Brain Structure and Function

, Volume 214, Issue 2, pp 245–262

Transgenic Drosophila models of Alzheimer’s disease and tauopathies

Authors

    • Laboratory of Neurogenetics and Pathobiology, Department of Biochemistry and Molecular Biology, Farber Institute for NeurosciencesThomas Jefferson University
    • Laboratory of Neurodegenerative and Metabolic Diseases, Department of Biochemistry and Molecular Biology, Farber Institute for NeurosciencesThomas Jefferson University
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