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Hypothesizing That Pediatric Autoimmune Neuropsychiatric Associated Streptococcal (PANDAS) Causes Rapid Onset of Reward Deficiency Syndrome (RDS) Behaviors and May Require Induction of “Dopamine Homeostasis”

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Open Journal of Immunology 2022年第3期12卷 65-75页

作者： Kenneth Blum Catherine A. Dennen Eric R. Braverman Ashim Gupta David Baron Bernard William Downs Debasis Bagchi Panayotis Thanos Maureen Pollock Jag Khalsa Igor Elman Abdalla Bowirrat Rajendra D. Badgaiyan Center for Mental Health and Sports Psychiatry Western University Health Sciences Pomona USA The Kenneth Blum Behavioral & Neurogenetic Institute Austin USA Department Psychiatry Boonshoff School of Medicine Wright University Dayton USA Institute of Psychology ELTE E&#246tv&#246s Loránd University Budapest Hungary Department of Psychiatry School of Medicine University of Vermont Burlington USA division of Nutrigenomics Victory Nutrition International Inc. Bonita Springs USA Department of Molecular Biology Adelson School of Medicine Ariel University Ariel Israel Department of Family Medicine Jefferson Health Northeast Philadelphia USA Future Biologics Lawrenceville USA Department of Pharmaceutical Sciences Texas Southern University Houston USA Department of Psychology & Behavioral neuropharmacology and Neuroimaging Laboratory on Addictions (BNNLA) Research Institute on Addictions University at Buffalo Buffalo USA Department of Microbiology Immunology and Tropical Medicine School of Medicine George Washington University Washington DC USA Cambridge Health Alliance Harvard Medical School Cambridge USA Department of Psychiatry Ichan School of Medicine at Mount Sinai New York USA Department of Psychiatry South Texas Veteran Health Care System Audie L. Murphy Memorial VA Hospital Long School of Medicine University of Texas Health Science Center San Antonio USA

Pediatric autoimmune neuropsychiatric disorders associated with group A streptococcal infections (PANDAS) is a concept that is used to characterize a subset of children with neuropsychiatric symptoms, tic disorders, or obsessive-compulsive disorder (OCD), whose symptoms are exacerbated by group A streptococcal (GAS) infection. PANDAS has been known to cause a sudden onset of reward deficiency syndrome (RDS). RDS includes multiple disorders that are characterized by dopaminergic signaling dysfunction in the brain reward cascade (BRC), which may result in addiction, depression, avoidant behaviors, anxiety, tic disorders, and/or OCD. According to research by Blum et al., the dopamine receptor D2 (DRD2) gene polymorphisms are important prevalent genetic determinants of RDS. The literature demonstrates that infections like Borrelia and Lyme, as well as other infections like group A beta-hemolytic streptococcal (GABHS), can cause an autoimmune reaction and associated antibodies target dopaminergic loci in the mesolimbic region of the brain, which interferes with brain function and potentially causes RDS-like symptoms/behaviors. The treatment of PANDAS remains controversial, especially since there have been limited efficacy studies to date. We propose an innovative potential treatment for PANDAS based on previous clinical trials using a pro-dopamine regulator known as KB220 variants. Our ongoing research suggests that achieving “dopamine homeostasis” by precision-guided DNA testing and pro-dopamine modulation could result in improved therapeutic outcomes.

关键词： PANDAS CANS Reward Deficiency Syndrome Group A Beta-Hemolytic Streptococcal (GABHS) Pro-Dopamine Regulation Dopamine Homeostasis Molecular Mimicry Lyme Borrelia

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在脑病理状态下星形胶质细胞介导的突触重塑

神经损伤与功能重建 2017年第4期12卷 F0003-F0003页

作者： Kim SK Nabekura J Koizumi S 唐颖馨(编译) Department of Physiology College of Korean MedicineKyung Hee UniversitySeoul02447Korea division of Homeostatic Development National Institute for Physiological SciencesOkazakiAichi444-8585Japan Department of Physiological Sciences The Graduate School for Advanced StudyHayamaKanagawa240-0193Japan Core Research for Evolutional Science and Technology Japan Science and Technology AgencyTokyo102-0076Japan Department of neuropharmacology Interdisciplinary Graduate School of MedicineUniversity of YamanashiYamanashi409-3898Japan 不详

