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Targeting the noradrenergic system for anti-inflammatory and neuroprotective effects: implications for Parkinson's disease

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Neural Regeneration research 2018年第8期13卷 1332-1337页

作者： Eoin O'Neill Andrew Harkin neuropsychopharmacology research group School of Pharmacy and Pharmaceutical Sciences & Trinity College Institute of Neuroscience Trinity College

Degeneration of the locus coeruleus noradrenergic system is thought to play a key role in the pathogenesis of Parkinson＇s disease （PD）, whereas pharmacological approaches to increase noradrenaline bioavailability may provide neuroprotection. Noradrenaline inhibits microglial activation and suppresses pro-inflamma- tory mediator production （e.g., tumor necrosis factor-a, interleukin-1β ＆ inducible nitric oxide synthase activity）, thus limiting the cytotoxicity of midbrain dopaminergic neurons in response to an inflamma- tory stimulus. Neighbouring astrocyte populations promote a neurotrophic environment in response to β2-adrenoceptor （β2-AR） stimulation via the production of growth factors （e.g., brain derived neurotrophic factor, cerebral dopamine neurotrophic factor ＆ glial cell derived neurotrophic factor which have shown promising neuroprotective and neuro-restorative effects in the nigrostriatal dopaminergic system. More recent findings have demonstrated a role for the β2-AR in down-regulating expression levels of the human a-synuclein gene SNCA and relative a-synuclein protein abundance. Given that a-synuclein is a major protein constituent of Lewy body pathology, a hallmark neuropathological feature in Parkinson＇s disease, these findings could open up new avenues for pharmacological intervention strategies aimed at alleviating the burden of a-synucleinopathies in the Parkinsonian brain. In essence, the literature reviewed herein supports our hypothesis of a tripartite neuroprotective role for noradrenaline in combating PD-related neuropathology and motor dysfunction via （1） inhibiting nigral microglial activation ＆ pro-inflammatory mediator production, （2） promoting the synthesis of neurotrophic factors from midbrain astrocytes and （3） downregulating a-synuclein gene expression and protein abundance in a β2-AR-dependent manner. Thus, taken together, either pharmacologically enhancing extra-synaptic noradrenaline bioavailability or targeting glial β2-ARs direct

关键词： noradrenaline microglia astrocytes inflammation Parkinson's disease neuroprotection animalmodel dopamie

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Regulation ofβ2-adrenoceptors in brain glia:implications for neuroinflammatory and degenerative disorders

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Neural Regeneration research 2020年第11期15卷 2035-2036页

作者： Karen M.Ryan Andrew Harkin Trinity College Institute of Neuroscience Trinity College Dublin neuropsychopharmacology research group School of Pharmacy and Pharmaceutical Sciences&Trinity College Institute of NeuroscienceTrinity College DublinDublinIreland

Noradrenaline:Within the central nervous system(CNS),the primary source of the catecholamine neurotransmitter noradrenaline is the locus coeruleus(LC)in the pontine tegmentum,with LC neurons projecting to almost all regions of the brain and spinal *** its release from LC neurons,noradrenaline has wide ranging *** example,noradrenaline is the endogenous agonist for G-coupledα-andβ-adrenoceptors that are expressed on many cell types,including neurons and glia,in both the peripheral nervous system and *** is via these receptors that noradrenaline exerts its anti-inflammatory and neurotrophic effects in the *** additionally has adrenoceptor-independent neuroprotective actions,and as such plays a role in free radical scavenging and reducing oxidative stress(Feinstein et al.,2016).

