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Updated: Jun 18, 2026

Assaying Locomotor, Learning, and Memory Deficits in Drosophila Models of Neurodegeneration
Published on: March 11, 2011
Transgenic Drosophila models of Alzheimer's disease and tauopathies
Kanae Iijima-Ando1, Koichi Iijima
1Laboratory of Neurogenetics and Pathobiology, Department of Biochemistry and Molecular Biology, Farber Institute for Neurosciences, Thomas Jefferson University, 900 Walnut Street, JHN410, Philadelphia, PA, 19107, USA. Kanae.Iijima-Ando@jefferson.edu
Abstract:
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.

