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Induced pluripotent stem cell-related approaches to generate dopaminergic neurons for Parkinson's disease

Neural Regeneration research 2025年第11期20卷 3193-3206页

作者： Ling-Xiao Yi Hui Ren Woon Genevieve Saw Li Zeng Eng King Tan Zhi Dong Zhou National Neuroscience Institute Singapore Nanyang Technology University Singapore Department of Neurology Singapore General HospitalSingapore Signature Research Program in Neuroscience and Behavioral Disorders Duke-NUS Medical SchoolSingapore

The progressive loss of dopaminergic neurons in affected patient brains is one of the pathological features of Parkinson's disease,the second most common human neurodegenerative *** the detailed pathogenesis accounting for dopaminergic neuron degeneration in Parkinson's disease is still unclear,the advancement of stem cell approaches has shown promise for Parkinson's disease research and *** induced pluripotent stem cells have been commonly used to generate dopaminergic neurons,which has provided valuable insights to improve our understanding of Parkinson's disease pathogenesis and contributed to anti-Parkinson's disease *** current review discusses the practical approaches and potential applications of induced pluripotent stem cell techniques for generating and differentiating dopaminergic neurons from induced pluripotent stem *** benefits of induced pluripotent stem cell-based research are *** dopaminergic neuron differentiation protocols from induced pluripotent stem cells are *** emerging three-dimension-based brain organoid models compared with conventional two-dimensional cell culture are ***,limitations,challenges,and future directions of induced pluripotent stem cell–based approaches are analyzed and proposed,which will be significant to the future application of induced pluripotent stem cell-related techniques for Parkinson's disease.

关键词： dopaminergic neurons induced pluripotent stem cells Parkinson's disease stem cell approaches

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Role of dopamine in the pathophysiology of Parkinson’s disease

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Translational Neurodegeneration 2023年第1期12卷 281-295页

作者： Zhi Dong Zhou Ling Xiao Yi Dennis Qing Wang Tit Meng Lim Eng King Tan National Neuroscience Institute of Singapore 11 Jalan Tan Tock SengSingapore 308433Singapore Department of Neurology Singapore General HospitalOutram RoadSingapore 169608Singapore Signature Research Program in Neuroscience and Behavioral Disorders Duke-NUS Graduate Medical School Singapore8 College RoadSingapore 169857Singapore Department of Neurology Zhujiang HospitalSouthern Medical UniversityGuangzhou 510280China Department of Biological Science National University of SingaporeSingapore 119077Singapore

A pathological feature of Parkinson’s disease(PD)is the progressive loss of dopaminergic neurons and decreased dopamine(DA)content in the substantia nigra pars compacta in PD *** is the neurotransmitter of dopaminergic *** evidence suggests that DA interacts with environmental and genetic factors to contribute to PD *** of DA synthesis,storage,transportation and metabolism have been shown to promote neurodegeneration of dopaminergic neurons in various PD *** is unstable and can undergo oxidation and metabolism to produce multiple reactive and toxic by-products,including reactive oxygen species,DA quinones,and 3,*** we summarize and highlight recent discoveries on DA-linked pathophysiologic pathways,and discuss the potential protective and therapeutic strategies to mitigate the complications associated with DA.

关键词： Dopamine Dopamine quinones 3,4-Dihydroxyphenylacetaldehyde Neurodegeneration Pathogenesis Parkinson’s disease Reactive oxygen species Therapeutic strategies

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FOXO-regulated DEAF1 controls muscle regeneration through autophagy

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Autophagy 2024年第12期20卷 2632-2654页

作者： Goh, Kah Yong Lee, Wen Xing Choy, Sze Mun Priyadarshini, Gopal Krishnan Chua, Kenon Tan, Qian Hui Low, Shin Yi Chin, Hui San Wong, Chee Seng Huang, Shu-Yi Fu, Nai Yang Nishiyama, Jun Harmston, Nathan Tang, Hong-Wen Program in Cancer and Stem Cell Biology Duke-NUS Medical School Department of Orthopaedic Surgery Singapore General Hospital Programme in Musculoskeletal Sciences Academic Clinical Program SingHealth/Duke-NUS Division of Science Yale-NUS College Program in Neuroscience and Behavioral Disorders Duke-NUS Medical School Department of Medical Research National Taiwan University Hospital Molecular Biosciences Division Cardiff School of Biosciences Cardiff University Division of Cellular & Molecular Research Humphrey Oei Institute of Cancer Research National Cancer Centre Singapore

