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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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Cell replacement for Parkinson's disease:advances and challenges

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Neural Regeneration Research 2023年第12期18卷 2693-2694页

作者： Bin Xiao Eng-King Tan Department of Neurology National Neuroscience InstituteSingapore Neuroscience and Behavioral Disorders Program Duke-NUS Medical SchoolSingapore

Parkinson's disease(PD), characterized by the loss of dopaminergic(DA) neurons in the substantia nigra pars compacta(SNpc) of the midbrain, is a prototype neurological disease that is suitable for cellular replacement therapy. Levodopa has been utilized to replace the insufficient dopamine released by degenerating DA neurons since the 1960s and it remains the cornerstone of PD treatment. However, as the disease progresses.

关键词： dopamine corners replace

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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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Hyperdense basilar artery sign as a reliable predictor of acute basilar artery occlusion: Case report and literature review

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Visual Journal of Emergency Medicine 2025年 38卷 102179-102179页

作者： Wu, Xiaoxin Sheng, Wenli Ye, Fei Department of Neurology The First Affiliated Hospital Sun Yat-sen University Guangzhou China Neuroscience and Behavioral Disorders Program Duke-NUS Medical School National University of Singapore Singapore Singapore

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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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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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Author reply to letter to the editor regarding "Efficacy and adverse effects of ketamine versus electroconvulsive therapy for major depressive disorder: A systematic review and meta-analysis."

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Journal of affective disorders 2024年 350卷 379-381页

作者： Luís Eduardo Gauer Stefanie Cavalcanti Debora de A Simoes Moreira Guilherme Teixeira João Quevedo Federal University of Paraná (UFPR) Curitiba PR Brazil. Translational Psychiatry Program Faillace Department of Psychiatry and Behavioral Sciences McGovern Medical School The University of Texas Health Science Center at Houston (UTHealth Houston) Houston TX USA Center of Excellence on Mood Disorders Faillace Department of Psychiatry and Behavioral Sciences McGovern Medical School The University of Texas Health Science Center at Houston (UTHealth Houston) Houston TX USA. Medical Sciences College of Santos Lusíada Foundation (UNILUS) Santos SP Brazil. University of Pernambuco (UPE) Recife PE Brazil. Center of Excellence on Mood Disorders Faillace Department of Psychiatry and Behavioral Sciences McGovern Medical School The University of Texas Health Science Center at Houston (UTHealth Houston) Houston TX USA Neuroscience Graduate Program The University of Texas MD Anderson Cancer Center UTHealth Houston Graduate School of Biomedical Sciences Houston TX USA Translational Psychiatry Laboratory Graduate Program in Health Sciences University of Southern Santa Catarina (UNESC) Criciúma SC Brazil. Electronic address: joao.l.dequevedo@uth.tmc.edu.

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A neural m⁶A/Ythdf pathway is required for learning and memory in Drosophila (vol 12, 1458, 2021)

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NATURE COMMUNICATIONS 2021年第1期12卷 1-18页

作者： Kan, Lijuan Ott, Stanislav Joseph, Brian Park, Eun Sil Dai, Wei Kleiner, Ralph E. Claridge-Chang, Adam Lai, Eric C. Department of Developmental Biology Sloan-Kettering Institute New York NY USA Program in Neuroscience and Behavioral Disorders Duke-NUS Medical School Singapore Singapore Louis V. Gerstner Jr. Graduate School of Biomedical Sciences Memorial Sloan Kettering Cancer Center New York NY USA Department of Chemistry Princeton University Princeton NJ USA Institute for Molecular and Cell Biology A*STAR Singapore Singapore Department of Physiology National University of Singapore Singapore Singapore

Epitranscriptomic modifications can impact behavior. Here, we used Drosophila melanogaster to study N6-methyladenosine (m6A), the most abundant modification of mRNA. Proteomic and functional analyses confirm its nuclear (Ythdc1) and cytoplasmic (Ythdf) YTH domain proteins as major m6A binders. Assays of short term memory in m6A mutants reveal neural-autonomous requirements of m6A writers working via Ythdf, but not Ythdc1. Furthermore, m6A/Ythdf operate specifically via the mushroom body, the center for associative learning. We map m6A from wild-type and Mettl3 mutant heads, allowing robust discrimination of Mettl3-dependent m6A sites that are highly enriched in 5’ UTRs. Genomic analyses indicate that Drosophila m6A is preferentially deposited on genes with low translational efficiency and that m6A does not affect RNA stability. Nevertheless, functional tests indicate a role for m6A/Ythdf in translational activation. Altogether, our molecular genetic analyses and tissue-specific m6A maps reveal selective behavioral and regulatory defects for the Drosophila Mettl3/Ythdf pathway.

关键词： RNA modification Short-term memory

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