星形胶质细胞是胶质细胞的主要类型,对神经元突触间的信号传递和联系起到反馈作用,构成"三重突触结构"。在大脑发育的过程中,星形胶质细胞的代谢型谷氨酸受体介导钙离子波并释放胶质递质或突触发生分子,介导神经元.胶质细胞间的联系,但... 详细信息

星形胶质细胞是胶质细胞的主要类型,对神经元突触间的信号传递和联系起到反馈作用,构成"三重突触结构"。在大脑发育的过程中,星形胶质细胞的代谢型谷氨酸受体介导钙离子波并释放胶质递质或突触发生分子,介导神经元.胶质细胞间的联系,但在成年大脑中,尚不清楚是否存在此信号通路。但越来越多的证据显示,当成年大脑处于病理状态下,成熟的星形胶质细胞也重新表现出非成熟星形胶质细胞的表型。星形胶质细胞表型的这种非成熟转变可以导致神经环路和突触的重塑。在本综述中,笔者总结了大脑发育过程中星形胶质细胞介导的突触重塑,讨论了成年脑病理过程中非成熟星形胶质细胞信号通路的重现,并重点讨论这些信号通路对病理过程中与脑功能改变有关的突触连接重塑的意义。

关键词：钙离子慢性疼痛树突棘代谢型谷氨酸受体5 血小板反应蛋白

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Structure-activity relationship of pyrazol-4-ylpyridine derivatives and identification of a radiofluorinated probe for imaging the muscarinic acetylcholine receptor M4

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Acta Pharmaceutica Sinica B 2023年第1期13卷 213-226页

作者： Ahmed Haider Xiaoyun Deng Olivia Mastromihalis Stefanie K.Pfister Troels E.Jeppesen Zhiwei Xiao Vi Pham Shaofa Sun Jian Rong Chunyu Zhao Jiahui Chen Yinlong Li Theresa R.Connors April T.Davenport James B.Daunais Vahid Hosseini Wenqing Ran Arthur Christopoulos Lu Wang Celine Valant Steven H.Liang Department of Radiology Division of Nuclear Medicine and Molecular Imaging Massachusetts General Hospital and Harvard Medical SchoolBostonMA 02114USA Department of Nuclear Medicine Tongji HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030China Drug Discovery Biology Monash Institute of Pharmaceutical SciencesMonash UniversityParkvilleVIC 3052Australia Neuromedicines Discovery Centre Monash Institute of Pharmaceutical SciencesMonash UniversityParkvilleVIC 3052Australia Hubei Collaborative Innovation Centre for Non-power Nuclear Technology College of Nuclear Technology&Chemistry and BiologyHubei University of Science and TechnologyXianning 437100China Department of Neurology Massachusetts General HospitalHarvard Medical SchoolBostonMA 02114USA Department of Physiology and Pharmacology Wake Forest School of MedicineWinston SalemNC 27157USA Terasaki Institute for Biomedical Innovation(TIBI) Los AngelesCA 90024USA Center of Cyclotron and PET Radiopharmaceuticals Department of Nuclear Medicine and PET/CT-MRI Centerthe First Affiliated Hospital of Jinan UniversityGuangzhou 510630China

