| 配分額 *注記 |
4,680千円 (直接経費: 3,600千円、間接経費: 1,080千円)
2023年度: 1,560千円 (直接経費: 1,200千円、間接経費: 360千円)
2022年度: 1,560千円 (直接経費: 1,200千円、間接経費: 360千円)
2021年度: 1,560千円 (直接経費: 1,200千円、間接経費: 360千円)
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| 研究開始時の研究の概要 |
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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| 研究実績の概要 |
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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