Journal
FRONTIERS IN BIOSCIENCE-LANDMARK
Volume 25, Issue -, Pages 134-146Publisher
IMR PRESS
DOI: 10.2741/4798
Keywords
Alzheimer's disease; Tauopathies; Amyloid-beta; APPL; BACE1; Drosophila
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Funding
- JSPS Core-to-Core Program B, Asia-Africa Science Platform
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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 amyloidbeta (A beta) that accumulate in the spaces between nerve cells. A beta 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 shortterm memory impairment, increase of wakefulness and consolidated sleep disruption by expressing human A beta 42 or human APP/BACE in Drosophila central nervous system. We herein discuss these Drosophila AD models.
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