IMR Press / FBL / Volume 25 / Issue 1 / DOI: 10.2741/4798

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.

Insights from Drosophila melanogaster model of Alzheimer's disease
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1 Faculty of Medical Technology, Hanoi Medical University, Hanoi, Vietnam
2 Center for Gene-Protein Research, Hanoi Medical University, Hanoi, Vietnam
3 Department of Physiology, Hanoi Medical University, Hanoi, Vietnam
4 Department of Applied Biology
5 The Center for Advanced Insect Research, Kyoto Institute of Technology, Matsugasaki, Sakyo-ku, Kyoto, 606-8585, Japan
Send correspondence to: Nguyen Trong Tue, Faculty of Medical Technology, Hanoi Medical University, No. 1, Ton That Tung, DongDa, Hanoi, Vietnam, Tel: 84 902185488, Fax: 0484 48525115, E-mail:
Front. Biosci. (Landmark Ed) 2020, 25(1), 134–146;
Published: 1 January 2020
(This article belongs to the Special Issue Cutting edge of insect biomedical science)

Alzheimer’s disease (AD) is a common chronic neurodegenerative disease that mainly affects the medial temporal lobe and associated neocortical structures. The disease process involves two abnormal structures, plaques and tangles, which damage and destroy nerve cells. Tangles are twisted fibers of tau protein that build up inside cells. Plaques are deposits of a protein fragment called amyloid-beta (Aβ) that accumulate in the spaces between nerve cells. Aβ derives from the amyloid precursor protein and is the main component of amyloid plaques in the AD brain. Although AD has been extensively examined, its pathogenetic mechanisms remain unclear and there are currently no effective drugs for this disorder. Many AD model systems have recently been established using Drosophila melanogaster by expressing the proteins involved in AD in the brain. These systems successfully reflect some of the symptoms associated with AD such as the onset of learning defects, age-dependent short-term memory impairment, increase of wakefulness and consolidated sleep disruption by expressing human Aβ42 or human APP/BACE in Drosophila central nervous system. We herein discuss these Drosophila AD models.

Alzheimer’s disease
Figure 1
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