CNS drug reviews最新文献

{"title":"Efficacy of Rimonabant and Other Cannabinoid CB1 Receptor Antagonists in Reducing Food Intake and Body Weight: Preclinical and Clinical Data","authors":"Mauro A. M. Carai,&nbsp;Giancarlo Colombo,&nbsp;Paola Maccioni,&nbsp;Gian Luigi Gessa","doi":"10.1111/j.1527-3458.2006.00091.x","DOIUrl":"10.1111/j.1527-3458.2006.00091.x","url":null,"abstract":"<div>\u0000 \u0000 <p>The present paper focuses on the different lines of evidence indicating that cannabinoid CB₁ receptor antagonists, including the prototype rimonabant, reduce food intake and body weight in laboratory animals. Recent clinical surveys demonstrated that rimonabant significantly reduced body weight also in overweight/obese humans. Treatment with rimonabant was associated with a beneficial effect on different metabolic parameters and cardiovascular risk factors linked to overweight. The data reviewed in this paper suggest that cannabinoid CB₁ receptor antagonists may constitute a novel class of drugs potentially effective in the treatment of obesity-related disorders.</p>\u0000 </div>","PeriodicalId":94307,"journal":{"name":"CNS drug reviews","volume":"12 2","pages":"91-99"},"PeriodicalIF":0.0,"publicationDate":"2006-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1527-3458.2006.00091.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26300003","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":"Humanin and Colivelin: Neuronal-Death-Suppressing Peptides for Alzheimer's Disease and Amyotrophic Lateral Sclerosis","authors":"Masaaki Matsuoka,&nbsp;Yuichi Hashimoto,&nbsp;Sadakazu Aiso,&nbsp;Ikuo Nishimoto","doi":"10.1111/j.1527-3458.2006.00113.x","DOIUrl":"10.1111/j.1527-3458.2006.00113.x","url":null,"abstract":"<div>\u0000 \u0000 <p>Humanin (HN), a 24-amino-acid neuroprotective peptide, was originally found in the occipital lobe of an autopsied Alzheimer's disease (AD) patient. HN inhibits neuronal death by binding to its specific receptor on the cell membrane and triggering a Jak2/STAT3 prosurvival pathway. The activation of this pathway may represent a therapeutic approach to AD. HN also exhibits neuroprotective activity against toxicity by familial amyotrophic lateral sclerosis (ALS)-related mutant superoxide dismutase (SOD1). Recent investigations established that AGA-(C8R)-HNG17, a 17-amno-acid derivative of HN, is 10⁵ times more potent as a neuroprotective than HN; at 10-picomolar and higher concentrations in vitro it completely suppresses neuronal death. Moreover, a 26-amino-acid peptide colivelin (CL), composed of activity-dependent neurotrophic factor (ADNF) C-terminally fused to AGA-(C8R)-HNG17, provides complete neuroprotection at 100-femtomolar or higher concentrations in vitro. A series of experiments using mouse AD and ALS models further established the efficacy of HN derivatives, including CL, against these diseases in vivo. HN and CL can be viewed as drug candidates for neuronal death suppression therapy in AD or ALS.</p>\u0000 </div>","PeriodicalId":94307,"journal":{"name":"CNS drug reviews","volume":"12 2","pages":"113-122"},"PeriodicalIF":0.0,"publicationDate":"2006-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1527-3458.2006.00113.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26242146","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":"Metabotropic Glutamate Receptor Subtype 5 Antagonists MPEP and MTEP","authors":"Paul M. Lea IV,&nbsp;Alan I. Faden","doi":"10.1111/j.1527-3458.2006.00149.x","DOIUrl":"10.1111/j.1527-3458.2006.00149.x","url":null,"abstract":"<div>\u0000 \u0000 <p>Glutamate regulates the function of central nervous system (CNS), in part, through the cAMP and/or IP3/DAG second messenger-associated metabotropic glutamate receptors (mGluRs). The mGluR5 antagonist 2-methyl-6-(phenylethynyl)-pyridine (MPEP) has been extensively used to elucidate potential physiological and pathophysiological functions of mGluR5. Unfortunately, recent evidence indicates significant non-specific actions of MPEP, including inhibition of NMDA receptors. In contrast, in vivo and in vitro characterization of the newer mGluR5 antagonist 3-[(2-methyl-1,3-thiazol-4-yl)ethynyl]pyridine (MTEP) indicates that it is more highly selective for mGluR5 over mGluR1, has no effect on other mGluR subtypes, and has fewer off-target effects than MPEP. This article reviews literature on both of these mGluR5 antagonists, which suggests their possible utility in neurodegeneration, addiction, anxiety and pain management.