There is an accumulating body of evidence implicating the muscarinic acetylcholine receptor4(M4)in schizophrenia and dementia with Lewy bodies,however,a clinically validated M4positron emission tomography(PET)radioligand is currently *** such,the aim of this study was to develop a suitable M4PET ligand that allows the non-invasive visualization of M4in the ***-activity relationship studies of pyrazol-4-yl-pyridine derivates led to the discovery of target compound 12—a subtype-selective positive allosteric modulator(PAM).The radiofluorinated analogue,[18F]12,was synthesized in 28±10%radiochemical yield,>37 GBq/μmol and an excellent radiochemical purity>99%.Initial in vitro autoradiograms on rodent brain sections were performed in the absence of carbachol and showed moderate specificity as well as a low selectivity of[18F]12 for the M4-rich ***,in the presence of carbachol,a significant increase in tracer binding was observed in the rat striatum,which was reduced by>60%under blocking conditions,thus indicating that orthosteric ligand interaction is required for efficient binding o f[18F]12 to the allosteric ***,however,the presence of carbachol was not required for high specific binding in the non-human primate(NHP)and human striatum,and did not further improve the specificity and selectivity of[18F]12 in higher *** results pointed towards significant species-differences and paved the way for a preliminary PET study in NHP,where peak brain uptake of[18F]12 was found in the putamen and temporal *** conclusion,we report on the identification and preclinical development of the first radiofluorinated M4PET radioligand with promising *** availability of a clinically validated M4PET radioligand harbors potential to facilitate drug development and provide a useful diagnostic tool for non-invasive imaging.

关键词： Muscarinicacetylcholine receptor Positronemission tomography Neuroimaging neuropharmacology Neurological disorders

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小胶质细胞在光/暗周期过程中调节海马突触传递和睡眠持续时间

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神经损伤与功能重建 2022年第5期17卷 310-310页

作者：杜一星(编译) Department of Physiology and Pharmacology Sapienza University of Rome Axe Neurosciences Centre de Recherche du CHU de Québec Université Laval Quebec City Department of Neurology San Raffaele of Cassino 4. National Research Council Institute of Biochemistry and Cell Biology (EMMA/Infrafrontier/IMPC ) International Campus "A. Buzzati-Traverso" INRAE Bordeaux INP NutriNeuro UMR 1286 Bordeaux University Tecniplast S.P.A. Buguggiate Department of Molecular Medicine Sapienza University INSERM Neurocentre Magendie Physiopathologie de la Plasticité Neuronale division of Medical Sciences University of Victoria The Department of Biochemistry and Molecular Biology The University of British Columbia Department of Physiology and Pharmacology Sapienza University Laboratory affiliated to Istituto Pasteur Italia Department of Neurophysiology Neuropharmacology Inflammaging IRCCS Neuromed

小胶质细胞是大脑的常驻巨噬细胞,通过感知神经元活动并支持突触重塑和可塑性积极促进脑实质的稳态。虽然已有研究表明星形胶质细胞在睡眠中的不同作用,但小胶质细胞在调节睡眠/觉醒周期和白天不同阶段调节突触活动中的作用尚未深入研... 详细信息

小胶质细胞是大脑的常驻巨噬细胞,通过感知神经元活动并支持突触重塑和可塑性积极促进脑实质的稳态。虽然已有研究表明星形胶质细胞在睡眠中的不同作用,但小胶质细胞在调节睡眠/觉醒周期和白天不同阶段调节突触活动中的作用尚未深入研究。以光作为授时提示,我们研究了用集落刺激因子-1受体拮抗剂PLX5622消除小胶质细胞对雄性小鼠睡眠/觉醒周期和海马突触传递的影响。我们的数据表明,小胶质细胞几乎完全的耗竭会增加NREM睡眠的持续时间并减少海马兴奋性神经传递。由于cx3cr1GFP/GFP小鼠显现与PLX5622处理的小鼠中发现的相同情况,趋化因子fractalkine受体CX3CR1在这些效应中起相关作用。此外,在光照阶段小胶质细胞表达较低水平的cx3cr1;当培养的小胶质细胞受到ATP(一种在睡眠期间释放的嘌呤能分子)的刺激时其cx3cr1表达降低。我们的研究结果表明,小胶质细胞参与调节睡眠,调整其cx3cr1表达以响应光/暗阶段,并以时相依赖性方式调节突触活动。

