Readjustment of "amyloid hypothesis" for developing methods to treat Alzheimer disease

2016 Fiscal Year Final Research Report

• Project/Area Number: 25460341
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: General pharmacology
• Research Institution: Saitama Medical University
• Principal Investigator: Maruyama Kei 埼玉医科大学, 医学部, 教授 (30211577)
• Co-Investigator(Renkei-kenkyūsha): Kondo Ryuichiro 九州大学, 農学研究科, 教授 (80091370) ; Kuniyoshi Shimizu 九州大学, 農学研究科, 教授 (20346836)
• Project Period (FY): 2013-04-01 – 2017-03-31
• Keywords: アルツハイマー病 / アミロイドβタンパク質 / タウタンパク質

Outline of Final Research Achievements

According to the "amyloid hypothesis", Alzheimer disease is developed by the deposition of amyloid beta protein (Aβ), followed by the accumulation of hyperphosphorylated tau and neuronal cell death. The hypothesis has been predominant for over ten years, but it is need to be readjust. We have generated two non-transgenic models: one with an increased Aβ production, and one with an increased phosphorylated tau. The former, which was generated by treatment of a natural resourse-derived compound, did not show abnormal behavior during the research duration. The latter was also used as an experimental model for sleep-disordered breathing, and we have shown that this model showed common gene expression pattern to ageing.

Free Research Field

神経病理学