Database : MEDLINE
Search on : central and nervous and system and agents [Words]
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[PMID]: 29501696
[Au] Autor:Bellini NK; Santos TM; da Silva MTA; Thiemann OH
[Ad] Address:Instituto de Física de São Carlos, Universidade de São Paulo, Caixa Postal 369, 13560-590, São Carlos, SP, Brazil.
[Ti] Title:The therapeutic strategies against Naegleria fowleri.
[So] Source:Exp Parasitol;187:1-11, 2018 Mar 01.
[Is] ISSN:1090-2449
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Naegleria fowleri is a pathogenic amoeboflagellate most prominently known for its role as the etiological agent of the Primary Amoebic Meningoencephalitis (PAM), a disease that afflicts the central nervous system and is fatal in more than 95% of the reported cases. Although being fatal and with potential risks for an increase in the occurrence of the pathogen in populated areas, the organism receives little public health attention. A great underestimation in the number of PAM cases reported is assumed, taking into account the difficulty in obtaining an accurate diagnosis. In this review, we summarize different techniques and methods used in the identification of the protozoan in clinical and environmental samples. Since it remains unclear whether the protozoan infection can be successfully treated with the currently available drugs, we proceed to discuss the current PAM therapeutic strategies and its effectiveness. Finally, novel compounds for potential treatments are discussed as well as research on vaccine development against PAM.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  2 / 61420 MEDLINE  
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[PMID]: 29460030
[Au] Autor:Vogel KR; Ainslie GR; Walters DC; McConnell A; Dhamne SC; Rotenberg A; Roullet JB; Gibson KM
[Ad] Address:Department of Neuroscience, University of Wisconsin, Madison, WI, USA.
[Ti] Title:Succinic semialdehyde dehydrogenase deficiency, a disorder of GABA metabolism: an update on pharmacological and enzyme-replacement therapeutic strategies.
[So] Source:J Inherit Metab Dis;, 2018 Feb 19.
[Is] ISSN:1573-2665
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:We present an update to the status of research on succinic semialdehyde dehydrogenase (SSADH) deficiency (SSADHD), a rare disorder of GABA metabolism. This is an unusual disorder featuring the accumulation of both GABA and its neuromodulatory analog, gamma-hydroxybutyric acid (GHB), and recent studies have advanced the potential clinical application of NCS-382, a putative GHB receptor antagonist. Animal studies have provided proof-of-concept that enzyme replacement therapy could represent a long-term therapeutic option. The characterization of neuronal stem cells (NSCs) derived from aldehyde dehydrogenase 5a1 (aldh5a1 ) mice, the murine model of SSADHD, has highlighted NSC utility as an in vitro system in which to study therapeutics and associated toxicological properties. Gene expression analyses have revealed that transcripts encoding GABA receptors are down-regulated and may remain largely immature in aldh5a1 brain, characterized by excitatory as opposed to inhibitory outputs, the latter being the expected action in the mature central nervous system. This indicates that agents altering chloride channel activity may be therapeutically relevant in SSADHD. The most recent therapeutic prospects include mTOR (mechanistic target of rapamycin) inhibitors, drugs that have received attention with the elucidation of the effects of elevated GABA on autophagy. The outlook for novel therapeutic trials in SSADHD continues to improve.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:Publisher
[do] DOI:10.1007/s10545-018-0153-8

  3 / 61420 MEDLINE  
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[PMID]: 29431424
[Au] Autor:Gale EM; Caravan P
[Ad] Address:The Athinoula A. Martinos Center for Biomedical Imaging, The Institute for Innovation in Imaging, Department of Radiology, Massachusetts General Hospital, Harvard Medical School , 149 Thirteenth Street, Suite 2301, Charlestown, Massachusetts 02129, United States.
[Ti] Title:Gadolinium-Free Contrast Agents for Magnetic Resonance Imaging of the Central Nervous System.
[So] Source:ACS Chem Neurosci;, 2018 Feb 12.
[Is] ISSN:1948-7193
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:We discuss how the recent revelation that gadolinium (Gd) from commercially available MRI contrast agents is irreversibly and cumulatively deposited in the central nervous system is driving innovation toward Gd-free contrast agents for neuroradiology.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:Publisher
[do] DOI:10.1021/acschemneuro.8b00044

