This study investigates the impact of decreased translational fidelity on neuronal function and aging. Mice harboring the Rps9(D95N) mutation exhibit error-prone protein synthesis, leading to synaptic dysfunction, neuronal hyperexcitability, and behavioral changes reminiscent of early Alzheimer's disease. These findings suggest that random protein misfolding due to translational errors may contribute to neurodegeneration.
Mice with the Rps9(D95N) mutation display cognitive deficits, altered circadian rhythms, and increased neuronal excitability, modeling early features of Alzheimer's disease and highlighting the role of translational fidelity in neurodegeneration.
Rps9(D95N) Knockin mouse model, engineered to express a ribosomal ambiguity mutation that increases translational errors, resulting in proteostasis imbalance and neurodegenerative phenotypes.
Alzheimer's disease, Neurodegeneration, Protein misfolding, Translational fidelity, Aging
Knockin model, Point mutation, Ribosomal ambiguity mutation, Error-prone translation, Proteostasis
From model design to experimental results
Tailor-made solutions adapted to scientific questions
Comprehensive dataset package
Generated with biopharma partners and in-house
Scientific follow-up and advice along the project
Collaborative approach for problem solving and development of innovative models
Breeding facilities in US and Europe
Certified health status from professional breeders
