CNS drug reviews最新文献

{"title":"The Neurobiology and Neuropharmacology of Alzheimer's Disease The ASPET — Ray Fuller Symposium New Orleans, LA, USA, April 19 — 20, 2002","authors":"A. Scriabine","doi":"10.1111/j.1527-3458.2002.tb00231.x","DOIUrl":"10.1111/j.1527-3458.2002.tb00231.x","url":null,"abstract":"","PeriodicalId":94307,"journal":{"name":"CNS drug reviews","volume":"8 3","pages":"331-336"},"PeriodicalIF":0.0,"publicationDate":"2006-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1527-3458.2002.tb00231.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"22135222","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}

{"title":"UFP-101, a Peptide Antagonist Selective for the Nociceptin/Orphanin FQ Receptor","authors":"Girolamo Calo,&nbsp;Remo Guerrini,&nbsp;Anna Rizzi,&nbsp;Severo Salvadori,&nbsp;Melissa Burmeister,&nbsp;Daniel R. Kapusta,&nbsp;David G. Lambert,&nbsp;Domenico Regoli","doi":"10.1111/j.1527-3458.2005.tb00264.x","DOIUrl":"10.1111/j.1527-3458.2005.tb00264.x","url":null,"abstract":"<div>\u0000 \u0000 <p>Nociceptin/orphanin FQ modulates various biological functions at central and peripheral levels by selectively activating a G-protein coupled receptor named N/OFQ peptide (NOP) receptor. For extending our knowledge on the biological roles of the N/OFQ - NOP receptor system the identification of selective NOP ligands, especially antagonists, is mandatory. [Nphe¹, Arg¹⁴, Lys¹⁵] N/OFQ-NH₂ (UFP-101) is a novel NOP ligand that was designed by combining, in the same molecule, the [Nphe¹] chemical modification which eliminates efficacy and the [Arg¹⁴, Lys¹⁵] substitution which increases ligand potency and duration of action <i>in vivo.</i> In the present article, we summarize the pharmacological features of UFP-101 as determined in a series of <i>in vitro</i> and <i>in vivo</i> assays. Moreover, some biological actions and possible therapeutic indications of NOP ligands are discussed on the basis of results obtained with UFP-101. Data obtained with this compound were compared with those generated using other NOP antagonists, especially J-113397 and [Nphe¹]N/OFQ(1-13)-NH₂, receptor or peptide knockout mice and other pharmacological tools useful for blocking N/OFQ – NOP receptor signaling.</p>\u0000 <p>The analysis of the available data demonstrates that UFP-101 is a useful pharmacological tool for the investigation of the central and peripheral biological functions regulated by the N/OFQ – NOP receptor system and for defining the therapeutic potential of NOP receptor ligands</p>\u0000 </div>","PeriodicalId":94307,"journal":{"name":"CNS drug reviews","volume":"11 2","pages":"97-112"},"PeriodicalIF":0.0,"publicationDate":"2006-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1527-3458.2005.tb00264.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24890911","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}

{"title":"Moclobemide and the Risk of Serotonin Toxicity (or Serotonin Syndrome)","authors":"Dr. Ken Gillman","doi":"10.1111/j.1527-3458.2004.tb00005.x","DOIUrl":"10.1111/j.1527-3458.2004.tb00005.x","url":null,"abstract":"","PeriodicalId":94307,"journal":{"name":"CNS drug reviews","volume":"10 1","pages":"83-85"},"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.tb00005.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24436914","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}