  4 / 61420 MEDLINE  
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[PMID]: 29486164
[Au] Autor:Nakashima KI; Iwao K; Inoue T; Haga A; Tsutsumi T; Mochita MI; Fujimoto T; Tanihara H
[Ad] Address:Department of Ophthalmology, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
[Ti] Title:Stimulation of the adenosine A3 receptor, not the A1 or A2 receptors, promote neurite outgrowth of retinal ganglion cells.
[So] Source:Exp Eye Res;170:160-168, 2018 Feb 24.
[Is] ISSN:1096-0007
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Among candidate neuroprotective agents, adenosine is thought to be a possible treatment for central nervous system disorders. Adenosine elicits biological effects through four G protein-coupled receptors (A , A , A , and A ). The A and A receptors stimulate adenylyl cyclase (AC) and increase cyclic adenosine monophosphate (cAMP) levels, whereas A and A receptors inhibit AC and decrease cAMP levels. Several studies have investigated the effects of adenosine receptors (AdoRs) in glaucoma, because modulation of A , A , or A receptor regulates intraocular pressure. In addition, AdoR-related phenomena may induce neuroprotective effects in retinal neurons. Notably, A , A , and A receptor agonists reportedly inhibit retinal ganglion cell (RGC) death in in vitro and in vivo glaucoma models. However, there is limited knowledge of the effects of AdoR activation on neurite outgrowth or the regeneration of RGCs. In this report, we described the role of an AdoR subtype in neurite outgrowth and RGC axonal regeneration. The distribution of AdoRs in the retina was evaluated by immunohistochemical analysis. Using primary cultured rat RGCs in vitro and an optic nerve crush model in vivo, neurite elongation was evaluated after stimulation by the following AdoR agonists: CHA, an A receptor agonist; CGS21680, an A receptor agonist; BAY60-6583, an A receptor agonist; and 2-Cl-IB-MECA, an A receptor agonist. To determine the mechanism of neurite promotion, the candidate molecules of signal transduction associated with the neurite elongation of AdoRs were evaluated by enzyme-linked immunosorbent assay (ELISA) and Western blot analysis, respectively. All four AdoRs (A , A , A , and A ) were present in the inner retinal layers. Among the agonists for AdoR, only 2-Cl-IB-MECA significantly promoted neurite outgrowth in primary cultured RGCs. Signaling pathway analyses showed that 2-Cl-IB-MECA caused upregulated phosphorylation of Akt in cultured RGCs. Additionally, LY294002, an inhibitor of Akt, suppressed the neurite-promoting effects of the A receptor agonist in RGCs. Moreover, 2-Cl-IB-MECA increased the number of regenerating axons in the optic nerve crush model. Taken together, these data indicate that activation of the A receptor, not the A or A receptors, promotes in vitro and in vivo neurite outgrowth during the regeneration of rat RGCs, which is caused by the activation of an Akt-dependent signaling pathway. Therefore, AdoR activation may be a promising candidate for the development of novel regenerative modalities for glaucoma and other optic neuropathies.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

