Assessment of psychomotor performance in [alpha]CaMK-II-4R tau mice: an insight into human tauopathies
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...
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Published in | Future neurology Vol. 7; no. 6; p. 773 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
London
Future Medicine Ltd
01.11.2012
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Subjects | |
Online Access | Get full text |
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Summary: | 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 [alpha]CaMK-II promoter in order to understand the pathophysiology of human tauopathies. Materials & methods: Wild-type (n = 24) and 24 [alpha]CaMK-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 [alpha]CaMK-II-4R tau mice developed a greater degree of anxiety and depression compared with wild-type mice. Conclusion: The cognitive and behavioral aspects of [alpha]CaMK-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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ISSN: | 1479-6708 1748-6971 |
DOI: | 10.2217/fnl.12.76 |