{"title":"LY503430: Pharmacology, Pharmacokinetics, and Effects in Rodent Models of Parkinson's Disease","authors":"Michael J. O'Neill,&nbsp;Tracey K. Murray,&nbsp;Michael P. Clay,&nbsp;Terry Lindstrom,&nbsp;Charles R. Yang,&nbsp;Eric S. Nisenbaum","doi":"10.1111/j.1527-3458.2005.tb00037.x","DOIUrl":"10.1111/j.1527-3458.2005.tb00037.x","url":null,"abstract":"<div>\u0000 \u0000 <p>Glutamate is the major excitatory transmitter in the brain. Recent developments in the molecular biology and pharmacology of the α-amino-3-hydroxy-5-methylisoxa-zole-4-propionic acid (AMPA)-subtype of glutamate receptors have led to the discovery of selective, potent and systemically active AMPA receptor potentiators. These molecules enhance synaptic transmission and play important roles in plasticity and cognitive processes. In the present studies we characterized a novel AMPA receptor potentiator, LY503430, on recombinant human GLU_A1-4 and native preparations <i>in vitro</i>, and then evaluated the potential neuroprotective effects of the molecule in rodent models of Parkinson's disease. Results indicated that at submicromolar concentrations LY503430 selectively enhanced glutamate-induced calcium influx into HEK293 cells transfected with human GLU_A1, GLU_A2, GLU_A3, or GLU_A4 AMPA receptors. The molecule also potentiated AMPA-mediated responses in native cortical, hippocampal and substantia nigra neurones. LY503430 had good oral bioavailability in both rats and dogs. We also report here that LY503430 provided dose-dependent functional and histological protection in animal models of Parkinson's disease. The neurotoxicity following unilateral infusion of 6-hyrdoxydopamine (6-OHDA) into either the substantia nigra or the striatum of rats and that following systemic 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in mice were reduced. Interestingly, LY503430 also had neurotrophic actions on functional and histological outcomes when treatment was delayed until well after (6 or 14 days) the lesion was established. LY503430 also produced some increase in brain derived neurotrophic factor (BDNF) in the substantia nigra and a dose-dependent increase in growth associated protein-43 (GAP-43) expression in the striatum. Therefore, we propose that AMPA receptor potentiators such as LY503430 offer the potential of a new disease modifying therapy for Parkinson's disease.</p>\u0000 </div>","PeriodicalId":94307,"journal":{"name":"CNS drug reviews","volume":"11 1","pages":"77-96"},"PeriodicalIF":0.0,"publicationDate":"2006-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1527-3458.2005.tb00037.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25262581","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}

{"title":"ABT-089: Pharmacological Properties of a Neuronal Nicotinic Acetylcholine Receptor Agonist for the Potential Treatment of Cognitive Disorders","authors":"Lynne E. Rueter,&nbsp;David J. Anderson,&nbsp;Clark A. Briggs,&nbsp;Diana L. Donnelly-Roberts,&nbsp;Gary A. Gintant,&nbsp;Murali Gopalakrishnan,&nbsp;Nan-Horng Lin,&nbsp;Mark A. Osinski,&nbsp;Glenn A. Reinhart,&nbsp;Michael J. Buckley,&nbsp;Ruth L. Martin,&nbsp;Jeffrey S. McDermott,&nbsp;Lee C. Preusser,&nbsp;Terese R. Seifert,&nbsp;Zhi Su,&nbsp;Bryan F. Cox,&nbsp;Michael W. Decker,&nbsp;James P. Sullivan","doi":"10.1111/j.1527-3458.2004.tb00011.x","DOIUrl":"10.1111/j.1527-3458.2004.tb00011.x","url":null,"abstract":"<div>\u0000 \u0000 <p>ABT-089 [2-methyl-3-(2-(S)-pyrrolidinylmethoxy)pyridine dihydrochloride salt] is a selective neuronal nicotinic receptor (NNR) modulator with cognitive enhancing properties in animal models of cognitive functioning. Amongst NNR subtypes, ABT-089 shows selectivity for the cytisine binding site on the α₄β₂ receptor subtype as compared to the α-bungarotoxin (α-BgT) binding sites on the α₇ and α₁β₁δγ receptor subtypes. In functional <i>in vitro</i> electrophysiological and cation flux assays, ABT-089 displays differential activity including agonism, partial agonism and antagonism depending upon the NNR subtype and assay. ABT-089 is as potent and efficacious as (–)-nicotine at evoking acetylcholine (ACh) release from hippocampal synaptosomes. Furthermore, ABT-089 is neuroprotective against excitotoxic glutamate insults, with even greater potency seen after chronic treatment. Similarly, ABT-089 is effective in models of cognitive functioning, including enhancement of baseline functioning as well as improvement of impaired cognitive functioning seen following septal lesioning and natural aging. In neuroprotective assays the compound is most potent by chronic administration. In stark contrast to the positive effects in the cognitive models, ABT-089 shows little propensity to induce adverse</p>\u0000 </div>","PeriodicalId":94307,"journal":{"name":"CNS drug reviews","volume":"10 2","pages":"167-182"},"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.tb00011.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24550747","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}

