Brain Structure and Function

, Volume 214, Issue 2, pp 245–262

Transgenic Drosophila models of Alzheimer’s disease and tauopathies

Review

DOI: 10.1007/s00429-009-0234-4

Cite this article as:
Iijima-Ando, K. & Iijima, K. Brain Struct Funct (2010) 214: 245. doi:10.1007/s00429-009-0234-4

Abstract

Alzheimer’s disease (AD) is the most common form of senile dementia. Aggregation of the amyloid-β42 peptide (Aβ42) and tau proteins are pathological hallmarks in AD brains. Accumulating evidence suggests that Aβ42 plays a central role in the pathogenesis of AD, and tau acts downstream of Aβ42 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.

Keywords

Alzheimer’s diseaseTauopathiesAmyloid-β42Microtubule associated protein tauDrosophila

Copyright information

© Springer-Verlag 2009

Authors and Affiliations

  1. 1.Laboratory of Neurogenetics and Pathobiology, Department of Biochemistry and Molecular Biology, Farber Institute for NeurosciencesThomas Jefferson UniversityPhiladelphiaUSA
  2. 2.Laboratory of Neurodegenerative and Metabolic Diseases, Department of Biochemistry and Molecular Biology, Farber Institute for NeurosciencesThomas Jefferson UniversityPhiladelphiaUSA