| Co-Investigator(Kenkyū-buntansha) |
豊田 倫子 国立研究開発法人理化学研究所, 脳科学総合研究センター, 客員研究員 (20392045)
前川 素子 国立研究開発法人理化学研究所, 脳科学総合研究センター, 研究員 (50435731)
大西 哲生 国立研究開発法人理化学研究所, 脳科学総合研究センター, 副チームリーダー (80373281)
豊島 学 国立研究開発法人理化学研究所, 脳科学総合研究センター, 研究員 (90582750)
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| Budget Amount *help |
¥61,490,000 (Direct Cost: ¥47,300,000、Indirect Cost: ¥14,190,000)
Fiscal Year 2016: ¥11,830,000 (Direct Cost: ¥9,100,000、Indirect Cost: ¥2,730,000)
Fiscal Year 2015: ¥11,830,000 (Direct Cost: ¥9,100,000、Indirect Cost: ¥2,730,000)
Fiscal Year 2014: ¥11,960,000 (Direct Cost: ¥9,200,000、Indirect Cost: ¥2,760,000)
Fiscal Year 2013: ¥11,700,000 (Direct Cost: ¥9,000,000、Indirect Cost: ¥2,700,000)
Fiscal Year 2012: ¥14,170,000 (Direct Cost: ¥10,900,000、Indirect Cost: ¥3,270,000)
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| Outline of Final Research Achievements |
We studied iPS cells derived from schizophrenia with the microdeletion of chromosome 22q11.2 and with impaired GLO1 gene whose protein product is involved in the scavenging of carbonyl stress. In these studies, we focused on the schizophrenia theory of “abnormal neurodevelopment”.We observed disturbed differentiation efficiencies in patients’iPS cell-derived neurospheres and neurons. Those defects of neural differentiations were partially rescued by an inhibitor of p38 (for 22q11.2 deletion) or by scavengers of carbonyl stress (for GLO1 mutation), suggesting an importance of rectifying abnormal neural differentiations in early neurodevelopmental stage.
We could also confirm that abnormal neural differentiations are seen in patients’ postmortem brains, by examining the expression ratio of neuronal and glial markers.
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