Abstract

Background: Tauopathies comprise of a group of senile neurodegenerative disorders that grossly affect memory and compromise motor activity. Early diagnosis and specific treatment of tauopathies remains a challenge for neuroscientists. Hyperphosphorylation of tau, a key microtubule-associated protein, has been confirmed to be responsible for characteristic pathological findings in these disorders. Aim: The objective of this study is to analyze the behavioral changes and motor performance of the four-repeat (4R) tau (with R406W mutation) rodent model induced by αCaMK-II promoter in order to understand the pathophysiology of human tauopathies. Materials & methods: Wild-type (n = 24) and 24 αCaMK-II-4R tau (transgenic; n = 24) mice were selected for the study. Each mouse was subjected to a series of behavioral tests, specifically, the accelerated rotarod, open field, elevated plus maze, light/dark transition and forced swimming tests. Results: The wild-type mice outperformed the transgenic mice in locomotor ability, cognition, learning and adaptability. The αCaMK-II-4R tau mice developed a greater degree of anxiety and depression compared with wild-type mice. Conclusion: The cognitive and behavioral aspects of αCaMK-II-4R tau mice obtained from this study can be projected to various tauopathies in general and certain sporadic forms of Alzheimer’s disease in particular, thus providing a critical in vivo model for determining the role of aberrant tau in neurodegeneration.

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