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2023 Fiscal Year Final Research Report

Demonstration of the neurodegeneration prevention effect of an orally administered neuron-specific potassium excretion promoter.

Research Project

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Project/Area Number 21K06723
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Review Section Basic Section 47060:Clinical pharmacy-related
Research InstitutionSetsunan University

Principal Investigator

Kuramoto Nobuyuki  摂南大学, 薬学部, 教授 (60324092)

Co-Investigator(Kenkyū-buntansha) 宇野 恭介  摂南大学, 薬学部, 講師 (30608774)
金城 俊彦  摂南大学, 薬学部, 助教 (70758599)
Project Period (FY) 2021-04-01 – 2024-03-31
Keywordsカリウム / ホメオスタシス / 神経細胞 / 脆弱性 / 保護効果 / ミトコンドリア / 高齢化
Outline of Final Research Achievements

We have investigated a possibility that lowering intracellular potassium ion (K+) level would perform protective effect on neuronal cell death. The potassium-chloride co-transporter (KCC) 2 stimulators were hypothesized to protect neurons by lowering K+, while a KCC2 inhibitors had such an effect. Although the inhibitor had the potential to increase cytosolic K+ levels, it was suggested that mitochondria may actually take up K+ and buffer the increase in cytosolic K+ levels, thereby protecting neurons. Although the expression level of K+ channels in the brains of aged mice changed, the K+ concentration in brain tissue did not change with age, suggesting that the K+ level was maintained even at the gene expression level.

Free Research Field

神経科学

Academic Significance and Societal Importance of the Research Achievements

高齢化に伴う認知機能の低下、各種神経精神疾患、運動機能障害は中枢神経系の神経細胞死によるものが大きい。神経細胞は幹細胞による補充が期待されず、脱落後は必然的に担当機能が不全となる。本研究により、神経細胞の老化や神経細胞死の進行の一因が神経細胞内K+濃度の変化に起因する可能性が示唆された。摂取した過剰なK+は尿として排出されるが、それまでの間、血中濃度を上げないように多くの細胞内に取り込まれ、一時的に保管される。すなわち腎機能が低下すると細胞内での蓄積が多くなる。したがって、本研究の遂行により、食事等由来K+摂取量の限度を定めることで高齢化社会における神経変性疾患抑制への関与が期待される。

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Published: 2025-01-30  

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