关键词： adrenoceptor protective endogenous

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Efficacy evaluation and neurobiological mechanism of psychedelics based on looming model

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中国药理学与毒理学杂志 2023年第7期37卷 533-534页

作者： XIA Ke YAN Haitao SU Ruibin Beijing Key Laboratory of neuropsychopharmacology State Key Laboratory of Toxicology and Medical Countermeasures Institute of Pharmacology and Toxicology Academy of Military Medical Sciences

OBJECTIVE To investigate the effect of psychedelics on innate fear behavior of mice in Looming model(LM) and its neurobiological mechanism. METHODS(1) Adult male C57BL/6J mice were randomly divided into saline group, DOM group, psilocybin group and mescaline group. The drugs of the corresponding groups were given ip injecction 5 min in advance and LM were used to test the effect of them on freezing time in shelter of mice.(2) The mice were performing ip given DOM or psilocybin following 5-HT2Areceptor antagonist M100907 ip30 min later involved looming experiments.(3) Quantified the expression of EGR1 protein in mouse brains by immunofluorescence staining, then use ibotenic acid(IBO) damaged the mouse brain regions based on the result above and performed looming experiments.(4) Specifically activate or inhibit CaMK Ⅱ, PV, VIP and SOM neurons of mice in saline or psilocybin groups respectively by chemical genetic methods and followed looming experiments. RESULTS(1) In LM, the freezing time in shelter of mice in DOM, psilocybin and mescaline groups was significantly shorter compared to the saline group(Pgroups, the freezing time in shelter of mice in M100907 + psilocybin/DOM groups was significantly prolonged(Pgroup and the M100907 + psilocybin/DOM groups.(3) Psilocybin significantly increased the expression of EGR1 protein in prelimbic cortex(PrL) compared with saline, and the damage of PrL could effectively antagonized the effect of psilocybin shortening the freezing time in LM.(4) Chemicalgenetic specific inhibition of CaMK Ⅱ, PV or VIP neurons in PrL could effectively antagonize the effect of psilocybin in LM,while chemicalgenetic specific activation of CaMK Ⅱneurons could significantly shorten the freezing time of saline-treated mice. CONCLUSION Psychedelics have capability

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8-Hydroxyquinolylnitrones as multifunctional ligands for the therapy of neurodegenerative diseases

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Acta Pharmaceutica Sinica B 2023年第5期13卷 2152-2175页

作者： Damijan Knez Daniel Diez-Iriepa Mourad Chioua Andrea Gottinger Milica Denic Fabien Chantegreil Florian Nachon Xavier Brazzolotto Anna Skrzypczak-Wiercioch Ane Meden Anja Pilar Janko Kos Simon akelj Jure Stojan Kinga Saat Julia Serrano Ana Patricia Fernández Aitana Sánchez-García Ricardo Martínez-Murillo Claudia Binda Francisco López-Muoz Stanislav Gobec JoséMarco-Contelles University of Ljubljana Faculty of PharmacyLjubljana 1000Slovenia Laboratory of Medicinal Chemistry(Institute of Organic Chemistry CSIC)Madrid 28006Spain Departamento de Química Orgánicay Química Inorgánica Alcaláde HenaresMadrid 28871Spain Department of Biology and Biotechnology University of PaviaPavia 27100Italy Département de Toxicologie et Risques Chimiques Institut de Recherche Biomédicale des ArméesParis 91220France Department of Animal Anatomy and Preclinical Sciences University Centre of Veterinary Medicine JU-UAUniversity of Agriculture in KrakowKrakow 30-059Poland Institute of Biochemistry Faculty of MedicineUniversity of LjubljanaLjubljana 1000Slovenia Department of Pharmacodynamics Chair of PharmacodynamicsFaculty of PharmacyJagiellonian University Medical CollegeKrakow 30-688Poland Department of Translational Neurobiology Neurovascular Research GroupCajal Institute(CSIC)Madrid 28002Spain Biotechnology and Vegetal Biology Department Escuela Técnica Superior de Ingeniería AgronómicaAlimentaria y de BiosistemasUniversidad Politécnica de MadridMadrid 28040Spain Faculty of Health Camilo JoséCela University of Madrid(UCJC)Neuropsychopharmacology Unit“Hospital 12 de Octubre”Research InstituteMadrid 28692Spain

