Relevant bibliographies by topics / Drugs acting on the central nervous system

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  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Drugs acting on the central nervous system'

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Published: 24 April 2022

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Journal articles on the topic "Drugs acting on the central nervous system"

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Gupta, S. P. "QSAR studies on drugs acting at the central nervous system." Chemical Reviews 89, no. 8 (December 1989): 1765–800. http://dx.doi.org/10.1021/cr00098a007.

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Samsam, Mohtashem. "Central Nervous System Acting Drugs in Treatment of Migraine Headache." Central Nervous System Agents in Medicinal Chemistry 12, no. 3 (August 1, 2012): 158–72. http://dx.doi.org/10.2174/187152412802430147.

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Zhu, Xing-Zu. "Development of natural products as drugs acting on central nervous system." Memórias do Instituto Oswaldo Cruz 86, suppl 2 (1991): 173–75. http://dx.doi.org/10.1590/s0074-02761991000600039.

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ALMEIDA, SEBASTIÃO S., JOHN TONKISS, and JANINA R. GALLER. "Malnutrition and Reactivity to Drugs Acting in the Central Nervous System." Neuroscience & Biobehavioral Reviews 20, no. 3 (January 1996): 389–402. http://dx.doi.org/10.1016/0149-7634(95)00054-2.

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Jann, Michael W., and Sara R. Grimsley. "Pharmacogenetics of Agents Acting on the Central Nervous System." Journal of Pharmacy Practice 6, no. 1 (February 1993): 2–16. http://dx.doi.org/10.1177/089719009300600103.

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This article will review the various agents affecting the central nervous system (CNS) such as the analgesics, antidepressants, anticonvulsants, antipsychotics, and benzodiazepines. Most of the research in pharmacogenetics with the CNS agents have been conducted in the antidepressants. The cytochrome 450 IID6 isozyme system has been shown to influence the disposition of the antidepressants and antipsychotics. Amitriptyline metabolism to nortriptyline and nortriptyline conversion to its 10-OH metabolite were shown to be influenced by the IID6 isozyme. Interestingly, imipramine metabolism to desipramine is only partially related to the IID6 isozyme. Biotransformation of imipramine to its 2-OH metabolite was shown to be affected by the IID6 isozyme, but its metabolism to the 10-OH remains to be investigated. Of the antipsychotic drugs, haloperidol and thioridazine are two agents most studied. Haloperidol is converted to a reduced metabolite via a ketone reductase enzyme. The reduced metabolite is oxidized back to Haloperidol. This oxidation pathway was reported to be affected by the IID6 isozyme. Thioridazine metabolism to mesoridazine and conversion of codeine to morphine appear to be also influenced by CP-450 IID6. Other 450 isozymes are reported to be involved with other CNS agents.
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Monzani, Agar, Gianfranco Gamberini, Daniela Braghiroli, Maria Di Bella, Lina Raffa, and Maurizio Sandrini. "Sulfonamides Acting on the Central Nervous System, VI." Archiv der Pharmazie 318, no. 4 (1985): 299–304. http://dx.doi.org/10.1002/ardp.19853180404.

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Kharkar, Prashant S. "Drugs acting on central nervous system (CNS) targets as leads for non-CNS targets." F1000Research 3 (March 21, 2014): 40. http://dx.doi.org/10.12688/f1000research.3-40.v2.

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Innovative drug discovery approaches are currently needed to rejuvenate the shrinking product pipelines of the pharmaceutical companies across the globe. Here a theme is presented – the use of central nervous system (CNS) drugs as leads for non-CNS targets. The approach is related to the use of existing drugs for new indications. Suitable chemical modifications of the CNS drugs abolish their CNS penetration. These novel analogs may then be screened for activity against non-CNS targets. Careful selection of the appropriate structural modifications remains the key to success.
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Garattini, Silvio, and Vittorio Bertele'. "Efficacy, safety and cost of new drugs acting on the central nervous system." European Journal of Clinical Pharmacology 59, no. 1 (March 22, 2003): 79–84. http://dx.doi.org/10.1007/s00228-003-0569-3.

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Saganuwan, Saganuwan Alhaji. "Chirality of Central Nervous System (CNS) Acting Drugs: A Formidable Therapeutic Hurdle Against CNS Diseases." Central Nervous System Agents in Medicinal Chemistry 19, no. 3 (October 31, 2019): 171–79. http://dx.doi.org/10.2174/1871524919666190624150214.

