Pathogenic roles of actin metabolism in cerebral small vessel disease

2015 Fiscal Year Final Research Report

• Project/Area Number: 26830039
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Nerve anatomy/Neuropathology
• Research Institution: National Cardiovascular Center Research Institute
• Principal Investigator: Yamamoto Yumi 国立研究開発法人国立循環器病研究センター, 研究所, 流動研究員 (10614927)
• Project Period (FY): 2014-04-01 – 2016-03-31
• Keywords: ＣＡＤＡＳＩＬ / 脳小血管病 / 脳梗塞

Outline of Final Research Achievements

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a hereditary cerebral small vessel disease caused by the mutations in NOTCH3 gene expressed in mural cells. Although many studies have conducted, the exact pathogenesis remains unclear. Here, we generated induced pluripotent stem cells (iPSCs) from CADASIL patients and differentiated them into mural cells (MCs) to replicate the pathology in vitro. Comparison between control and CADASIL MCs revealed altered migration and adhesion ability of CADASIL MCs. Those results suggests that actin metabolism is deeply involved in the pathogenesis of CADASIL.

Free Research Field

細胞生物学