Could neuronal cell senescence be a pathogenetic factor for age-associated neurodegenerative diseases?

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K08425
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Experimental pathology
• Research Institution: Kagawa University
• Principal Investigator: Chiba Yoichi 香川大学, 医学部, 講師 (30372113)
• Co-Investigator(Kenkyū-buntansha): 上野 正樹 香川大学, 医学部, 教授 (30322267)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: 細胞老化 / 神経変性疾患 / 神経細胞

Outline of Final Research Achievements

To investigate whether neuronal cell senescence contributes to the pathogenesis of age-associated neurodegenerative diseases, we analyzed the expression of cell senescence markers in cultured primary cortical neurons from E17 embryos of SAMP8 mice, a model for age-associated neurodegeneration. Primary neurons from mouse embryos were successfully maintained in serum-free media for up to 8 weeks. The ratio of senescence-associated β-galactosidase-positive neurons from SAMP8 mice was significantly increased after 28 days in vitro (DIV) when compared to those from control SAMR1 mice. The expression of γ-H2AX, a marker for DNA damage foci, was increased in nuclei of cultured neurons after 28 DIV, although no significant difference between neurons from SAMP8 and SAMR1 mice. Other cell senescence markers, such as heterochromatin-associated mH2A and lipid peroxidation product 4-HNE, did not show significant difference between neurons from SAMP8 and SAMR1 mice.

Free Research Field

実験病理学