</p>\u0000 </div>","PeriodicalId":94307,"journal":{"name":"CNS drug reviews","volume":"12 2","pages":"149-166"},"PeriodicalIF":0.0,"publicationDate":"2006-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1527-3458.2006.00149.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26242150","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":"Preclinical and Clinical Pharmacology of DOV 216,303, a “Triple” Reuptake Inhibitor","authors":"Phil Skolnick,&nbsp;Philip Krieter,&nbsp;Joseph Tizzano,&nbsp;Anthony Basile,&nbsp;Piotr Popik,&nbsp;Pal Czobor,&nbsp;Arnold Lippa","doi":"10.1111/j.1527-3458.2006.00123.x","DOIUrl":"10.1111/j.1527-3458.2006.00123.x","url":null,"abstract":"<div>\u0000 \u0000 <p>DOV 216,303 [(±)-1-(3,4-dichlorophenyl)-3-azabicyclo-[3.1.0]hexane hydrochloride] is the prototype of a class of compounds referred to as “triple” reuptake inhibitors. Such compounds inhibit the reuptake of norepinephrine (NE), serotonin (5-HT), and dopamine (DA), the three neurotransmitters most closely linked to major depressive disorder. DOV 216,303 inhibits [³H]NE, [³H]5-HT, and [³H]DA uptake to the corresponding human recombinant transporters (expressed in HEK 293 cells) with IC₅₀ values of ∼20, 14, and 78 nM, respectively. DOV 216,303 is active in tests predictive of antidepressant activity including the mouse forced swim test and reversal of tetrabenazine-induced ptosis and locomotor depression. The pharmacodynamic, pharmacokinetic, and toxicological profile of DOV 216,303 in animals prompted us to initiate clinical studies. In both single and multiple dose studies using normal volunteers, DOV 216,303 was safe and well-tolerated. Furthermore, both C_max and AUC values were dose-proportional between 5–150 mg. The plasma concentrations of DOV 216,303 at doses &gt;10 mg were in excess of the IC₅₀ values for inhibition of biogenic amine reuptake. In a Phase II study designed to explore the safety and tolerability of DOV 216,303 in depressed individuals, patients received either 100 mg DOV 216,303 (50 mg b.i.d.) or 40 mg citalopram (20 mg, b.i.d.) for two weeks. A placebo arm was not employed in this study because several institutional review boards required administration of an active control to severely depressed individuals. Time dependent reductions in HAM-D scores (the primary outcome measure) were observed in both the DOV 216,303 and citalopram groups compared to baseline scores (p &lt; 0.0001). The side effect profile was not remarkably different between treatment arms. These findings provide preliminary evidence of a clinically meaningful antidepressant action with a molecule capable of inhibiting the three transmitters most closely linked to major depressive disorder.</p>\u0000 </div>","PeriodicalId":94307,"journal":{"name":"CNS drug reviews","volume":"12 2","pages":"123-134"},"PeriodicalIF":0.0,"publicationDate":"2006-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1527-3458.2006.00123.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26242147","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 Activity of 3-Aminopyridine-2-Carboxaldehyde Thiosemicarbazone (PAN-811), a Cancer Therapeutic Agent","authors":"Zhi-Gang Jiang,&nbsp;Michael S. Lebowitz,&nbsp;Hossein A. Ghanbari","doi":"10.1111/j.1527-3458.2006.00077.x","DOIUrl":"10.1111/j.1527-3458.2006.00077.x","url":null,"abstract":"<p>3-aminopyridine-2-carboxaldehyde thiosemicarbazone (3-AP) is a highly-hydrophobic small molecule that was originally developed for cancer therapy (Triapine®, Vion Pharmaceuticals) due to its ability to inhibit ribonucleotide reductase, a key enzyme required for DNA synthesis. 