We describe the development of quinolylnitrones(QNs)as multifunctional ligands inhibiting cholinesterases(ChEs:acetylcholinesterase and butyrylcholinesterase—h BChE)and monoamine oxidases(hMAO-A/B)for the therapy of neurodegenerative *** identified QN 19,a simple,low molecular weight nitrone,that is readily synthesized from commercially available *** 19 has no typical pharmacophoric element to suggest ChE or MAO inhibition,yet unexpectedly showed potent inhibition of h BChE(IC50=1.06±0.31 nmol/L)and h MAO-B(IC_(50)=4.46±0.18μmol/L).The crystal structures of 19 with hBChE and hMAO-B provided the structural basis for potent binding,which was further studied by enzyme *** 19 acted as a free radical scavenger and biometal chelator,crossed the blood—brain barrier,was not cytotoxic,and showed neuroprotective properties in a 6-hydroxydopamine cell model of Parkinson's *** addition,in vivo studies showed the anti-amnesic effect of 19 in the scopolamine-induced mouse model of AD without adverse effects on motoric function and ***,chronic treatment of double transgenic APPswe-PS1δE9 mice with 19 reduced amyloid plaque load in the hippocampus and cortex of female mice,underscoring the disease-modifying effect of QN 19.

关键词： Quinolylnitrone Butyrylcholinesterase Monoamine oxidase B Alzheimer's disease Multifunctional ligands 6-Hydroxydopamine model Passive avoidance task Novel object recognition

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G αi, and G βγ, subunits have opposite effects on dexmedetomidine-induced sedation

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中国药理学与毒理学杂志 2018年第4期32卷 294-294页

作者： Meng LIU Yi YANG Bo TAN Yu-lei LI Pei-lan ZHOU Rui-bin SU State Key Laboratory of Toxicology and Medical Countermeasures Beijing Key Laboratory of Neuropsychopharmacology Beijing Institute of Pharmacology and Toxicology Beijing 100850 China

OBJECTIVE To explore the mechanism of G_(αi) and G_(βγ) subunits on dexmedetomidine(DMED)-induced *** Kunming mice were randomly placed into three groups(DMED group,DMED+dbcAMP/rolipram/gallein/M119 group,dbcAMP/rolipram/gallein/M119 group) to explore the regulation of dbcAMP/rolipram/gallein/M119 on DMED-induced sedation by establishing loss of righting reflex(LORR) ***/rolipram was intracerebroventricular injected and gallein/M119 was intraperitoneal injected 15 min before DMED intravenous *** CHO-α2 A-AR cells,after administration of DMED/gallein/M119,the regulation on the cAMP accumulation stimulated by Forskolin(FSK) was detected,so was the intracellular calcium ion concentration([Ca2 + ]*** levels of pERK/pCREB were detected by Western Blot to explore the key signal molecules involved in DMED-induced *** The ED50 of DMED-induced LORR(200.0 nmol·kg^(-1)) was increased to 375.0 or433.3 nmol·kg^(-1) by pre-treatment with cAMP analog dbcAMP(50 nmol/5μl per mouse) or *** 4 inhibitor rolipram(100 nmol/5μl per mouse).In addition,the ED50 of DMED-induced LORR was decreased to 113.6 or 136.5 nmol·kg^(-1) when pre-treated with G_(βγ) subunits inhibitor M119(100 mg·kg^(-1))or gallein(100 mg·kg^(-1)) *** of dbcAMP,rolipram,gallein or M119 alone had little effect on LORR of ***(10 μmol·L^(-1)) significantly inhibited forskolin-stimulated cAMP *** in CHO-α2A-AR *** with G_(βγ) subunits inhibitors or DMED alone,[Ca^(2+)]i and pERK1/2 significantly increased after co-administration of G_(βγ) subunits inhibitors with ***(5 μmol·L^(-1))or rolipram(5 μmol·L^(-1)) alone had little effect on ERK1/2 phosphorylation,but decreased DMEDinduced ERK1/2 phosphorylation after co-administration with DMED.G_(βγ) subunit inhibitors treatment increased DMED-induced phosphorylation of CREB,whereas dbcAMP or rolipram had little effect on pCREB induced by *** G_(

关键词：右旋美托咪定镇静作用临床分析科学研究

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Impact of living with bipolar patients: Making sense of caregivers' burden

