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CRISPR-Based Genome-Editing Tools for Huntington’s Disease research and Therapy

Neuroscience Bulletin 2022年第11期38卷 1397-1408页

作者： Yiyang Qin Shihua Li Xiao-Jiang Li Su Yang guangdong key laboratory of non-human primate research Guangdong-Hongkong-Macao Institute of CNS RegenerationJinan UniversityGuangzhou 510632China

Huntington’s disease(HD)is an autosomal dominantly-inherited neurodegenerative disease,which is caused by CAG trinucleotide expansion in exon 1 of the Huntingtin(HTT)*** HD is a rare disease,its monogenic nature makes it an ideal model in which to understand pathogenic mechanisms and to develop therapeutic strategies for neurodegenerative *** regularly-interspaced short palindromic repeats(CRISPR)is the latest technology for genome *** simple to use and highly efficient,CRISPR-based genome-editing tools are rapidly gaining popularity in biomedical research and opening up new avenues for disease ***,we review the development of CRISPR-based genome-editing tools and their applications in HD research to offer a translational perspective on advancing the genome-editing technology to HD treatment.

关键词： Huntington’s disease CRISPR Animal models

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Differential development and electrophysiological activity in cultured cortical neurons from the mouse and cynomolgus monkey

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Neural Regeneration research 2021年第12期16卷 2446-2452页

作者： Xue-Yan Zhang Jun Li Cai-Juan Li Ying-Qi Lin Chun-Hui Huang Xiao Zheng Xi-Chen Song Zhu-Chi Tu Xiao-Jiang Li Sen Yan guangdong key laboratory of non-human primate Models Guangdong-Hongkong-Macao Institute of CNS RegenerationJinan UniversityGuangzhouGuangdong ProvinceChina key laboratory of CNS Regeneration Ministry of EducationJinan UniversityGuangzhouGuangdong ProvinceChina

In vitro cultures of primary cortical neurons are widely used to investigate neuronal ***,it has yet to be fully investigated whether there are significant differences in development and function between cultured rodent and primate cortical neurons,and whether these differences influence the utilization of cultured cortical neurons to model pathological *** in vitro culture techniques combined with immunofluorescence and electrophysiological methods,our study found that the development and maturation of primary cerebral cortical neurons from cynomolgus monkeys were slower than those from *** used a microelectrode array technique to compare the electrophysiological differences in cortical neurons,and found that primary cortical neurons from the mouse brain began to show electrical activity earlier than those from the cynomolgus *** cultured monkey cortical neurons developed slowly in vitro,they exhibited typical pathological features-revealed by immunofluorescent staining-when infected with adeno-associated viral vectors expressing mutant huntingtin(HTT),the Huntington’s disease protein.A quantitative analysis of the cultured monkey cortical neurons also confirmed that mutant HTT significantly reduced the length of ***,compared with the primary cortical neurons of mice,cultured monkey cortical neurons have longer developmental and survival times and greater sustained physiological activity,such as electrophysiological *** findings also suggest that primary cynomolgus monkey neurons cultured in vitro can simulate a cell model of human neurodegenerative disease,and may be useful for investigating time-dependent neuronal death as well as treatment via neuronal *** mouse experiments and protocols were approved by the Animal Care and Use Committee of Jinan University of China(IACUC Approval No.20200512-04)on May 12,*** monkey experiments were approved by the IACUC protocol(IACUC Approval N

关键词： Axion-MEA electrical activities human disease model Huntington’s disease HTT monkey neuron morphometric analysis mouse neuron neurodegenerative diseases primary culture

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PINK1 kinase dysfunction triggers neurodegeneration in the primate brain without impacting mitochondrial homeostasis

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Protein & Cell 2022年第1期13卷 26-46页

作者： Weili Yang Xiangyu Guo Zhuchi Tu Xiusheng Chen Rui Han Yanting Liu Sen Yan Qi Wang Zhifu Wang Xianxian Zhao Yunpeng Zhang Xin Xiong Huiming Yang Peng Yin Huida Wan Xingxing Chen Jifeng Guo Xiao-Xin Yan Lujian Liao Shihua Li Xiao-Jiang Li guangdong key laboratory of non-human primate research Guangdong-Hongkong-Macao Institute of CNS RegenerationJinan UniversityGuangzhou 510632China key laboratory of Brain Functional Genomics of Ministry of Education Shanghai Key Laboratory of Brain Functional Genomicsand Shanghai Key Laboratory of Regulatory BiologySchool of Life SciencesEast China Normal UniversityShanghai 100021China Department of Neurology Xiangya HospitalCentral South UniversityChangsha 410008China Department of Anatomy and Neurobiology Xiangya School of MedicineCentral South UniversityChangsha 410008China

In vitro studies have established the prevalent theory that the mitochondrial kinase PINK1 protects neurodegeneration by removing damaged mitochondria in Parkinson's disease(PD).However,difficulty in detecting endogenous PINK1 protein in rodent brains and cell lines has prevented the rigorous investigation of the in vivo role of *** we report that PINK1 kinase form is selectively expressed in the human and monkey ***/Cas9-mediated deficiency of PINK1 causes similar neurodegeneration in the brains of fetal and adult monkeys as well as cultured monkey neurons without affecting mitochondrial protein expression and ***,PINK1 mutations in the primate brain and human cells reduce protein phosphorylation that is important for neuronal function and *** findings suggest that PINK1 kinase activity rather than its mitochondrial function is essential for the neuronal survival in the primate brains and that its kinase dysfunction could be involved in the pathogenesis of PD.

关键词： Parkinson's disease neurogenesis neurodegeneration mitochondria non-human primates

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