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Updated: Aug 24, 2026

Mass Histology to Quantify Neurodegeneration in Drosophila
Published on: December 15, 2016
Age-dependent neurodegeneration and Alzheimer-amyloid plaque formation in transgenic Drosophila
Isabell Greeve1, Doris Kretzschmar, Jakob-Andreas Tschäpe
1Center for Molecular Neurobiology, University of Hamburg, 20251 Hamburg, Germany.
Abstract:
Beta-amyloid peptides that are cleaved from the amyloid precursor protein (APP) play a critical role in Alzheimer's disease (AD) pathophysiology. Here, we show that in Drosophila, the targeted expression of the key genes of AD, APP, the beta-site APP-cleaving enzyme BACE, and the presenilins led to the generation of beta-amyloid plaques and age-dependent neurodegeneration as well as to semilethality, a shortened life span, and defects in wing vein development. Genetic manipulations or pharmacological treatments with secretase inhibitors influenced the activity of the APP-processing proteases and modulated the severity of the phenotypes. This invertebrate model of amyloid plaque pathology demonstrates Abeta-induced neurodegeneration as a basic biological principle and may allow additional genetic analyses of the underlying molecular pathways.
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