CNS drug reviews最新文献

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Alcohol and Neurodegeneration 酒精与神经变性
CNS drug reviews Pub Date : 2006-06-07 DOI: 10.1111/j.1527-3458.1999.tb00112.x
Fulton T. Crews
{"title":"Alcohol and Neurodegeneration","authors":"Fulton T. Crews","doi":"10.1111/j.1527-3458.1999.tb00112.x","DOIUrl":"10.1111/j.1527-3458.1999.tb00112.x","url":null,"abstract":"","PeriodicalId":94307,"journal":{"name":"CNS drug reviews","volume":"5 4","pages":"379-394"},"PeriodicalIF":0.0,"publicationDate":"2006-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1527-3458.1999.tb00112.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79559523","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 41
ACKNOWLEDGMENT OF REVIEWERS 审稿人致谢
CNS drug reviews Pub Date : 2006-06-07 DOI: 10.1111/j.1527-3458.1999.tb00114.x
{"title":"ACKNOWLEDGMENT OF REVIEWERS","authors":"","doi":"10.1111/j.1527-3458.1999.tb00114.x","DOIUrl":"https://doi.org/10.1111/j.1527-3458.1999.tb00114.x","url":null,"abstract":"","PeriodicalId":94307,"journal":{"name":"CNS drug reviews","volume":"5 4","pages":"404"},"PeriodicalIF":0.0,"publicationDate":"2006-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1527-3458.1999.tb00114.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"137654018","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Experimental Biology‘99 Washington, DC, April 17–21, 1999 《实验生物学》1999年4月17-21日,华盛顿特区
CNS drug reviews Pub Date : 2006-06-07 DOI: 10.1111/j.1527-3458.1999.tb00098.x
Alexander Scriabine
{"title":"Experimental Biology‘99 Washington, DC, April 17–21, 1999","authors":"Alexander Scriabine","doi":"10.1111/j.1527-3458.1999.tb00098.x","DOIUrl":"https://doi.org/10.1111/j.1527-3458.1999.tb00098.x","url":null,"abstract":"","PeriodicalId":94307,"journal":{"name":"CNS drug reviews","volume":"5 2","pages":"185-188"},"PeriodicalIF":0.0,"publicationDate":"2006-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1527-3458.1999.tb00098.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"137654681","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Heteromerization of GABAB Receptors: A New Principle for G Protein-Coupled Receptors. Satellite Symposium to the 28th Annual Meeting of the Society for Neuroscience Los Angeles, CA, November 5–7, 1998 GABAB受体的异聚化:G蛋白偶联受体的新原理。神经科学学会第28届年会卫星研讨会,洛杉矶,加州,1998年11月5-7日
CNS drug reviews Pub Date : 2006-06-07 DOI: 10.1111/j.1527-3458.1998.tb00077.x
Klemens Kaupmann, Bernard Bettler
{"title":"Heteromerization of GABAB Receptors: A New Principle for G Protein-Coupled Receptors. Satellite Symposium to the 28th Annual Meeting of the Society for Neuroscience Los Angeles, CA, November 5–7, 1998","authors":"Klemens Kaupmann, Bernard Bettler","doi":"10.1111/j.1527-3458.1998.tb00077.x","DOIUrl":"10.1111/j.1527-3458.1998.tb00077.x","url":null,"abstract":"The fourth international γ-aminobutyric acid (GABAB) symposium, organized as a satellite meeting to the Annual Society for Neuroscience Meeting in Los Angeles, was the first reunion of the GABAB-receptor community after the long-awaited cloning of a receptor cDNA in early 1997. The organizing committee consisted of N. G. Bowery, J. Gallagher, S. J. Enna, F. Froestl, and H. Bittiger. The symposium included several speakers who joined the GABAB field more recently and many presentations reported studies that made use of the now available genetic tools. In the opening lecture, W. Froestl (Novartis, Basel, Switzerland) outlined the development of radioligands that had been used to clone the first GABAB receptors, GABABR1a and b. Recent data on the structure, function, and distribution of these receptors were summarized by B. Bettler (Novartis, Basel, Switzerland). The two receptors derive from the same gene by alternative N-terminal splicing and share ligand-binding properties and coupling preferences; in addition, their distribution corresponds to the one of native GABAB receptors. In the retina, GABABR1a/b receptors are localized on either side of the synapse, demonstrating that these receptors do not represent exclusive preor postsynaptic subtypes. While the cloned receptors had many of the expected properties, there remained some discrepancies. For