2015 Fiscal Year Final Research Report
Investigation of inhibitory materials for Abeta amyloidgenesis including inhibitory function of GM1 ganglioside expression
| Project/Area Number |
25870906
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Neurochemistry/Neuropharmacology
Pharmacology in pharmacy
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| Research Institution | Hokuriku University |
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Principal Investigator |
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Keywords | アルツハイマー病 / 神経細胞 / GM1ガングリオシド / アミロイドβ蛋白 / アストロサイト / ネプリライシン |
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| Outline of Final Research Achievements |
We suggested that propofol, thiopental and midazolam inhibits amyloid β-protein assembly by decreasing GM1 ganglioside expression in detergent-resistant membrane microdomains of neurons, and that leptin inhibits amyloid β-protein assembly by decreasing GM1 ganglioside expression in neuronal membrane.
We suggested that ketamine suppresses Aβ degradation of NEP by reducing p38 MAPK-mediated pathway activity, and that leptin decreases Aβ degradation by NEP through activation of ERK, and that simvastatin and atorvastatin induce the increase of Aβ degradation of NEP on the extracellular of astrocytes by inducing ERK-mediated pathway activity and that these reagents regulate the differential mechanisms between the secretion of NEP, the induction of cholesterol reduction, and the morphological changes in the cultured astrocytes.
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| Free Research Field |
神経化学
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