Effect of ATBF1 on the neuronal death and APP trafficking using ATBF1 KO mouse

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K06714
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Neurophysiology / General neuroscience
• Research Institution: Nagoya City University
• Principal Investigator: Jung Cha-Gyun 名古屋市立大学, 大学院医学研究科, 准教授 (00464579)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: アルツハイマー病 / ATBF1 / APP代謝 / Aβ産生 / 神経細胞死

Outline of Final Research Achievements

In the present study, we determined the functional role of ATBF1 in neuronal death using ATBF1 knockout mouse. The density of TUNEL positive and activated caspase3 positive cells was comparable between brains of wild-type and knockout mice at E19. However, cultured cortical neurons isolated from ATBF1 KO mice protected against neuronal death induced by Aβ42 compared with wild-type mice. Moreover, ATBF1 binds to Smad2,3,4 for down-regulating Bcl2 (pro-apoptotic factor) expression, thereby inhibiting neuronal death. Our findings suggest that ATBF1 may be a suitable target for therappeutic intervention of AD.

Free Research Field

アルツハイマー病、神経科学