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Background: Over fifty percent of drugs being used clinically are chiral and 90% of them are racemates. Unfortunately, they have both adverse and beneficial effects on body systems. Methods: Because of the erratic effects of chiral compounds on body functional systems, literature search was carried out with a view to identify CNS chiral drugs, their clinical advantages and disadvantages, unique physicochemical properties and structural modifications into safer drugs. Results: Findings have shown that majority of CNS and non-CNS acting drugs have chiral functional groups that may occur as either dextrorotatory (clockwise) or levorotatory (anticlockwise) or racemates which are inert. Sometimes, the enantiomers (optical isomers) could undergo keto-enol tautomerism, appearing in either acidic or basic or inert form. Chiral CNS acting drugs have agonistic and antagonistic effects, clinical advantages, disadvantages, and special clinical applications, possible modifications for better therapeutic effects and possible synthesis of more potent drugs from racemates. Clockwise chirality may be more effective and safer than the drugs with anticlockwise chirality. When chiral drugs are in racemate state they become inert and may be safer than when they are single. Also, diastereoisomers may be more dangerous than stereoisomers. Conclusion: Therefore, chiral compounds should be adequately studied in lab rodents and primates, and their mechanisms of actions should be comprehensively understood before being used in clinical setting. Since many of them are toxic, their use should be based on principle of individualized medicine. Their molecular weights, functional groups, metabolites, polymers and stereoisomers could be valuable tools for their modifications.
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KONTANI, Hitoshi, Mikiko NAKAGAWA, and Takeshi SAKAI. "Effects of Central Nervous System-Acting Drugs on Urinary Bladder Contraction in Unanesthetized Rats." Japanese Journal of Pharmacology 50, no. 3 (1989): 327–32. http://dx.doi.org/10.1016/s0021-5198(19)42447-5.

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Dissertations / Theses on the topic "Drugs acting on the central nervous system"

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Gray, J. A. "Interactions between GABA and monamines in the central nervous system and their relationship to the mode of action of antidepressant drugs." Thesis, University of Oxford, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.233447.

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Schroeder, Frederick Albert. "A Role for Histone Modification in the Mechanism of Action of Antidepressant and Stimulant Drugs: a Dissertation." eScholarship@UMMS, 2007. https://escholarship.umassmed.edu/gsbs_diss/370.

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Depression and stimulant drug addiction each result in massive losses of health, productivity and human lives every year. Despite decades of research, current treatment regimes for depression are ineffective in approximately half of all patients. Therapy available to stimulant drug addicts is largely ineffective and moreover, dedicated treatments for drug dependence (including abuse of cocaine) are non-existent. Thus, there is a pressing need to further understanding of the molecular mechanisms underlying these disorders in order to develop novel, targeted therapeutic strategies. Chromatin remodeling, including changes in histone acetylation, has been proposed to play a role in both the etiology and treatment of depression and stimulant abuse. Histone acetyltransferases (HATs) and histone deacetylases (HDACs) regulate numerous cellular processes, including transcription, cell cycle progression and differentiation. Moreover, histone acetylation has been shown to regulate hippocampal neurogenesis, a cellular response associated with the pathogenesis and treatment of depression and stimulant abuse (Hsieh et al., 2004, Yamaguchi et al., 2004, Fischer et al., 2007). Ultimately, such basic cellular processes impact higher order function, namely cognition and emotion. Indeed, recent studies suggest that HDAC activity in selected forebrain regions, including ventral striatum and hippocampus, modulate stimulant- and antidepressantinduced behavior (Kumar et al., 2005, Tsankova et al., 2006a, Fischer et al., 2007). These reports highlight an association between chromatin remodeling and diverse behavioral changes, including changes induced by the pleiotropic HDAC inhibitor, sodium butyrate (SB), (Kumar et al., 2005, Tsankova et al., 2006a, Fischer et al., 2007). However, behavioral, brain-metabolic and molecular effects of SB treatment in the context of rodent models of depression, dopaminergic sensitization and repeated cocaine administration remained unclear. The work described in this thesis illustrates the potential for chromatin modifying drugs in mechanisms underlying the experimental pharmacology of depression and stimulant addiction. Specifically, the data presented here support the view that treatment with the short chain fatty acid, sodium butyrate enhances: (1) antidepressant-like behavioral effects of the selective serotonin reuptake inhibitor (SSRI), fluoxetine (2) locomotor sensitization induced by repeated administration of the dopamine D1/D5 receptor agonist SKF82958; and(3) brain metabolic activation upon repeated cocaine administration as evidenced by fMRI in awake rats. Furthermore, this report provides evidence that these treatment paradigms will result in chromatin modification changes associated with active transcription, in addition to increased mRNA levels of plasticity-associated genes, including brain-derived neurotrophic factor (BDNF) at key brain regions implicated in the pathogenesis of depression and stimulant addiction. To date, little is known regarding the underlying mechanisms of action mediating the enhancing effects of sodium butyrate on the various antidepressant- and stimulantrelated paradigms. Our findings underscore the potential of chromatin-modifying drugs to profoundly affect the behavioral response of an animal to antidepressant and stimulant drugs and warrants consideration in the context of developing novel therapeutic strategies.
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Lloyd, Edward John, and mikewood@deakin edu au. "A common structural basis for central nervous system drug design." Deakin University. School of Biological Sciences, 1986. http://tux.lib.deakin.edu.au./adt-VDU/public/adt-VDU20050902.115505.