The commonality between various muscle diseases is the loss of muscle mass, function, and regeneration, which severely restricts mobility and impairs the quality of life. With muscle stem cells (MuSCs) playing a key role in facilitating muscle repair, targeting regulators of muscle regeneration has been shown to be a promising therapeutic approach to repair muscles. However, the underlying molecular mechanisms driving muscle regeneration are complex and poorly understood. Here, we identified a new regulator of muscle regeneration, Deaf1 (Deformed epidermal autoregulatory factor-1)–a transcriptional factor downstream of foxo signaling. We showed that Deaf1 is transcriptionally repressed by FOXOs and that DEAF1 targets to Pik3c3 and Atg16l1 promoter regions and suppresses their expression. Deaf1 depletion therefore induces macroautophagy/autophagy, which in turn blocks MuSC survival and differentiation. In contrast, Deaf1 overexpression inactivates autophagy in MuSCs, leading to increased protein aggregation and cell death. The fact that Deaf1 depletion and its overexpression both lead to defects in muscle regeneration highlights the importance of fine tuning DEAF1-regulated autophagy during muscle regeneration. We further showed that Deaf1 expression is altered in aging and cachectic MuSCs. Manipulation of Deaf1 expression can attenuate muscle atrophy and restore muscle regeneration in aged mice or mice with cachectic cancers. Together, our findings unveil an evolutionarily conserved role for DEAF1 in muscle regeneration, providing insights into the development of new therapeutic strategies against muscle atrophy. Abbreviations: DEAF1: Deformed epidermal autoregulatory factor-1;FOXO: Forkhead box O;MuSC: Muscle Stem Cell;PAX7: Paired box 7;PIK3C3: Phosphatidylinositol 3-kinase catalytic subunit type 3. © 2024 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group.

关键词： Autophagy cancer cachexia Deaf1 FOXO muscle sarcopenia

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Glucose-6-phosphate dehydrogenase regulates mitophagy by maintaining PINK1 stability

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Life Metabolism 2025年第1期4卷 17-34页

作者： Yik-Lam Cho Hayden Weng Siong Tan Jicheng Yang Basil Zheng Mian Kuah Nicole Si Ying Lim Naiyang Fu Boon-Huat Bay Shuo-Chien Ling Han-Ming Shen Department of Physiology Yong Loo Lin School of MedicineNational University of SingaporeSingapore 117593Singapore Department of Anatomy Yong Loo Lin School of MedicineNational University of SingaporeSingapore 117594Singapore Cancer and Stem Cell Biology Program Duke-NUS Medical SchoolSingapore 169857Singapore NUS Centre for Cancer Research Yong Loo Lin School of MedicineNational University of SingaporeSingapore 117599Singapore Programs in Neuroscience and Behavioral Disorders Duke-NUS Medical SchoolSingapore 169857Singapore Healthy Longevity Translational Research Programme Yong Loo Lin School of MedicineNational University of SingaporeSingapore 117549Singapore Faculty of Health Sciences MOE Frontier Centre for Precision OncologyUniversity of MacaoMacao 999078China

Glucose-6-phosphate dehydrogenase(G6PD)is the rate-limiting enzyme in the pentose phosphate pathway(PPP)in *** metabolism is closely implicated in the regulation of mitophagy,a selective form of autophagy for the degradation of damaged *** PPP and its key enzymes such as G6PD possess important metabolic functions,including biosynthesis and maintenance of intracellular redox balance,while their implication in mitophagy is largely ***,via a whole-genome CRISPR-Cas9 screening,we identified that G6PD regulates PINK1(phosphatase and tensin homolog[PTEN]-induced kinase 1)-Parkinmediated *** function of G6PD in mitophagy was verified via multiple approaches.G6PD deletion significantly inhibited mitophagy,which can be rescued by G6PD ***,while the catalytic activity of G6PD is required,the known PPP functions per se are not involved in mitophagy ***,we found a portion of G6PD localized at mitochondria where it interacts with PINK1.G6PD deletion resulted in an impairment in PINK1 stabilization and subsequent inhibition of ubiquitin phosphorylation,a key starting point of ***,we found that G6PD deletion resulted in lower cell viability upon mitochondrial depolarization,indicating the physiological function of G6PD-mediated mitophagy in response to mitochondrial *** summary,our study reveals a novel role of G6PD as a key positive regulator in mitophagy,which bridges several important cellular processes,namely glucose metabolism,redox homeostasis,and mitochondrial quality control.

