|Budget Amount *help
¥16,380,000 (Direct Cost: ¥12,600,000、Indirect Cost: ¥3,780,000)
Fiscal Year 2017: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
Fiscal Year 2016: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
Fiscal Year 2015: ¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2014: ¥5,720,000 (Direct Cost: ¥4,400,000、Indirect Cost: ¥1,320,000)
|Outline of Final Research Achievements
Previous observational studies have implied that angiotensin II type 1 receptor (AT1) blocker (ARB) is superior to the other types of antihypertensives in attenuating the progression of Alzheimer’s disease (AD). The receptor of AGE (RAGE) is shown to be involved in the pathogenesis of AD by binding to amyloid β (Aβ). In this study, we planned to clarify the hypotheses that Aβ activates AT1 via an interaction between AT1 and RAGE on cellular membrane, and that ARB prevents the progression of AD by inhibiting the interaction. In vitro analysis revealed that the binding of Aβ to RAGE activates cellular signaling and undergoes endocytosis by activating AT1, and that ARBs partially inhibited the phenomenon. Further investigation will be required to investigate whether this phenomenon contributes to the progression of AD using mice models.