  5 / 61420 MEDLINE  
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[PMID]: 29455234
[Au] Autor:Wang S; Wang X; Liu M; Bai O
[Ad] Address:Department of Hematology, The First Hospital of Jilin University, No. 71 Xinmin Street, Chaoyang District, Changchun, 130021, Jilin, People's Republic of China.
[Ti] Title:Blastic plasmacytoid dendritic cell neoplasm: update on therapy especially novel agents.
[So] Source:Ann Hematol;97(4):563-572, 2018 Apr.
[Is] ISSN:1432-0584
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:Blastic plasmacytoid dendritic cell neoplasm (BPDCN) is a rare and aggressive hematopoietic malignancy mainly affecting elderly patients. Most patients present with asymptomatic skin lesions as the first symptom and has a high frequency of bone marrow involvement. BPDCN is typically characterized by CD4+ and CD 56+ co-expression without common lymphoid or myeloid lineage markers. There is no consensus on the optimal therapeutic strategy for BPDCN. It is highly responsive to chemotherapy but the median event-free survival is very short. Allogeneic stem cell transplantation may improve the prognosis of BPDCN but the rate of relapse is still high. There are no specific targeted agents approved for patients with BPDCN, but advances in the understanding of the pathobiology of BPDCN and the results of early clinical studies have revealed novel targets and potentially effective agents. Novel targeted therapies may improve outcomes for patients with BPDCN in the future.
[Mh] MeSH terms primary: Antineoplastic Agents/therapeutic use
Dendritic Cells/drug effects
Drugs, Investigational/therapeutic use
Hematologic Neoplasms/drug therapy
[Mh] MeSH terms secundary: Animals
Antineoplastic Agents/pharmacology
Antineoplastic Combined Chemotherapy Protocols/pharmacology
Antineoplastic Combined Chemotherapy Protocols/therapeutic use
Cell Line, Tumor
Central Nervous System Neoplasms/diagnosis
Central Nervous System Neoplasms/prevention & control
Central Nervous System Neoplasms/secondary
Dendritic Cells/pathology
Drugs, Investigational/pharmacology
Hematologic Neoplasms/diagnosis
Hematologic Neoplasms/pathology
Hematologic Neoplasms/surgery
Hematopoietic Stem Cell Transplantation/adverse effects
Humans
Prognosis
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Nm] Name of substance:0 (Antineoplastic Agents); 0 (Drugs, Investigational)
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:180219
[St] Status:MEDLINE
[do] DOI:10.1007/s00277-018-3259-z

  6 / 61420 MEDLINE  
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[PMID]: 29363337
[Au] Autor:Patti F; Chisari CG; D'Amico E; Zappia M
[Ad] Address:a Department "GF Ingrassia", Section of Neurosciences, Multiple Sclerosis Center , University of Catania , Catania , Italy.
[Ti] Title:Pharmacokinetic drug evaluation of daclizumab for the treatment of relapsing-remitting multiple sclerosis.
[So] Source:Expert Opin Drug Metab Toxicol;14(3):341-352, 2018 Mar.
[Is] ISSN:1744-7607
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:INTRODUCTION: Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system. Despite the availability of several disease-modifying therapies for relapsing MS, there is a need for highly efficacious targeted therapy with a favorable benefit-risk profile and a high level of treatment adherence. Daclizumab is a humanized monoclonal antibody directed against CD25, the α subunit of the high-affinity interleukin 2 (IL-2) receptor, that reversibly modulates IL-2 signaling. Areas covered: Daclizumab blocks the activation and expansion of autoreactive T cells that plays a role in the immune pathogenesis of MS. As its modulatory effects on the immune system, daclizumab's potential for use in MS was tested extensively showing a high efficacy in reducing relapse rate, disability progression and the number and volume of gadolinium-enhancing lesions on brain magnetic resonance imaging. Moreover, phase II and III trials showed a favorable pharmacokinetic (PK) profile with slow clearance, linear pharmacokinetics at doses above 100 mg and high subcutaneous bioavailability, not influenced by age, sex or other clinical parameters. Expert opinion: Among the new emerging drugs for MS, daclizumab also, thanks to a favorable PK profile, may represent an interesting and promising therapeutic option in the wide MS therapies armamentarium.
[Mh] MeSH terms primary: Antibodies, Monoclonal, Humanized/administration & dosage
Immunoglobulin G/administration & dosage
Immunosuppressive Agents/administration & dosage
Multiple Sclerosis, Relapsing-Remitting/drug therapy
[Mh] MeSH terms secundary: Animals
Antibodies, Monoclonal, Humanized/pharmacokinetics
Antibodies, Monoclonal, Humanized/pharmacology
Biological Availability
Dose-Response Relationship, Drug
Humans
Immunoglobulin G/pharmacology
Immunosuppressive Agents/pharmacokinetics
Immunosuppressive Agents/pharmacology
Interleukin-2 Receptor alpha Subunit/immunology
Magnetic Resonance Imaging
Medication Adherence
Multiple Sclerosis, Relapsing-Remitting/physiopathology
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Nm] Name of substance:0 (Antibodies, Monoclonal, Humanized); 0 (IL2RA protein, human); 0 (Immunoglobulin G); 0 (Immunosuppressive Agents); 0 (Interleukin-2 Receptor alpha Subunit); CUJ2MVI71Y (daclizumab)
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:180125
[St] Status:MEDLINE
[do] DOI:10.1080/17425255.2018.1432594