example, the coupling of the cloned receptors to presumed effector K and Ca channels in heterologous cells proved surprisingly difficult. Moreover while the antagonist pharmacology of cloned and native GABAB receptors matched neatly, the agonist affinity at the recombinant receptors was drastically reduced. The identification of a second GABAB receptor, GABABR2, now reconciles these puzzling observations. Three representatives of pharmaceutical companies (F. Mar-","PeriodicalId":94307,"journal":{"name":"CNS drug reviews","volume":"4 4","pages":"376-379"},"PeriodicalIF":0.0,"publicationDate":"2006-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1527-3458.1998.tb00077.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35217601","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 2
The Pharmacology and Mechanism of Action of Zolpidem 唑吡坦的药理作用及作用机制
CNS drug reviews Pub Date : 2006-06-07 DOI: 10.1111/j.1527-3458.1998.tb00074.x
David J. Sanger, Henri Depoortere
{"title":"The Pharmacology and Mechanism of Action of Zolpidem","authors":"David J. Sanger, Henri Depoortere","doi":"10.1111/j.1527-3458.1998.tb00074.x","DOIUrl":"10.1111/j.1527-3458.1998.tb00074.x","url":null,"abstract":"","PeriodicalId":94307,"journal":{"name":"CNS drug reviews","volume":"4 4","pages":"323-340"},"PeriodicalIF":0.0,"publicationDate":"2006-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1527-3458.1998.tb00074.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35217606","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 53
Neuropharmacological Profile of an Atypical Antipsychotic, NRA0562 一种非典型抗精神病药的神经药理学特征,NRA0562
CNS drug reviews Pub Date : 2006-06-07 DOI: 10.1111/j.1527-3458.2003.tb00261.x
Shiho Hirota, Naoya Kawashima, Shigeyuki Chaki, Shigeru Okuyama
{"title":"Neuropharmacological Profile of an Atypical Antipsychotic, NRA0562","authors":"Shiho Hirota,&nbsp;Naoya Kawashima,&nbsp;Shigeyuki Chaki,&nbsp;Shigeru Okuyama","doi":"10.1111/j.1527-3458.2003.tb00261.x","DOIUrl":"10.1111/j.1527-3458.2003.tb00261.x","url":null,"abstract":"<div>\u0000 \u0000 <p>Schizophrenia is a serious and disabling psychiatric disorder affecting approximately 1% of the world's population. Anew generation of atypical antipsychotics has been introduced over the past decade. These atypical antipsychotics have comparable or greater efficacy than traditional antipsychotics in the treatment of the psychotic symptoms of schizophrenia and a much improved neurologic side effect profile. This paper reviews the pharmacological efficacy and safety of a potential atypical antipsychotic, NRA0562.</p>\u0000 <p>NRA0562 has a high affinity for dopamine D<sub>1</sub>, D<sub>2L</sub>, D<sub>4.2</sub>, 5-HT<sub>2A</sub> receptors as well as α<sub>1</sub>-adrenoceptors, and has a moderate affinity for H<sub>1</sub> receptors. NRA0562 strongly binds to 5-HT<sub>2A</sub> receptors and α<sub>1</sub>-adrenoceptors in the frontal cortex, its binding to striatal D<sub>2</sub> receptors is weaker, similar to that of clozapine.</p>\u0000 <p>NRA562 displayed potent antipsychotic activities in animal models of schizophrenia, such as methamphetamine (MAP)-induced hyperactivity, apomorphine-induced disruption of pre-pulse inhibition and conditioned avoidance test. NRA0562 is more potent in reversing the inhibitory effects of MAP at A10 than at A9 dopamine neurons. It increased Fos-like immunoreactivity in the nucleus accumbens more effectively than in the dorsolateral striatum, indicating that NRA0562 has the profile of an atypical antipsychotic. <i>In vivo</i> assays for extrapyramidal side effect liability showed that NRA0562 has a low rate of neurological side effects. Thus, NRA0562 may have unique antipsychotic activity with a lower propensity for extrapyramidal side effects.</p>\u0000 </div>","PeriodicalId":94307,"journal":{"name":"CNS drug reviews","volume":"9 4","pages":"375-388"},"PeriodicalIF":0.0,"publicationDate":"2006-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1527-3458.2003.tb00261.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24100969","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 4
