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International Journal of Alzheimer’s Disease
Volume 2012, Article ID 970980, 14 pages
Review Article

Drosophila Models of Tauopathies: What Have We Learned?

1Laboratory of Behavioral and Developmental Genetics, Center for Human Genetics, University of Leuven, 3000 Leuven, Belgium
2VIB Center for the Biology of Disease, 3000 Leuven, Belgium
3INSERM U744, Institut Pasteur de Lille, Université Lille Nord de France, 1 Rue du Professeur Calmette, 59019 Lille Cedex, France

Received 21 February 2012; Accepted 8 April 2012

Academic Editor: David Blum

Copyright © 2012 Marc Gistelinck et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Aggregates of the microtubule-associated protein Tau are neuropathological hallmark lesions in Alzheimer's disease (AD) and related primary tauopathies. In addition, Tau is genetically implicated in a number of human neurodegenerative disorders including frontotemporal dementia (FTD) and Parkinson's disease (PD). The exact mechanism by which Tau exerts its neurotoxicity is incompletely understood. Here, we give an overview of how studies using the genetic model organism Drosophila over the past decade have contributed to the molecular understanding of Tau neurotoxicity. We compare the different available readouts for Tau neurotoxicity in flies and review the molecular pathways in which Tau has been implicated. Finally, we emphasize that the integration of genome-wide approaches in human or mice with high-throughput genetic validation in Drosophila is a fruitful approach.