关键词： G6PD mitophagy PINK1 ROS NADPH PPP

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Depth-targeted intracortical microstroke by two-photon photothrombosis in rodent brain

Depth-targeted intracortical microstroke by two-photon photo...

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Clinical and Translational Biophotonics, Translational 2022

作者： Fukuda, Masahiro Matsumura, Takayoshi Suda, Toshio Hirase, Hajime International Research Center for Medical Sciences Kumamoto University 2-2-1 Honjo Chuo-ku Kumamoto860-0811 Japan Signature Program in Neuroscience and Behavioral Disorders Duke-NUS Medical School 8 college Road Singapore169857 Singapore Division of Inflammation Research Center for Molecular Medicine Jichi Medical University 3311-1 Yakushiji Tochigi Shimotsuke329-0498 Japan Cancer Science Institute of Singapore National University of Singapore 14 Medical Drive #12-01 Singapore117599 Singapore Center for Translational Neuromedicine Faculty of Health and Life Sciences University of Copenhagen Blegdamsvej 3B Copenhagen N2200 Denmark

We have developed depth-targeted Photothrombosis (DTPT) technique that can target a single vessel in the cortical parenchyma by two-photon excitation. Rose Bengal-mediated DTPT could be induced at 720 nm scanning with... 详细信息

ISBN: (纸本)9781557528209

关键词： Photons

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Analysis of sleep spindles in children with Asperger’s syndrome

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Sleep Science 2023年第3期14卷 201-206页

作者： Rodolfo Cebreros-Paniagua Fructuoso Ayala-Guerrero Erik Leonardo Mateos-Salgado Christopher Isaac Villamar-Flores Carlos Alberto Gutiérrez-Chávez Ulises Jiménez-Correa National Autonomous University of Mexico Psychology Faculty - Mexico City - Mexico. Autonomous University of the State of Mexico Psychology Faculty - Toluca - State of Mexico - Mexico. National Autonomous University of Mexico Sleep Disorders Clinic Medicine Faculty Research Division - Mexico City - Mexico. National Autonomous University of Mexico Postgraduate Program in Behavioral Neuroscience Psychology Faculty - Mexico City - Mexico.

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Effectiveness of a brief behavioral intervention for insomnia (BBII) during the COVID-19 pandemic: Mexican case report

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Sleep Science 2023年第3期13卷 210-213页

作者： Horacio Balam Álvarez-García Ulises Jiménez-Correa Katie Moraes de Almondes National Autonomous University of Mexico Sleep Disorders Clinic Medicine Faculty Research Division - Mexico City - Mexico. National Autonomous University of Mexico Postgraduate program in Behavioral Neuroscience Psychology Faculty - Mexico City. Onofre Lopes University Hospital AMBSONO Sleep Clinic - Natal - Rio Grande do Norte - Brazil. Federal University of Rio Grande do Norte Department of Psicobiología and Postgraduate Program in Psicobiología - Natal - Rio Grande do Norte - Brazil.