3-AP has a high affinity for divalent cations, chelating the Fe²⁺ at the R2 subunit of the enzyme and inhibiting formation of a tyrosyl radical essential for ribonucleotide reduction. We have demonstrated that 3-AP is also a potent neuroprotectant (as such, it is referred to as “PAN-811”). In vitro it completely blocks ischemic neurotoxicity at a concentration of 0.5 μM (EC₅₀ ≊ 0.35 μM) and hypoxic toxicity at 1.2 μM (EC₅₀ ≊ 0.75 μM). Full protection of primary cortical and striatal neurons can be achieved with 3-AP when it is added to the medium at up to six hours after an ischemic insult. 3-AP also suppresses cell death induced by neurotoxic agents, including staurosporine, veratridine and glutamate, indicating activity against a central target(s) in the neurodegenerative process. 3-AP acts via neutralization of two important intracellular effectors of excitatory neurotoxicity; calcium and free radicals. Its reported ability to elevate anti-apoptotic proteins is likely to be a consequence of the suppression of excessive intracellular free calcium. In a rat model of transient ischemia, a single bolus delivery of 3-AP 1 h after the initiation of ischemic attack reduced infarct volume by 59% when administered i.c.v. (50 μg per rat) and by 35% when administered i.v. (1 mg/kg). In Phase I clinical trials in cancer therapy 3-AP had no cardiovascular, CNS or other major adverse effects. Thus, 3-AP has a high potential for development as a novel, potent neuroprotectant for the treatment of neurodegenerative diseases.</p>","PeriodicalId":94307,"journal":{"name":"CNS drug reviews","volume":"12 1","pages":"77-90"},"PeriodicalIF":0.0,"publicationDate":"2006-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1527-3458.2006.00077.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26140610","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":"A New Look at the 5α-Reductase Inhibitor Finasteride","authors":"Deborah A. Finn,&nbsp;Amy S. Beadles-Bohling,&nbsp;Ethan H. Beckley,&nbsp;Matthew M. Ford,&nbsp;Katherine R. Gililland,&nbsp;Rebecca E. Gorin-Meyer,&nbsp;Kristine M. Wiren","doi":"10.1111/j.1527-3458.2006.00053.x","DOIUrl":"10.1111/j.1527-3458.2006.00053.x","url":null,"abstract":"<p>Finasteride is the first 5α-reductase inhibitor that received clinical approval for the treatment of human benign prostatic hyperplasia (BPH) and androgenetic alopecia (male pattern hair loss). These clinical applications are based on the ability of finasteride to inhibit the Type II isoform of the 5α-reductase enzyme, which is the predominant form in human prostate and hair follicles, and the concomitant reduction of testosterone to dihydrotestosterone (DHT). In addition to catalyzing the rate-limiting step in the reduction of testosterone, both isoforms of the 5α-reductase enzyme are responsible for the reduction of progesterone and deoxycorticosterone to dihydroprogesterone (DHP) and dihydrodeoxycorticosterone (DHDOC), respectively. Recent preclinical data indicate that the subsequent 3α-reduction of DHT, DHP and DHDOC produces steroid metabolites with rapid non-genomic effects on brain function and behavior, primarily via an enhancement of γ-aminobutyric acid (GABA)ergic inhibitory neurotransmission. Consistent with their ability to enhance the action of GABA at GABA_A receptors, these steroid derivatives (termed neuroactive steroids) possess anticonvulsant, antidepressant and anxiolytic effects in addition to altering aspects of sexual- and alcohol-related behaviors. Thus, finasteride, which inhibits both isoforms of 5α-reductase in rodents, has been used as a tool to manipulate neuroactive steroid levels and determine the impact on behavior. Results of some preclinical studies and clinical observations with finasteride are described in this review article. The data suggest that endogenous neuroactive steroid levels may be inversely related to symptoms of premenstrual and postpartum dysphoric disorder, catamenial epilepsy, depression, and alcohol withdrawal.</p>","PeriodicalId":94307,"journal":{"name":"CNS drug reviews","volume":"12 1","pages":"53-76"},"PeriodicalIF":0.0,"publicationDate":"2006-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1527-3458.2006.00053.