Abstract
Parkinson’s disease (PD) is the second most common neurodegenerative disease, and it is associated with sleep behavior disorders. In Drosophila melanogaster disease model, human α-synuclein A30P overexpressing flies (A30P PD model) have been shown for levy body aggregation and movement disorders. We measured sleep rhythms in the A30P PD model flies using the Drosophila Activity Monitoring system and found that they develop sleep defects at 20 days after eclosion. Furthermore, the total amount of sleep is significantly reduced in middle-aged PD model flies and the reduction has been attributed to nighttime sleep. The number and length of sleep bouts also decreased in middle-aged A30P PD model flies. Feeding of the oriental traditional herbal medicines (Kampo), Kamikihito and Unkei-to significantly ameliorate the level of sleep defects in A30P PD model flies. The Kamikihito and Unkei-to recovered 60-min sleep bouts number in the A30P PD model flies to the level of young (5 days after eclosion) flies. Kamikihito recovered sleep both in wild-type and PD model flies. Unkei-to ameliorates not only sleep but also motor function in PD model flies. The data suggest that Kamikihito and Unkei-to might be useful for the sleep defects in human PD patients as well as healthy human.
Highlights
Parkinson’s disease (PD) is a neurodegenerative disease characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta, protein aggregation in neurons (Lewy bodies), and movement disorders, such as tremor at rest, bradykinesia, and rigidity
The similar increase was evident in A30P PD model flies at 20 days, but the daytime sleep level at 5 days was similar to that of control flies at 20 days (Figure 1A)
As described in Section “Materials and Methods,” human α-synuclein A30P overexpressing PD model Drosophila showed the essential features of human disorder [9, 18]
Summary
Parkinson’s disease (PD) is a neurodegenerative disease characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta, protein aggregation in neurons (Lewy bodies), and movement disorders, such as tremor at rest, bradykinesia, and rigidity. Over 90% of patients with PD develop sleep rhythm abnormality such as increased daytime sleep, sleep fragmentation, and the loss of slow-wave sleep (SWS) [2]. Sleep quality is very important to maintain homeostasis, and sleep deprivation in mice causes increased oxidative stress and changes in antioxidant enzyme activities [3]. Sleep disorder deficits have been suggested signature for early PD, because patients with REM sleep behavior disorder are associated with a high risk of developing PD [4, 5]. These human data suggest that the possibility of early sleep deficits may be occurred in Drosophila PD models
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