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Transgenic Drosophila models of Alzheimer’s disease and tauopathies

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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.

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Acknowledgments

We apologize to those authors whose work we could not cite because of space constraints. We would like to dedicate this manuscript to the memory of our friend, Goemon Ando. This work was supported by start-up funds from the Farber Institute for Neurosciences, a pilot research grant from the Thomas Jefferson University, and grants from Gilbert Foundation/the American Federation for Aging Research, the Alzheimer’s Association (NIRG-08-91985) and the National Institute of Health (R01AG032279).

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Iijima-Ando, K., Iijima, K. Transgenic Drosophila models of Alzheimer’s disease and tauopathies. Brain Struct Funct 214, 245–262 (2010). https://doi.org/10.1007/s00429-009-0234-4

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