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26140611","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 Effects of Edaravone: a Novel Free Radical Scavenger in Cerebrovascular Injury","authors":"Hiroshi Yoshida,&nbsp;Hidekatsu Yanai,&nbsp;Yoshihisa Namiki,&nbsp;Kayoko Fukatsu-Sasaki,&nbsp;Nobuyuki Furutani,&nbsp;Norio Tada","doi":"10.1111/j.1527-3458.2006.00009.x","DOIUrl":"10.1111/j.1527-3458.2006.00009.x","url":null,"abstract":"<p>Recanalization and neuroprotection have been mainly targeted for the specific treatment of acute ischemic stroke. Free radicals play a crucial role in brain ischemic injury by exacerbating membrane damage through peroxidation of unsaturated fatty acids of cell membrane, leading to neuronal death and brain edema. Free radicals have been implicated in stroke pathophysiology as pivotal contributors to cell injury. Edaravone (3-methyl-1-phenyl-2-pyrazolin-5-one) is a novel potent free radical scavenger that has been clinically used to reduce the neuronal damage following ischemic stroke. Edaravone exerts neuroprotective effects by inhibiting endothelial injury and by ameliorating neuronal damage in brain ischemia. Edaravone provides the desirable features of NOS: it increases eNOS (beneficial NOS for rescuing ischemic stroke) and decreases nNOS and iNOS (detrimental NOS). Post- reperfusion brain edema and hemorrhagic events induced by thrombolytic therapy may be reduced by edaravone pretreatment. Increased productions of superoxide and NO in the brain after reperfusion and a concomitant surge in oxygen free radicals with increased NO during recirculation lead to formation of peroxynitrite, a superpotent radical. Edaravone, which inhibits oxidation and enhances NO production derived from increased eNOS expression, may improve and conserve cerebral blood flow without peroxynitrite generation during reperfusion. Clinical experience with edaravone suggests that this drug has a wide therapeutic time window. The combination therapy (a thrombolytic plus edaravone) is likely to target brain edema, reduce stroke death and improve the recovery from neurological deficits in stoke patients.</p>","PeriodicalId":94307,"journal":{"name":"CNS drug reviews","volume":"12 1","pages":"9-20"},"PeriodicalIF":0.0,"publicationDate":"2006-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1527-3458.2006.00009.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26139674","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":"Bryostatin-1: Pharmacology and Therapeutic Potential as a CNS Drug","authors":"Miao-Kun Sun,&nbsp;Daniel L. Alkon","doi":"10.1111/j.1527-3458.2006.00001.x","DOIUrl":"10.1111/j.1527-3458.2006.00001.x","url":null,"abstract":"<p>Bryostatin-1 is a powerful protein kinase C (PKC) agonist, activating PKC isozymes at nanomolar concentrations. Pharmacological studies of bryostatin-1 have mainly been focused on its action in preventing tumor growth. Emerging evidence suggests, however, that bryostatin-1 exhibits additional important pharmacological activities. In preclinical studies bryostatin-1 has been shown at appropriate doses to have cognitive restorative and antidepressant effects. The underlying pharmacological mechanisms may involve an activation of PKC isozymes, induction of synthesis of proteins required for long-term memory, restoration of stress-evoked inhibition of PKC activity, and reduction of neurotoxic amyloid accumulation and tau protein hyperphosphorylation. The therapeutic potential of bryostatin-1 as a CNS drug should be further explored.</p>","PeriodicalId":94307,"journal":{"name":"CNS drug reviews","volume":"12 1","pages":"1-8"},"PeriodicalIF":0.0,"publicationDate":"2006-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1527-3458.2006.00001.