Clinical Pharmacology, Clinical Efficacy, and Behavioral Toxicity of Alprazolam: A Review of the Literature 阿普唑仑的临床药理学、临床疗效和行为毒性:文献综述。
CNS drug reviews Pub Date : 2006-06-07 DOI: 10.1111/j.1527-3458.2004.tb00003.x
Joris C. Verster, Edmund R. Volkerts
{"title":"Clinical Pharmacology, Clinical Efficacy, and Behavioral Toxicity of Alprazolam: A Review of the Literature","authors":"Joris C. Verster,&nbsp;Edmund R. Volkerts","doi":"10.1111/j.1527-3458.2004.tb00003.x","DOIUrl":"10.1111/j.1527-3458.2004.tb00003.x","url":null,"abstract":"<div>\u0000 \u0000 <p>Alprazolam is a benzodiazepine derivative that is currently used in the treatment of generalized anxiety, panic attacks with or without agoraphobia, and depression. Alprazolam has a fast onset of symptom relief (within the first week); it is unlikely to produce dependency or abuse. No tolerance to its therapeutic effect has been reported. At discontinuation of alprazolam treatment, withdrawal and rebound symptoms are common. Hence, alprazolam discontinuation must be tapered.</p>\u0000 <p>An exhaustive review of the literature showed that alprazolam is significantly superior to placebo, and is at least equally effective in the relief of symptoms as tricyclic antidepressants (TCAs), such as imipramine. However, although alprazolam and imipramine are significantly more effective than placebo in the treatment of panic attacks, Selective Serotonin Reuptake Inhibitors (SSRIs) appear to be superior to either of the two drugs. Therefore, alprazolam is recommended as a second line treatment option, when SSRIs are not effective or well tolerated.</p>\u0000 <p>In addition to its therapeutic effects, alprazolam produces adverse effects, such as drowsiness and sedation. Since alprazolam is widely used, many clinical studies investigated its cognitive and psychomotor effects. It is evident from these studies that alprazolam may impair performance in a variety of skills in healthy volunteers as well as in patients. Since the majority of alprazolam users are outpatients, this behavioral impairment limits the safe use of alprazolam in patients routinely engaged in potentially dangerous daily activities, such as driving a car.</p>\u0000 </div>","PeriodicalId":94307,"journal":{"name":"CNS drug reviews","volume":"10 1","pages":"45-76"},"PeriodicalIF":0.0,"publicationDate":"2006-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1527-3458.2004.tb00003.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24407184","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 123
Preclinical and Clinical Pharmacology of Cyamemazine: Anxiolytic Effects and Prevention of Alcohol and Benzodiazepine Withdrawal Syndrome Cyamemazine的临床前和临床药理学:抗焦虑作用和预防酒精和苯二氮卓戒断综合征
CNS drug reviews Pub Date : 2006-06-07 DOI: 10.1111/j.1527-3458.2004.tb00023.x
Michel Bourin, Eric Dailly, Martine Hascöet
{"title":"Preclinical and Clinical Pharmacology of Cyamemazine: Anxiolytic Effects and Prevention of Alcohol and Benzodiazepine Withdrawal Syndrome","authors":"Michel Bourin,&nbsp;Eric Dailly,&nbsp;Martine Hascöet","doi":"10.1111/j.1527-3458.2004.tb00023.x","DOIUrl":"10.1111/j.1527-3458.2004.tb00023.x","url":null,"abstract":"<div>\u0000 \u0000 <p>Several studies have suggested that the antipsychotic compound, cyamemazine, possesses anxiolytic properties in humans. The original pharmacological profile of cyamemazine (D<sub>2</sub>, 5-HT<sub>2A</sub>, 5-HT<sub>2C</sub>, and 5-HT<sub>3</sub> receptor antagonist), which was established by binding, microdialysis and behavioral studies, is consistent with these observations. In the light/dark exploration test, cyamemazine demonstrated anxiolytic-like activity by acute, but not chronic administration. By chronic administration, however, cyamemazine increased the time spent in the open arms of the elevated plus maze (EPM) test demonstrating anxiolytic-like activity. The discrepancy between the results obtained in these tests by acute and chronic administration, could be due to a combination of dopamine D<sub>2</sub> receptor antagonism with antagonism of the 5-HT<sub>2C</sub> and 5-HT<sub>3</sub> receptors. The action of cyamemazine on both the dopaminergic system and 5-HT<sub>3</sub> receptors could also explain the activity of cyamemazine in the management of alcohol withdrawal demonstrated in preclinical studies. This potential indication for cyamemazine and its activity in benzodiazepine withdrawal syndrome have recently been investigated in clinical trials and the results of these studies are presented in this review.