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朱剑虹:细胞治疗和细胞器置换技术用于神经系统疾病和损伤的预防和治疗
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The current cell therapy aims at restoring neural regeneration and replacement of lost neural cells within the appropriate time window in traumatic brain injury patients. Furthermore, neurorepair attempts to restore retinal neuron axonal function in the optic nerve injury in those patients with significant visional impairment.

Mitochondria – bacteria sized cellular organelles residing in most of our cells-- convert fuel from food into the body's most biologically useful form of energy or ATP. Only in the past few years, with advances in cellular and molecular biology, have we appreciated the complexity of genetic mechanisms and cl inical presentations in mitochondrial disorders. For example, large numbers of mitochondria DNA (mtDNA) deletions in brain and muscle, become fatal or in young adulthood with epilepsy, while a maternally inherited point mutation in patients with Leber's hereditary optic neuropathy, a cause of blindness in young adults. Mutated mtDNAs may also have roles in the progressive symptoms of late-onset neurodegenerative diseases, such as Parkinson's and Alzheimer's diseases.

Currently, these diseases are refractory or incurable; however, nuclear genome transfer between patients' and healthy eggs to replace mutant mtDNAs holds promises. Considering that a polar body contains few mitochondria and shares the same genomic material as an oocyte, we perform polar body transfer to prevent the transmission of mtDNA variants.

We compare the effects of different types of germline genome transfer, including spindle-chromosome transfer, pronuclear transfer, and polar body transfer, in mice. Genetic analysis confirms that the F1 generation from polar body transfer possesses m i n i m a l d o n o r m t D N A c a r r y o v e r . M o r e o v e r , t h e m t D N A g e n o t y p e r e m a i n s stable in F2 progeny after polar body transfer. Our investigation demonstrates that promising pre-clinical studies of cell therapy have been translating partially into positive outcomes in clinical trials, and mitochondrial replacement has great potential to prevent inherited mitochondrial diseases.
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讲师介绍
  • 讲师:朱剑虹(教授)

    教育部长江学者,复旦大学特聘教授, 复旦大学医学神经生物学国家重点实验室副主任,复旦大学附属华山医院神经外科教授。他曾在德国柏林洪堡大学获得细胞生物学博士学位和在苏州大学医学院取得神经外科博士学位。 朱剑虹教授长期从事神经外科和神经生物学临床、研究和教学工作,尤其在神经干细胞生物学、神经损伤修复和中枢神经系统肿瘤方面作了深入研究。先后主持了国家基础研究计划(973项目)课题,上海市科委重大研究项目的研究和国家自然科学基金项目。