Current mouse models of Alzheimer's disease (AD) that are engineered to overproduce amyloid-β do not recapitulate all the features of familial AD. Cohen et al. developed a new transgenic rat model of AD that expressed two mutant human genes known to cause familial AD — the genes encoding amyloid precursor protein and presenilin 1. The rat model showed many features of familial AD, such as progressive neurodegeneration, cerebral amyloidosis and tauopathy, as well as apoptotic neuronal loss in the brain and cognitive decline, and so it could be a useful model for translational AD research.
References
Cohen, R. M. et al. A transgenic Alzheimer rat with plaques, tau pathology, behavioral impairment, oligomeric Aβ, and frank neuronal loss. J. Neurosci. 33, 6245–6256 (2013)
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Harrison, C. Capturing AD features in a novel rat model. Nat Rev Drug Discov 12, 424 (2013). https://doi.org/10.1038/nrd4041
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DOI: https://doi.org/10.1038/nrd4041