Research Article

Expression of human amyloid precursor protein in Drosophila melanogaster nerve cells causes a decrease in presynaptic gene mRNA levels

Published: August 10, 2015
Genet. Mol. Res. 14 (3) : 9225-9232 DOI: https://doi.org/10.4238/2015.August.10.2
Cite this Article:
(2015). Expression of human amyloid precursor protein in Drosophila melanogaster nerve cells causes a decrease in presynaptic gene mRNA levels. Genet. Mol. Res. 14(3): gmr5379. https://doi.org/10.4238/2015.August.10.2
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Abstract

Amyloid precursor protein (APP) is a key player in Alzheimer’s disease. The proteolytic cleavage of APP results in various short peptide fragments including the toxic amyloid-beta peptide, which is a main component of senile plaques. However, the functions of APP and its processed fragments are not yet well understood. Here, using real-time polymerase chain reaction, we demonstrate that exogenous expression of APP, its mutant form APP-Swedish, or two truncated forms in Drosophila melanogaster causes a significant (P ≤ 0.05) drop in the mRNA levels of the presynaptic proteins synaptotagmin-1 and neuronal synaptobrevin. The results obtained from this study suggest a potential role of APP or its fragments in the regulation of synaptic gene transcription.

Amyloid precursor protein (APP) is a key player in Alzheimer’s disease. The proteolytic cleavage of APP results in various short peptide fragments including the toxic amyloid-beta peptide, which is a main component of senile plaques. However, the functions of APP and its processed fragments are not yet well understood. Here, using real-time polymerase chain reaction, we demonstrate that exogenous expression of APP, its mutant form APP-Swedish, or two truncated forms in Drosophila melanogaster causes a significant (P ≤ 0.05) drop in the mRNA levels of the presynaptic proteins synaptotagmin-1 and neuronal synaptobrevin. The results obtained from this study suggest a potential role of APP or its fragments in the regulation of synaptic gene transcription.