Invertebrate Neuroscience

, Volume 7, Issue 3, pp 165–171

A comparison of the neuronal dysfunction caused by Drosophila tau and human tau in a Drosophila model of tauopathies

  • Kiren K. Ubhi
  • Hassan Shaibah
  • Tracey A. Newman
  • David Shepherd
  • Amritpal Mudher
Original Paper

DOI: 10.1007/s10158-007-0052-4

Cite this article as:
Ubhi, K.K., Shaibah, H., Newman, T.A. et al. Invert Neurosci (2007) 7: 165. doi:10.1007/s10158-007-0052-4

Abstract

Hyperphosphorylation and aggregation of tau into tangles is a feature of disorders such as Alzheimer’s disease and other Tauopathies. To model these disorders in Drosophila melanogaster, human tau has been over-expressed and a variety of phenotypes have been observed including neurotoxicity, disrupted neuronal and synaptic function and locomotor impairments. Neuronal dysfunction has been seen prior to neuronal death and in the absence of tangle formation. The Drosophila tau protein shares a large degree of homology with human tau but differs in the crucial microtubule binding domains. Although like human tau Drosophila tau can induce neurotoxicity, little is known about its ability to disrupt neuronal function. In this study we demonstrate that like human tau, over-expression of Drosophila tau results in disrupted axonal transport, altered neuromuscular junction morphology and locomotor impairments. This indicates that like human tau, over-expression of Drosophila tau compromises neuronal function despite significant differences in microtubule binding regions.

Keywords

NeurodegenerationAlzheimer’sTauAxonal transport

Copyright information

© Springer-Verlag 2007

Authors and Affiliations

  • Kiren K. Ubhi
    • 1
  • Hassan Shaibah
    • 1
  • Tracey A. Newman
    • 1
  • David Shepherd
    • 1
  • Amritpal Mudher
    • 1
  1. 1.Department of NeuroscienceUniversity of Southampton, School of Biological SciencesSouthamptonUK