Electronic versions

  • Kiren K. Ubhi
  • Hassan Shaibah
  • Tracey A. Newman
  • David Shepherd
    University of Southampton
  • Amritpal Mudher

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

  • Animals, Animals, Genetically Modified, Axonal Transport/physiology, Disease Models, Animal, Drosophila/metabolism, Drosophila Proteins/metabolism, Humans, Immunohistochemistry, Larva, Movement/physiology, Neuromuscular Junction/pathology, Neurons/metabolism, Tauopathies/metabolism, tau Proteins/metabolism
Original languageEnglish
Pages (from-to)165-71
Number of pages7
JournalInvertebrate neuroscience
Volume7
Issue number3
DOIs
Publication statusPublished - Sept 2007
Externally publishedYes
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