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World Journal of Psychiatry 2014年第1期4卷 1-12页

作者： Maurizio Pompili Désirée Harnic Xenia Gonda Alberto Forte Giovanni Dominici Marco Innamorati Konstantinos N Fountoulakis Gianluca Serafini Leo Sher Luigi Janiri Zoltan Rihmer Mario Amore Paolo Girardi Department of Neurosciences Mental Health and Sensory Organs Suicide Prevention Center Sant’Andrea Hospital Sapienza University of Rome 00189 Rome Italy Department of Psychiatry Catholic University Medical School 00189 Rome Italy Department of Clinical and Theoretical Mental Health and Department of Pharmacodynamics Semmelweis University H-1086 Budapest Hungary neuropsychopharmacology and Neurochemistry research group National Academy of Sciences and Semmelweis University H-1086 Budapest Hungary National Institute of Psychiatry and Addictions Laboratory for Suicide Research and Prevention H-1135 Buda-pest Hungary 3rd Department of Psychiatry Aristotle University of Thessaloniki GR-54006 Thessaloniki Greece Department of Psychiatry Icahn School of Medicine at Mount Sinai New York NY 10029 United States Department of Clinical and Theoretical Mental Health Semmelweis University H-1125 Budapest Hungary Department of Neuroscience Rehabilitation Ophthalmology Genetics Maternal and Child Health Section of Psychiatry University of Genova I-16146 Genova Italy

The aim of the present review was to examine objective and subjective burdens in primary caregivers(usually family members) of patients with bipolar disorder(BD) and to list which symptoms of the patients are considered more burdensome by the caregivers. In order to provide a critical review about caregiver's burden in patients with bipolar disorder, we performed a detailed Pub Med, Bio Med Central, ISI Web of Science, Psyc INFO, Elsevier Science Direct and Cochrane Library search to identify all papers and book chapters in English published during the period between 1963 and November 2011. The highest levels of distress were caused by the patient's behavior and the patient's role dysfunction(work, education and social relationships). Furthermore, the caregiving role compromises other social roles occupied by the caregiver, becoming part of the heavy social cost of bipolar affective disorder. There is a need to better understand caregivers' views and personal perceptions of the stresses and demands arising from caring for someone with BD in order to develop practical appropriate interventions and to improve the training of caregivers.