{"title":"Animal Model of Brain Aging: Senescence-Accelerated Mouse (SAM)","authors":"Masaomi Miyamoto,&nbsp;Hideki Takahashi,&nbsp;Hiroyuki Ohta,&nbsp;Junko Sakamoto","doi":"10.1111/j.1527-3458.1998.tb00076.x","DOIUrl":"10.1111/j.1527-3458.1998.tb00076.x","url":null,"abstract":"Senescence-accelerated mouse (SAM), a murine model of accelerated senescence, was established by Takeda et al. (59) at Kyoto University. In 1968, several pairs of the AKR/J strain of mice were donated by the Jackson Laboratory (Bar Harbor, ME) to the Department of Pathology (currently the Department of Senescence Biology), Chest Disease Research Institute (currently Institute for Frontier Medical Sciences), Kyoto University, Japan. While continuing sister-brother mating to maintain the inbred strain, researchers were aware that in certain litters most of the mice showed a moderate-to-severe degree of loss of activity, hair loss, lack of glossiness, skin coarseness, periophthalmic lesions, increased lordokyphosis, and early death. In 1975, five litters of mice with severe exhaustion were selected as the progenitors of the senescence-prone series (P series). Litters in which the aging process was normal were selected as progenitors of the senescence-resistant series (R series). Thereafter, selective breeding was based on the data of the grading score of senescence (16), life span, and pathogenic phenotypes in addition to the routine sister-brother mating (56,57,59). SAM consists of senescence-accelerated-prone mouse (SAMP) and senescence-accelerated-resistant mouse (SAMR), the latter of which shows normal aging characteristics. At present, there are 12 lines of SAM: nine SAMP substrains, including SAMP1, SAMP2, SAMP3, SAMP6, SAMP7, SAMP8, SAMP9, SAMP10, and SAMP11; and three SAMR substrains, including SAMR1, SAMR4, and SAMR5 (56). SAM strains manifest various phenotypes that are characteristic enough to differentiate the SAM strains (Table 1): senile amyloidosis in SAMP1, SAMP2, SAMP10, and SAMP11 (14,15,60); impaired immune response in SAMP1, SAMP2 (18,19), and SAMP8 (1); contracted kidney in SAMP1,","PeriodicalId":94307,"journal":{"name":"CNS drug reviews","volume":"4 4","pages":"361-375"},"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.tb00076.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35217600","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}

{"title":"S 17092: A Prolyl Endopeptidase Inhibitor as a Potential Therapeutic Drug for Memory Impairment. Preclinical and Clinical Studies","authors":"Philippe Morain,&nbsp;Pierre Lestage,&nbsp;Guillaume De Nanteuil,&nbsp;Roeline Jochemsen,&nbsp;Jean-Loïc Robin,&nbsp;David Guez,&nbsp;Pierre-Alain Boyer","doi":"10.1111/j.1527-3458.2002.tb00214.x","DOIUrl":"10.1111/j.1527-3458.2002.tb00214.x","url":null,"abstract":"<div>\u0000 \u0000 <p>Any treatment that could positively modulate central neuropeptides levels would provide a promising therapeutic approach to the treatment of cognitive deficits associated with aging and/or neurodegenerative diseases. Therefore, based on the activity in rodents, S 17092 (2S,3aS,7aS)-1 ([(R.R)-2-phenylcyclopropyl]carbonyl)-2-[(thiazolidin-3-yl)car-bonyl]octahydro-<i>1H</i>-indole) has been selected as a potent inhibitor of cerebral prolyl-endopeptidase (PEP). By retarding the degradation of neuroactive peptides, S 17092 was successfully used in a variety of memory tasks. These tasks explored short-term, long-term, reference and working memory in aged mice, as well as in rodents and monkeys with chemically induced amnesia or spontaneous memory deficits. S 17092 has also been safely administered to humans, and showed a clear peripheral expression of its mechanism of action through its inhibitory effect upon PEP activity in plasma. S 17092 exhibited central effects, as evidenced by EEG recording in healthy volunteers, and could improve a delayed verbal memory task. Collectively, the preclinical and clinical effects of S 17092 have suggested a promising role for this compound as an agent for the treatment of cognitive disorders associated with cerebral aging.</p>\u0000 </div>","PeriodicalId":94307,"journal":{"name":"CNS drug reviews","volume":"8 1","pages":"31-52"},"PeriodicalIF":0.0,"publicationDate":"2006-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1527-3458.2002.tb00214.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41224625","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}

