| Project/Area Number |
21K15617
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 51030:Pathophysiologic neuroscience-related
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| Research Institution | University of Tsukuba |
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Principal Investigator |
Liu ChihーYao 筑波大学, 国際統合睡眠医科学研究機構, 研究員 (50895513)
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| Project Period (FY) |
2021-04-01 – 2022-03-31
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| Project Status |
Discontinued (Fiscal Year 2021)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2023: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2022: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2021: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | Sleep / REM sleep / Sublaterodorsal nucleus / Parkinson's disease / Alpha-synuclein / alpha-synuclein |
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| Outline of Research at the Start |
Since the discovery of REM sleep behavior disorder (RBD) as an early marker of alpha-synclein-related disease such as Parkinson's disease (PD), which is one of the major neurodegenerative diseases no matter in Japan or all over the world, more people are aware of the significance of RBD-like symptoms and seek for medical consultation and intervention so as to slow down the progress of RBD to PD. This proposed research aims to provide direct scientific evidence about a potential neural mechanism that could be one important factor underlying the association between RBD and PD.
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| Outline of Annual Research Achievements |
Mammalian sleep is composed of rapid eye movement (REM) sleep and non-REM (NREM) sleep, both of which can be compromised differentially in various psychiatric and neurological disorders. I recently found that ablation of a specific neuronal population in the sublaterodorsal nucleus (SLD) resulted in significant loss of REM sleep, suggesting a genetically defined neuronal population is discovered to be essential for generating REM sleep. In the SLD neuron-ablated mice, REM sleep without muscle atonia is frequently observed, reminiscent of REM sleep behavior disorder in Parkinson's disease (PD). Moreover, lower anxiety-like and lower depression-like behaviors are found, consistent with previous observations in which REM sleep deprivation produced anxiolytic-like and antidepressant-like effect. Next, I found that the ablated neuronal population are composed of both GABAergic and glutamatergic neurons with varied percentages. Therefore, these results provide us more information about the pathogenesis of PD, during which the alpha-synuclein accumulation may occur in the level of the SLD, producing various motor and non-motor symptoms. Furthermore, the genetic identification of SLD neurons may lead to the development of novel diagnostic methods and therapeutics for PD.
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