This study investigates the role of tubulin-alpha4a (Tuba4a) polyglutamylation in tauopathies. Researchers generated a Knockin mouse model with mutations preventing polyglutamylation of Tuba4a. These mice exhibited reduced binding of tau and GSK3 kinase to neuronal microtubules, leading to decreased tau phosphorylation. Crossbreeding with a human tauopathy model reversed tau hyperphosphorylation, oligomerization, and microglial activation, highlighting tubulin polyglutamylation as a potential therapeutic target in tauopathies.
Preventing Tuba4a polyglutamylation reduces tau hyperphosphorylation and microglial activation, suggesting a novel therapeutic approach for tauopathies.
Tuba4aΔpolyGlu Knockin mouse model with point mutations abolishing polyglutamylation of Tuba4a, developed to study the impact on tau pathology.
Tauopathies, Neurodegeneration, Microglial activation, Tubulin modifications
Knockin model, Point mutations, Polyglutamylation-deficient Tuba4a, Tau pathology assessment
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