关键词： cx3cr1 脑电图长期增强小胶质细胞耗竭微型兴奋性突触后电流睡觉眠自发兴奋性突触后电流

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小胶质细胞控制成年小鼠海马中的谷氨酸能突触

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神经损伤与功能重建 2021年第10期16卷 F0003-F0003页

作者： Bernadette Basilico Laura Ferrucci Patrizia Ratano Maria T Golia Alfonso Grimaldi Maria Rosito Valentina Ferretti Ingrid Reverte Caterina Sanchini Maria C Marrone Maria Giubettini Valeria De Turris Debora Salerno Stefano Garofalo Marie-Kim St-Pierre Micael Carrier Massimiliano Renzi Francesca Pagani Brijesh Modi Marcello Raspa Ferdinando Scavizzi Cornelius T Gross Silvia Marinelli Marie-Ève Tremblay Daniele Caprioli Laura Maggi Cristina Limatola Silvia Di Angelantonio Davide Ragozzino Department of Physiology and Pharmacology Sapienza University of RomeRomeItaly. Neurophysiology and neuropharmacology Inflammaging Unit IRCCS NeuromedMediterranean Neurological InstitutePozzilliISItaly. Center for Life Nano-and Neuro-science Istituto Italiano di TecnologiaRomeItaly. Dipartimento di Biologia e Biotecnologie“Charles Darwin” Sapienza University of RomeRomeItaly. Santa Lucia Foundation(IRCCS Fondazione Santa Lucia) RomeItaly. European Brain Research Institute(EBRI)‘Rita Levi-Montalcini’ RomeItaly. CrestOptics S.p.A RomeItaly. Centre de Recherche du CHU de Québec Axe Neurosciences QuébecQuebec CityCanada. Département de Médecine Moléculaire UniversitéLaval QuébecQuebec CityCanada.1 National Research Council Institute of Biochemistry and Cell Biology(CNR-IBBC/EMMA/Infrafrontier/IMPC)International Campus“A.Buzzati-Traverso”Monterotondo(Rome)Italy.1 Epigenetics and Neurobiology Unit European Molecular Biology Laboratory(EMBL)MonterotondoItaly.1 division of Medical Sciences University of VictoriaVictoriaCanada.1 Department of Physiology and Pharmacology Sapienza UniversityLaboratory affiliated to Istituto Pasteur ItaliaRomeItaly.

小胶质细胞是调节大脑突触发育和可塑性的重要细胞类型,但其影响突触的正常功能的机制尚不清楚。在本研究中,我们通过PLX5622造成小胶质细胞耗竭,并观察其对成年野生型小鼠海马CA3-CA1突触的影响。在小胶质细胞耗竭后,与树突棘密度降低... 详细信息

小胶质细胞是调节大脑突触发育和可塑性的重要细胞类型,但其影响突触的正常功能的机制尚不清楚。在本研究中,我们通过PLX5622造成小胶质细胞耗竭,并观察其对成年野生型小鼠海马CA3-CA1突触的影响。在小胶质细胞耗竭后,与树突棘密度降低相关的自发和诱发谷氨酸能活动的减少,出现未成熟突触特征以及突触的可塑性提高。小胶质细胞耗竭的小鼠在新物体识别任务的获取方面表现出缺陷。海马星形胶质细胞出现增生,但并没有神经炎症反应。在Cx3cr1-/-小鼠中,PLX不能导致海马出现上述改变。这说明CX3CL1/CX3CR1轴在小胶质细胞对突触功能的控制中有重要作用。PLX5622停用后,小胶质细胞的重新增殖,海马突触恢复,小鼠的学习功能也出现恢复。综上所述,小胶质细胞对维持成人大脑的突触的正常功能用重要的作用,去除小胶质细胞会导致谷氨酸能突触组织和活动的可逆变化。

关键词：谷氨酸能传递海马体学习小胶质细胞神经元-小胶质细胞相互作用突触

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