{"title":"Taltirelin Hydrate (TA-0910): An Orally Active Thyrotropin-Releasing Hormone Mimetic Agent with Multiple Actions","authors":"Kiyoshi Kinoshita,&nbsp;Michio Yamamura,&nbsp;Juko Sugihara,&nbsp;Mamoru Suzuki,&nbsp;Yuzo Matsuoka","doi":"10.1111/j.1527-3458.1998.tb00039.x","DOIUrl":"10.1111/j.1527-3458.1998.tb00039.x","url":null,"abstract":"","PeriodicalId":94307,"journal":{"name":"CNS drug reviews","volume":"4 1","pages":"25-41"},"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.tb00039.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73098549","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}

{"title":"Mesulergine: A Review","authors":"Panagiota Galanopoulou,&nbsp;George Giannakopoulos","doi":"10.1111/j.1527-3458.1999.tb00102.x","DOIUrl":"10.1111/j.1527-3458.1999.tb00102.x","url":null,"abstract":"","PeriodicalId":94307,"journal":{"name":"CNS drug reviews","volume":"5 3","pages":"233-248"},"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.tb00102.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77415574","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}

{"title":"Neuroprotective Profile of Enoxaparin, a Low Molecular Weight Heparin, in In Vivo Models of Cerebral Ischemia or Traumatic Brain Injury in Rats: a Review","authors":"Jean-Marie Stutzmann,&nbsp;Veronique Mary,&nbsp;Florence Wahl,&nbsp;Odile Grosjean-Piot,&nbsp;André Uzan,&nbsp;Jeremy Pratt","doi":"10.1111/j.1527-3458.2002.tb00213.x","DOIUrl":"10.1111/j.1527-3458.2002.tb00213.x","url":null,"abstract":"<div>\u0000 \u0000 <p>The development of treatments for acute neurodegenerative diseases (stroke and brain trauma) has focused on (i) re-establishing blood flow to ischemic areas as quickly as possible (i.e. mainly antithrombotics or thrombolytics for stroke therapy) and (ii) on protecting neurons from cytotoxic events (i.e. neuroprotective therapies such as anti-excitotoxic or anti-inflammatory agents for stroke and neurotrauma therapies). This paper reviews the preclinical data for enoxaparin in <i>in vivo</i> models of ischemia and brain trauma in rats. Following a photothrombotic lesion in the rat, enoxaparin significantly reduced edema at 24 h after lesion when the treatment was started up to 18 h after insult. Enoxaparin was also tested after an ischemic insult using the transient middle cerebral artery occlusion (tMCAO) model in the rat. Enoxaparin, 2 × 1.5 mg/kg i.v., significantly reduced the lesion size and improved the neuroscore when the treatment was started up to 5 h after ischemia. Enoxaparin, administered at 5h after insult, reduced cortical lesion size in a dose-dependent manner. In permanent MCAO, enoxaparin (5 and 24 h after insult) significantly reduced lesion size and improved neuroscore. A slight and reversible elevation of activated partial thromboplastin time (APTT) suggests that enoxaparin is neuroprotective at a non-hemorrhagic dose. Traumatic brain injury (TBI) is often accompanied by secondary ischemia due in part to edema-induced compression of blood vessels. When enoxaparin, at 0.5 mg/kg i.v. + 4 × 1 mg/kg s.c., was administered later than 30h after TBI, it significantly reduced edema in hippocampus and parietal cortex. At one week after TBI the lesion size was significantly reduced and the neurological deficit significantly improved in enoxaparin treated animals. Finally, the cognitive impairment was significantly improved by enoxaparin at 48 h to 2 weeks after TBI. The anticoagulant properties of unfractionated heparin and specifically enoxaparin can explain their anti-ischemic effects in experimental models. Furthermore, unfractionated heparin and specifically enoxaparin, have, in addition to anticoagulant, many other pharmacological effects (i.e. reduction of intracellular Ca²⁺ release; antioxidant effect; anti-inflammatory or neurotrophic effects) that could act in synergy to explain the neuroprotective activity of enoxaparin in acute neurodegenerative diseases. Finally, we demonstrated, that in different <i>in vivo</i> models of acute neurodegenerative diseases, enoxaparin reduces brain edema and lesion size and improves motor and cognitive functional recovery with a large therapeutic window of opportunity (compatible with a clinical application). Taking into account these experimental data in models of ischemia and brain trauma, the clinical use of enoxaparin in acute neurodegenerative diseases warrants serious consideration.</p>\u0000 </div>","PeriodicalId":94307,"journal":{"name":"CNS drug reviews","volume":"8 1","pages":"1-30"},"PeriodicalIF":0.0,"publicationDate":"2006-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1527-3458.2002.tb00213.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80496877","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}