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Synaptic abnormalities in a Drosophila model of Alzheimer’s disease
Journal article   Open access   Peer reviewed

Synaptic abnormalities in a Drosophila model of Alzheimer’s disease

Siddhita D Mhatre, Vivek Satyasi, Mark Killen, Brie E Paddock, Robert D Moir, Aleister J Saunders and Daniel R Marenda
Disease models & mechanisms, v 7(3), pp 373-385
Mar 2014
PMID: 24487408
url
https://doi.org/10.1242/dmm.012104View
Published, Version of Record (VoR) Open

Abstract

APP Synapse NMJ Alzheimer’s disease Drosophila BACE
Alzheimer’s disease (AD) is an age-related neurodegenerative disease characterized by memory loss and decreased synaptic function. Advances in transgenic animal models of AD have facilitated our understanding of this disorder, and have aided in the development, speed and efficiency of testing potential therapeutics. Recently, we have described the characterization of a novel model of AD in the fruit fly, Drosophila melanogaster , where we expressed the human AD-associated proteins APP and BACE in the central nervous system of the fly. Here we describe synaptic defects in the larval neuromuscular junction (NMJ) in this model. Our results indicate that expression of human APP and BACE at the larval NMJ leads to defective larval locomotion behavior, decreased presynaptic connections, altered mitochondrial localization in presynaptic motor neurons and decreased postsynaptic protein levels. Treating larvae expressing APP and BACE with the γ-secretase inhibitor L-685,458 suppresses the behavioral defects as well as the pre- and postsynaptic defects. We suggest that this model will be useful to assess and model the synaptic dysfunction normally associated with AD, and will also serve as a powerful in vivo tool for rapid testing of potential therapeutics for AD.

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Collaboration types
Domestic collaboration
Web of Science research areas
Cell Biology
Medicine, Research & Experimental
Pathology
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