsRbrc (RBRC06344)Ĭourtesy of Takaomi C.Today’s tool for functional analysis / Today’s model for human disease. ![]()
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