关键词： Bipolar disorder Caregivers Burden Prevention

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神经精神药理学治疗药物监测共识指南:2017版

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实用药物与临床 2022年第1期25卷 1-20页

作者： C.Hiemke N.Bergemann H.W.Clement A.Conca J.Deckert K.Domschke G.Eckermann K.Egberts M.Gerlach C.Greiner G.Gründer E.Haen U.Havemann-Reinecke G.Hefner R.Helmer G.Janssen E.Jaquenoud G.Laux T.Messer R.M ssner M.J.Müller M.Paulzen B.Pfuhlmann P.Riederer A.Saria B.Schoppek G.Schoretsanitis M.Schwarz M.Silva Gracia B.Stegmann W.Steimer J.C.Stingl M.Uhr S.Ulrich S.Unterecker R.Waschgler G.Zernig G.Zurek P.Baumann 李文标(主译) 果伟(译) 贺静(译) 鲍爽(译) 路钊(译) 牛梦溪(译) 阮灿军(译) 臧彦楠(译) 王勇(译) 张玲(译) 刘辰庚(译) 李洁(译) 汤宜朗(审校) 王传跃(审校) 王刚(审校) Department of Psychiatry and Psychotherapy University Medical Center of MainzMainzGermany Institute of Clinical Chemistry and Laboratory Medicine University Medical Center of MainzMainzGermany Kitzberg Hospitals Center for Psychosomatic Medicine and PsychotherapyBad MergentheimGermany Department of Child and Adolescent Psychiatry University of FreiburgFreiburgGermany Servizio Psichiatrico del Comprensorio Sanitario di Bolzano BolzanoItaly Department of Psychiatry Psychotherapy and PsychosomaticsUniversity Hospital of WürzburgGermany Department of Psychiatry and Psychotherapy Medical Center-University of FreiburgFaculty of MedicineUniversity of FreiburgFreiburgGermany Psychiatric Hospital KaufbeurenGermany Department of Child and Adolescent Psychiatry Psychosomatics and PsychotherapyCenter of Mental HealthUniversity Hospital of WürzburgGermany Federal Institute for Drugs and Medical Devices(BfArM) BonnGermany Department of Psychiatry Psychotherapy and PsychosomaticsRWTH Aachen UniversityAachenand JARA–Translational Brain MedicineAachenGermany Clinical Pharmacology Department of Psychiatry and Psychotherapy and Department of Pharmacology and ToxicologyUniversity of RegensburgRegensburgGermany Department of Psychiatry and Psychosomatics University of G ttingenG ttingenGermany Psychiatric Hospital Vitos KlinikEichbergEltvilleGermany Center of Epilepsy BielefeldGermany Medical Laboratory Stein Limbach GroupM nchengladbachGermany Psychiatric Hospital K nigsfeldenBruggAargauSwitzerland Institute of Psychological Medicine Haag in OberbayernGermany Danuviuskliniken Psychiatric HospitalPfaffenhofenGermany Department of Psychiatry and Psychotherapy University of TübingenTübingenGermany Psychiatric Hospitals Oberberggruppe BerlinGermany Psychiatric Hospital Weisser Hirsch DresdenGermany Experimental Psychiatry Unit Department of Psychiatry1Medical University of InnsbruckInnsbruckAustria kbo-Isar-Amper Klinikum München-Ost Psychiatric HospitalMunich-HaarGermany Department of

治疗药物监测(Therapeutic Drug Monitoring,TDM)通过定量测定和解释血药浓度以优化药物治疗。TDM着眼于药代动力学的个体差异,使个体化药物治疗成为可能。在精神病学和神经病学领域中,有可能明显获益于TDM的主要患者群体包括少年儿童... 详细信息

治疗药物监测(Therapeutic Drug Monitoring,TDM)通过定量测定和解释血药浓度以优化药物治疗。TDM着眼于药代动力学的个体差异,使个体化药物治疗成为可能。在精神病学和神经病学领域中,有可能明显获益于TDM的主要患者群体包括少年儿童、孕妇、老年患者、智障患者、药物滥用者、涉法精神病患者、已知或怀疑药代动力学异常的患者以及合并躯体疾病影响药代动力学的患者。常规剂量下治疗无效,用药依从性难以判断,药物耐受性不佳,以及可能存在药代动力学方面的药物-药物相互作用等情况都是治疗药物监测的典型指征。然而,只有将TDM充分整合到临床治疗过程中,才能发挥其优化药物治疗的潜在优势。为了向临床医生和实验室提供有效的TDM信息,神经精神药理学与药物精神病学协会(Arbeitsgemeinschaft für Neuropsychopharmakologie und Pharmakopsychiatrie,AGNP)的TDM专家组在2004年发表了第一版《精神科治疗药物监测指南》。2011年进行了更新之后,现在再次更新。遵循新版指南,可能会改善神经精神药物治疗的效果,加快很多患者的康复,并降低医疗费用。

关键词：抗凝药物妊娠期静脉血栓栓塞疾病抗抑郁药抗癫痫药抗帕金森病药抗精神病药血药浓度共识指南药物分析基因型分析神经药物遗传药理学药代动力学表型分析血浆药物浓度精神药物参考范围血清药物浓度治疗药物监测治疗窗