</p>\u0000 </div>","PeriodicalId":94307,"journal":{"name":"CNS drug reviews","volume":"10 3","pages":"219-229"},"PeriodicalIF":0.0,"publicationDate":"2006-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1527-3458.2004.tb00023.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24767677","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 30
The Cellular Biochemistry of Cholesterol and Statins: Insights into the Pathophysiology and Therapy of Alzheimer's Disease 胆固醇和他汀类药物的细胞生化:阿尔茨海默病的病理生理学和治疗的见解
CNS drug reviews Pub Date : 2006-06-07 DOI: 10.1111/j.1527-3458.2004.tb00009.x
Benjamin Wolozin, James Brown III, Catherine Theisler, Simone Silberman
{"title":"The Cellular Biochemistry of Cholesterol and Statins: Insights into the Pathophysiology and Therapy of Alzheimer's Disease","authors":"Benjamin Wolozin,&nbsp;James Brown III,&nbsp;Catherine Theisler,&nbsp;Simone Silberman","doi":"10.1111/j.1527-3458.2004.tb00009.x","DOIUrl":"10.1111/j.1527-3458.2004.tb00009.x","url":null,"abstract":"<p>The causes of late onset Alzheimer disease (AD) are poorly understood. Although β-amyloid (Aβ) is thought to play a critical role in the pathophysiology of AD, no genetic evidence directly ties Aβ to late onset AD. This suggests that the accumulation of Aβ and neurodegeneration associated with AD might result from an abnormality that indirectly affects Aβ production or accumulation. Increasing evidence suggests that abnormalities in the metabolism of cholesterol and related molecules, such as cholseterol esters and 24(S) hydroxycholesterol might contribute to the pathophysiology of late onset AD by increasing production of Aβ. 24(S) Hydroxycholesterol is a member of a family of oxidized cholesterol catabolites, termed oxysterols, which function to regulate export of cholesterol from the cell and transcription of genes related to cholesterol metabolism. Cholesterol esters are cholesterol derivatives used for cholesterol storage. Levels of 24(S) hydroxycholesterol increase with AD. Polymorphisms in several different genes important for cholesterol physiology are associated with an increased load or level of Aβ in AD. These genes include apolipoprotein E, cholesterol 24 hydroxylase (Cyp46), acyl-CoA:choles-terol acetyltransferase (ACAT), and the cholesterol transporter ABCA1. Other studies show that levels of cholesterol, or its precursors, are elevated in subjects early in the course of AD. Finally, studies of the processing of amyloid precursor protein show that cholesterol and its catabolites modulate amyloid precursor protein processing and Aβ production. These lines of evidence raise the possibility that genetic abnormalities in cholesterol metabolism might contribute to the pathophysiology of AD.</p>","PeriodicalId":94307,"journal":{"name":"CNS drug reviews","volume":"10 2","pages":"127-146"},"PeriodicalIF":0.0,"publicationDate":"2006-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1527-3458.2004.tb00009.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24550746","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 50
CNS Drugs at the Experimental Biology 2003 Meeting San Diego, CA April 11–15, 2003 2003年4月11-15日,加州圣地亚哥,实验生物学会议上的中枢神经系统药物
CNS drug reviews Pub Date : 2006-06-07 DOI: 10.1111/j.1527-3458.2003.tb00256.x
Alexander Scriabine
{"title":"CNS Drugs at the Experimental Biology 2003 Meeting San Diego, CA April 11–15, 2003","authors":"Alexander Scriabine","doi":"10.1111/j.1527-3458.2003.tb00256.x","DOIUrl":"10.1111/j.1527-3458.2003.tb00256.x","url":null,"abstract":"","PeriodicalId":94307,"journal":{"name":"CNS drug reviews","volume":"9 3","pages":"313-318"},"PeriodicalIF":0.0,"publicationDate":"2006-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1527-3458.2003.tb00256.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24059418","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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