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26139673","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":"Pharmacological Profile of the Selective FAAH Inhibitor KDS-4103 (URB597)","authors":"Daniele Piomelli,&nbsp;Giorgio Tarzia,&nbsp;Andrea Duranti,&nbsp;Andrea Tontini,&nbsp;Marco Mor,&nbsp;Timothy R. Compton,&nbsp;Olivier Dasse,&nbsp;Edward P. Monaghan,&nbsp;Jeff A. Parrott,&nbsp;David Putman","doi":"10.1111/j.1527-3458.2006.00021.x","DOIUrl":"10.1111/j.1527-3458.2006.00021.x","url":null,"abstract":"<p>In the present article, we review the pharmacological properties of KDS-4103 (URB597), a highly potent and selective inhibitor of the enzyme fatty-acid amide hydrolase (FAAH), which catalyzes the intracellular hydrolysis of the endocannabinoid anandamide. In vitro, KDS-4103 inhibits FAAH activity with median inhibitory concentrations (IC₅₀) of 5 nM in rat brain membranes and 3 nM in human liver microsomes. In vivo, KDS-4103 inhibits rat brain FAAH activity after intraperitoneal (i.p.) administration with a median inhibitory dose (ID₅₀) of 0.15 mg/kg. The compound does not significantly interact with other cannabinoid-related targets, including cannabinoid receptors and anandamide transport, or with a broad panel of receptors, ion channels, transporters and enzymes. By i.p. administration to rats and mice KDS-4103 elicits significant, anxiolytic-like, antidepressant-like and analgesic effects, which are prevented by treatment with CB1 receptor antagonists. By contrast, at doses that significantly inhibit FAAH activity and substantially raise brain anandamide levels, KDS-4103 does not evoke classical cannabinoid-like effects (e.g., catalepsy, hypothermia, hyperphagia), does not cause place preference, and does not produce generalization to the discriminative effects of the active ingredient of cannabis, Δ9-tetrahydrocannabinol (Δ9-THC). These findings suggest that KDS-4103 acts by enhancing the tonic actions of anandamide on a subset of CB₁ receptors, which may normally be engaged in controlling emotions and pain. KDS-4103 is orally available in rats and cynomolgus monkeys. Sub-chronic repeated dose studies (1500 mg/kg, per os) in these two species have not demonstrated systemic toxicity. Likewise, no toxicity was noted in bacterial cytotoxicity tests in vitro and in the Ames test. Furthermore, no deficits were observed in rats on the rotarod test after acute i.p. treatment with KDS-4103 at doses up to 5 mg/kg or in a functional observation battery after oral doses up to 1500 mg/kg. The results suggest that KDS-4103 will offer a novel approach with a favorable therapeutic window for the treatment of anxiety, depression and pain.</p>","PeriodicalId":94307,"journal":{"name":"CNS drug reviews","volume":"12 1","pages":"21-38"},"PeriodicalIF":0.0,"publicationDate":"2006-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1527-3458.2006.00021.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26140608","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":"Pharmacological Characterization of DM232 (Unifiram) and DM235 (Sunifiram), New Potent Cognition Enhancers","authors":"M. N. Romanelli,&nbsp;N. Galeotti,&nbsp;C. Ghelardini,&nbsp;D. Manetti,&nbsp;E. Martini,&nbsp;F. Gualtieri","doi":"10.1111/j.1527-3458.2006.00039.x","DOIUrl":"10.1111/j.1527-3458.2006.00039.x","url":null,"abstract":"<p>DM232 (unifiram) and DM235 (sunifiram) are potent cognition-enhancers, which are four order of magnitude more potent than piracetam. These compounds, although not showing affinity in binding studies for the most important central receptors or channels, are able to prevent amnesia induced by modulation of several neurotransmission systems. These compounds are able to increase the release of acetylcholine from rat cerebral cortex, and, as far as unifiram is concerned, to increase the amplitude of fEPSP in rat hippocampal slices. In vitro experiments, performed on hippocampal slices, also supported the hypothesis of a role of the AMPA receptors for the cognition-enhancing properties of unifiram and sunifiram.</p>","PeriodicalId":94307,"journal":{"name":"CNS drug reviews","volume":"12 1","pages":"39-52"},"PeriodicalIF":0.0,"publicationDate":"2006-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1527-3458.2006.00039.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26140609","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}