  7 / 61420 MEDLINE  
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[PMID]: 29521236
[Au] Autor:Lemos A; Meloc R; Preto AJ; Almeida JG; Moreira IS; Cordeiro MNDS
[Ad] Address:LAQV/REQUIMTE, Department of Chemistry and Biochemistry, Faculty of Sciences, University of Porto, Rua do Campo Alegre s/n, 4169-007 Porto. Portugal.
[Ti] Title:In silico studies targeting G-protein coupled receptors for drug research against Parkinson's disease.
[So] Source:Curr Neuropharmacol;, 2018 Mar 08.
[Is] ISSN:1875-6190
[Cp] Country of publication:United Arab Emirates
[La] Language:eng
[Ab] Abstract:Parkinson's Disease (PD) is a long-term neurodegenative brain disorder that mainly affects the motor system. The causes are still unknown, and even though currently there is no cure, several therapeutic options are available to manage its symptoms. The development of novel anti-parkinsonian agents and an understanding of their proper and optimal use are, indeed, highly demanding. For the last decades, L-3,4-DihydrOxyPhenylAlanine or levodopa (L-DOPA) has been the gold-standard therapy for the symptomatic treatment of motor dysfunctions associated to PD. However, the development of dyskinesias and motor fluctuations (wearing-off and on-off phenomena) associated to long-term L-DOPA replacement therapy have limited its antiparkinsonian efficacy. The investigation for non-dopaminergic therapies has been largelyexplored as an attempt to counteract the motor side effects associated to dopamine replacement therapy. Being one of the largest cell membrane protein families, G-Protein-Coupled Receptors (GPCRs) have become a relevant target for drug discovery focused in a wide range of therapeutic areas, including Central Nervous System (CNS) diseases. The modulation of specific GPCRs potentially implicated in PD, excluding dopamine receptors, may provide promising non-dopaminergic therapeutic alternatives for symptomatic treatment of PD. In this review, we focused on the impact of specific GPCR subclasses, including dopamine receptors, adenosine receptors, muscarinic acetylcholine receptors, metabotropic glutamate receptors, and 5-hydroxytryptamine receptors, on the pathophysiology of PD and the importance of structure- and ligand-based in silico approaches for the development of small molecules to target these receptors.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher
[do] DOI:10.2174/1570159X16666180308161642

  8 / 61420 MEDLINE  
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[PMID]: 29504046
[Au] Autor:C Conley A; A Newhouse P
[Ad] Address:Center for Cognitive Medicine, Department of Psychiatry, Vanderbilt University Medical Center, 1601 23rd Ave., Nashville, TN, 37212, USA.
[Ti] Title:Advances in Drug Discovery and Development in Geriatric Psychiatry.
[So] Source:Curr Psychiatry Rep;20(2):10, 2018 Mar 05.
[Is] ISSN:1535-1645
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:PURPOSE OF REVIEW: This article reviews recent advances in drug discovery and development for geriatric psychiatry. Drug discovery for disorders of the central nervous system is a long and challenging process, with a high attrition rate from the preclinical stages through to marketing a compound. Developing drugs for geriatric neuropsychiatric conditions presents additional challenges, due to the complexity of the symptoms, comorbid diagnoses, and the variability of the population. Despite there being limited success over the past two decades, a number of new approaches have identified potential targets for preclinical development and ultimately clinical testing. RECENT FINDINGS: Recent approaches have tried to address specific mechanisms that relate to the disease progression. These approaches include combining a number of ligands into to multi-target compounds, or targeting specific types of cells such as protein kinases or myeloid cells. In addition, the increased use of induced pluripotent stem cell cultures has enabled new compounds to be tested on disease-specific tissues, increasing the success rate of the lead compounds going through the preclinical stages. New pharmacological agents designed with advanced screening techniques and the shift towards systems pharmacology is changing the landscape of drug discovery in geriatric psychiatry. There is potential for these new agents to produce targeted effects in the framework of disorders that have long been untreatable.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review
[do] DOI:10.1007/s11920-018-0871-5