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神经精神药理学治疗药物监测共识指南:2017版

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实用药物与临床 2022年第2期25卷 97-118页

作者： C.Hiemke N.Bergemann H.W.Clement A.Conca J.Deckert K.Domschke G.Eckermann K.Egberts M.Gerlach C.Greiner G.Gründer E.Haen U.Havemann-Reinecke G.Hefner R.Helmer G.Janssen E.Jaquenoud G.Laux T.Messer R.M ssner M.JMüller M.Paulzen B.Pfuhlmann P.Riederer A.Saria B.Schoppek G.Schoretsanitis M.Schwarz M.Silva Gracia B.Stegmann W.Steimer J.C.Stingl M.Uhr S.Ulrich S.Unterecker R.Waschgler G.Zernig G.Zurek P.Baumann 李文标(译) 果伟(译) 贺静(译) 鲍爽(译) 路钊(译) 牛梦溪(译) 阮灿军(译) 臧彦楠(译) 王勇(译) 张玲(译) 刘辰庚(译) 李洁(译) 汤宜朗(译) 王传跃(译) 王刚(译) Department of Psychiatry and Psychotherapy University Medical Center of MainzMainzGermany Institute of Clinical Chemistry and Laboratory Medicine University Medical Center of MainzMainzGermany Kitzberg Hospitals Center for Psychosomatic Medicine and PsychotherapyBad MergentheimGermany Department of Child and Adolescent Psychiatry University of FreiburgFreiburgGermany Servizio Psichiatrico del Comprensorio Sanitario di Bolzano BolzanoItaly Department of Psychiatry Psychotherapy and PsychosomaticsUniversity Hospital of WürzburgGermany Department of Psychiatry and Psychotherapy Medical Center-University of FreiburgFaculty of MedicineUniversity of FreiburgFreiburgGermany Psychiatric Hospital KaufbeurenGermany Department of Child and Adolescent Psychiatry Psychosomatics and PsychotherapyCenter of Mental HealthUniversity Hospital of WürzburgGermany Federal Institute for Drugs and Medical Devices(BfArM) BonnGermany Department of Psychiatry Psychotherapy and PsychosomaticsRWTH Aachen UniversityAachenand JARA–Translational Brain MedicineAachenGermany Clinical Pharmacology Department of Psychiatry and Psychotherapy and Department of Pharmacology and ToxicologyUniversity of RegensburgRegensburgGermany Department of Psychiatry and Psychosomatics University of G ttingenG ttingenGermany Psychiatric Hospital Vitos KlinikEichbergEltvilleGermany Center of Epilepsy BielefeldGermany Medical Laboratory Stein Limbach GroupM nchengladbachGermany Psychiatric Hospital K nigsfeldenBruggAargauSwitzerland Institute of Psychological Medicine Haag in OberbayernGermany Danuviuskliniken Psychiatric HospitalPfaffenhofenGermany Department of Psychiatry and Psychotherapy University of TübingenTübingenGermany Psychiatric Hospitals Oberberggruppe BerlinGermany Psychiatric Hospital Weisser Hirsch DresdenGermany Experimental Psychiatry Unit Department of Psychiatry1Medical University of InnsbruckInnsbruckAustria kbo-Isar-Amper Klinikum München-Ost Psychiatric HospitalMunich-HaarGermany Department of

2.2剂量相关参考浓度范围对于TDM结果的解释,除了治疗参考浓度范围外还有另一个浓度范围,即所谓的剂量相关参考浓度范围。治疗参考浓度范围的应用是药效动力学问题,而剂量相关参考浓度范围的运用是药代动力学问题。后者比较的是测得的... 详细信息

2.2剂量相关参考浓度范围对于TDM结果的解释,除了治疗参考浓度范围外还有另一个浓度范围,即所谓的剂量相关参考浓度范围。治疗参考浓度范围的应用是药效动力学问题,而剂量相关参考浓度范围的运用是药代动力学问题。后者比较的是测得的药物浓度与理论预期药物浓度范围。参照药代动力学研究,优先考虑没有合并用药或药物基因组异常的患者群(“正常”患者),在日维持剂量(Daily maintenance dose,D m)、给药间隔(Dosing interval,d i)、总清除率(Total clearance,CL)和生物利用度(Bioavailability,F)已知情况下,某种药物在某个“正常”患者体内的预期平均稳态浓度(Average steady-state concentration,C av)可通过下面的公式计算。

关键词：治疗药物监测药效动力学给药间隔维持剂量生物利用度药物浓度药代动力学合并用药

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