Transgenic Drosophila models of Alzheimer's disease and tauopathies.

Laboratory 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.
Brain Structure and Function (Impact Factor: 7.84). 12/2009; 214(2-3):245-62. DOI: 10.1007/s00429-009-0234-4
Source: PubMed

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.

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