  9 / 61420 MEDLINE  
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[PMID]: 29215336
[Au] Autor:Sayilan Özgün G; Özgün E; Tabakçioglu K; Süer Gökmen S; Eskiocak S; Çakir E
[Ad] Address:Department of Medical Biochemistry, Trakya University School of Medicine, Edirne, Turkey.
[Ti] Title:Caffeine Increases Apolipoprotein A-1 and Paraoxonase-1 but not Paraoxonase-3 Protein Levels in Human-Derived Liver (HepG2) Cells.
[So] Source:Balkan Med J;34(6):534-539, 2017 12 01.
[Is] ISSN:2146-3131
[Cp] Country of publication:Turkey
[La] Language:eng
[Ab] Abstract:BACKGROUND: Apolipoprotein A-1, paraoxonase-1 and paraoxonase-3 are antioxidant and anti-atherosclerotic structural high-density lipoprotein proteins that are mainly synthesized by the liver. No study has ever been performed to specifically examine the effects of caffeine on paraoxonase enzymes and on liver apolipoprotein A-1 protein levels. AIMS: To investigate the dose-dependent effects of caffeine on liver apolipoprotein A-1, paraoxonase-1 and paraoxonase-3 protein levels. STUDY DESIGN: experimental study. METHODS: HepG2 cells were incubated with 0 (control), 10, 50 and 200 µM of caffeine for 24 hours. Cell viability was evaluated by 3-(4,5-Dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide assay. Apolipoprotein A-1, paraoxonase-1 and paraoxonase-3 protein levels were measured by western blotting. RESULTS: We observed a significant increase on apolipoprotein A-1 and paraoxonase-1 protein levels in the cells incubated with 50 µM of caffeine and a significant increase on paraoxonase-1 protein level in the cells incubated with 200 µM of caffeine. CONCLUSION: Our study showed that caffeine does not change paraoxonase-3 protein level, but the higher doses used in our study do cause an increase in both apolipoprotein A-1 and paraoxonase-1 protein levels in liver cells.
[Mh] MeSH terms primary: Apolipoprotein A-I/drug effects
Aryldialkylphosphatase/drug effects
Caffeine/pharmacology
Central Nervous System Stimulants/pharmacology
Hep G2 Cells/drug effects
Liver/pathology
[Mh] MeSH terms secundary: Analysis of Variance
Blotting, Western
Cell Survival/drug effects
Dose-Response Relationship, Drug
Humans
In Vitro Techniques
Lipoproteins, HDL
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Apolipoprotein A-I); 0 (Central Nervous System Stimulants); 0 (Lipoproteins, HDL); 3G6A5W338E (Caffeine); EC 3.1.8.1 (Aryldialkylphosphatase); EC 3.1.8.1 (PON1 protein, human); EC 3.1.8.1 (PON3 protein, human)
[Em] Entry month:1801
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[Js] Journal subset:IM
[Da] Date of entry for processing:171208
[St] Status:MEDLINE
[do] DOI:10.4274/balkanmedj.2016.1217

  10 / 61420 MEDLINE  
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[PMID]: 28455692
[Au] Autor:Casaca-Carreira J; Temel Y; Hescham SA; Jahanshahi A
[Ad] Address:School for Mental Health and Neuroscience, Maastricht University, Maastricht, the Netherlands.
[Ti] Title:Transependymal Cerebrospinal Fluid Flow: Opportunity for Drug Delivery?
[So] Source:Mol Neurobiol;55(4):2780-2788, 2018 Apr.
[Is] ISSN:1559-1182
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Drug delivery to the central nervous system (CNS) is complicated by the blood-brain barrier. As a result, many agents that are found to be potentially effective at their site of action cannot be sufficiently or effectively delivered to the CNS and therefore have been discarded and not developed further for clinical use, leaving many CNS diseases untreated. One way to overcome this obstacle is intracerebroventricular (ICV) delivery of the therapeutics directly to cerebrospinal fluid (CSF). Recent experimental and clinical findings reveal that CSF flows from the ventricles throughout the parenchyma towards the subarachnoid space also named minor CSF pathway, while earlier, it was suggested that only in pathological conditions such as hydrocephalus this form of CSF flow occurs. This transependymal flow of CSF provides a route to distribute ICV-infused drugs throughout the brain. More insight on transependymal CSF flow will direct more rational to ICV drug delivery and broaden its clinical indications in managing CNS diseases.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1704
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review
[do] DOI:10.1007/s12035-017-0501-y


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