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乌头碱诱发心律失常毒性新分子机制#

乌头碱诱发心律失常毒性新分子机制#

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第四届（2023年）中国安全药理学学术年会

作者：王相冲 Jianjun Wu Heming Wei 许彦芳苏素文河北医科大学药理教研室 Neuroscience & Behavioral Disorders Program Duke-NUS Medical School Singapore Research Laboratory KK Women's & Children's HospitalSingapore

目的:乌头类中药被誉为"回阳救逆"第一要药,其应用历史悠久、临床疗效显著。然而,其主要活性成分乌头碱有明显的毒性,主要表现为中枢神经系统和心血管系统的毒性反应,特别是其心脏毒性,可引起致死性心律失常,严重危害人类健... 详细信息

目的:乌头类中药被誉为"回阳救逆"第一要药,其应用历史悠久、临床疗效显著。然而,其主要活性成分乌头碱有明显的毒性,主要表现为中枢神经系统和心血管系统的毒性反应,特别是其心脏毒性,可引起致死性心律失常,严重危害人类健康。然而,乌头碱致心律失常的机制尚不明确。因此,本研究采用整体动物实验和体外细胞实验相结合的方法,对乌头碱致心律失常的分子细胞学机制进行探讨。

关键词：心律失常浓度依赖性心室肌细胞乌头碱钙电流钠电流动作电位时程分子机制

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Blood tests of brain function: Neuronal extracellular vesicles

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Biomarkers in Neuropsychiatry 2022年 7卷 100058-100058页

作者： Levine, Amir Strawn, Jeffrey R. Department of Psychiatry Columbia University and New York State Psychiatric Institute New York NY United States Anxiety Disorders Research Program College of Medicine University of Cincinnati Cincinnati OH United States Department of Psychiatry and Behavioral Neuroscience College of Medicine University of Cincinnati Cincinnati OH United States

Extracellular vesicles (EVs) are tiny (<1 µm) membrane-bound vesicles released by all tissues (including the brain) that cross the blood-brain barrier and facilitate cell-to-cell communication within and among tissues. They represent the body's “Twitter system,” rapidly disseminating packets of information throughout the brain and body. Not unlike Twitter, EVs convey short messages through their cargos (e.g., RNAs, proteins, lipids, and metabolites), which direct the molecular activity of recipient cells in both health and disease. Extracellular vesicles serve as mediators of brain function and represent a reservoir for CNS-specific biomarkers that can be sequestered from plasma to guide diagnosis and treatment, representing a new frontier in the molecular study of psychiatric illness and in the development of biomarkers. The EV field has immense potential to revolutionize diagnostic approaches in psychiatry, facilitate precision treatment, predict response, and discover much-needed novel therapeutics. © 2022

关键词： Anxiety Biomarker Depression Extracellular vesicles L1CAM

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Molecular targets for modulating the protein translation vital to proteostasis and neuron degeneration in Parkinson’s disease

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Translational Neurodegeneration 2019年第1期8卷 63-76页

作者： Zhi Dong Zhou Thevapriya Selvaratnam Ji Chao Tristan Lee Yin Xia Chao Eng-King Tan Department of Research National Neuroscience Institute11 Jalan Tan Tock SengSingapore 308433Singapore Department of Neurology Singapore General HospitalOutram RoadSingapore 169608Singapore Signature Research Program in Neuroscience and Behavioural Disorders Duke-NUS Medical School Singapore8 College RoadSingaporeSingapore

Parkinson’s disease(PD)is the most common neurodegenerative movement disorder,which is characterized by the progressive loss of dopaminergic neurons in the Substantia Nigra pars compacta concomitant with Lewy body formation in affected brain *** detailed pathogenic mechanisms underlying the selective loss of dopaminergic neurons in PD are unclear,and no drugs or treatments have been developed to alleviate progressive dopaminergic neuron degeneration in ***,the formation ofα-synuclein-positive protein aggregates in Lewy body has been identified as a common pathological feature of PD,possibly stemming from the consequence of protein misfolding and dysfunctional *** is the mechanism for maintaining protein homeostasis via modulation of protein translation,enhancement of chaperone capacity and the prompt clearance of misfolded protein by the ubiquitin proteasome system and *** protein translation and impaired capacities of chaperone or protein degradation can disturb proteostasis processes,leading to pathological protein aggregation and neurodegeneration in *** recent years,multiple molecular targets in the modulation of protein translation vital to proteostasis and dopaminergic neuron degeneration have been *** potential pathophysiological and therapeutic significance of these molecular targets to neurodegeneration in PD is highlighted.

关键词： Molecular targets Neuron degeneration Parkinson’s disease Protein aggregation Protein translation Proteostasis

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