Transgenic Drosophila models of Alzheimer's disease and tauopathies

Brain Struct Funct. 2010 Mar;214(2-3):245-62. doi: 10.1007/s00429-009-0234-4. Epub 2009 Dec 5.


Alzheimer's disease (AD) is the most common form of senile dementia. Aggregation of the amyloid-beta42 peptide (Abeta42) and tau proteins are pathological hallmarks in AD brains. Accumulating evidence suggests that Abeta42 plays a central role in the pathogenesis of AD, and tau acts downstream of Abeta42 as a modulator of the disease progression. Tau pathology is also observed in frontotemporal dementia with Parkinsonism linked to chromosome 17 (FTDP-17) and other related diseases, so called tauopathies. Although most cases are sporadic, genes associated with familial AD and FTDP-17 have been identified, which led to the development of transgenic animal models. Drosophila has been a powerful genetic model system used in many fields of biology, and recently emerges as a model for human neurodegenerative diseases. In this review, we will summarize key features of transgenic Drosophila models of AD and tauopathies and a number of insights into disease mechanisms as well as therapeutic implications gained from these models.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Alzheimer Disease / genetics*
  • Alzheimer Disease / metabolism
  • Alzheimer Disease / pathology
  • Amyloid beta-Peptides / genetics
  • Animals
  • Animals, Genetically Modified / genetics*
  • Disease Models, Animal
  • Drosophila / genetics*
  • Genetic Predisposition to Disease / genetics
  • Humans
  • Nerve Degeneration / genetics
  • Nerve Degeneration / metabolism
  • Nerve Degeneration / pathology
  • Plaque, Amyloid / genetics
  • Plaque, Amyloid / metabolism
  • Tauopathies / genetics*
  • Tauopathies / metabolism
  • Tauopathies / pathology
  • tau Proteins / genetics


  • Amyloid beta-Peptides
  • tau Proteins