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The main theme of this thesis is that there is a common structural basis for drugs acting on the central nervous system (CNS), and that this concept may be used to design new CNS-active drugs which have greater specificity and hence less side-effects. To develop these ideas, the biological basis of how drugs modify CMS neurotransmission is described, and illustrated using dopaminergic pathways. An account is then given of the use of physicochemical concepts in contemporary drug design. The complete conformational analysis of several antipsychotic drugs is used to illustrate some of these techniques in the development of a model for antipsychotic drug action. After reviewing current structure-activity studies in several classes of CNS drugs (antipsychotics, anti-depressants, stimulants, hal1ucinogens, anticonvulsants and analgesics), a hypothesis for a common structural basis of CNS drug action is proposed- This is based on a topographical comparison of the X-ray structures of eight representative CNS-active drugs, and consists of three parts: 1.there is a common structural basis for the activity of many different CNS-active drug classes; 2. an aromatic ring and a nitrogen atom are the primary binding groups whose topographical arrangement is fundamental to the activity of these drug classes; 3. the nature and placement of secondary binding determines different classes of CNS drug activity. A four-Point model for this common structural basis is then defined using 14- CNS-active drug structures that include the original eight used in proposing the hypothesis. The coordinates of this model are: R1 (0. 3.5, 0), R2 (0, -3.5, O), N (4.8. -0.3, 1.4), and R3 (6.3, 1.3, 0), where R1 and R2 represent the point locations of a hydrophobic interaction of the common aromatic ring with a receptor, and R3 locates the receptor point for a hydrogen bond involving the common nitrogen, N. Extended structures were used to define the receptor points R1, R2 and R3, and the complete conformational space of each of the 14 molecules was considered. It is then shoun that the model may be used to predict whether a given structure is likely to show CNS activity: a search over 1,000 entries in the current Merck Index shows a high probability (82%) of CNS activity in compounds fitting the structural model. Analysis of CNS neurotransmitters and neuropeptides shows that these fit the common model well. Based on the available evidence supporting chemical evolution, protein evolution, and the evolution of neurotransmitter functions, it is surmised that the aromatic ring/nitrogen atom pharmacophore proposed in the common model supports the idea of the evolution of CNS receptors and their neurotransmitters, possibly from an aromatic amine or acety1cho1ine acting as a primaeval communicating molecule. The third point in the hypothesis trilogy is then addressed. The extensive conformation-activity analyses that have resulted in well-defined models for five separate CNS drug classes are used to map out the locations of secondary binding groups relative to the common model for anti-psychotics, antidepressants, analgesics, anticholinergics, and anticonvulsants. With this information, and knowledge derived from receptor-binding data, it is postulated that drugs having specified activity could be designed. In order to generate novel structures having a high probability of CNS-activity, a process of drug design is described in which known CNS structures are superimposed topographically using the common model as a template. Atoms regarded as superfluous may be selectively deleted and the required secondary binding groups added in predicted locations to give novel structures. It is concluded that this process provides the basis for the rational design of new lead compounds which could further be optimized for potent and specific CNS activity.
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Tiraboschi, Juan Manuel. "Penetration and antiviral activity of antiretroviral drugs in the Central Nervous System." Doctoral thesis, Universitat de Barcelona, 2015. http://hdl.handle.net/10803/396308.

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INTRODUCTION: With successful treatment and near-normal life expectancy of people living with HIV, the focus of care has shifted towards minimizing toxicity from long term exposure to antiretrovirals (ARVs) and preventing co-morbidities. The prevalence of neurocognitive abnormalities has been reported to remain high, including in patients treated with cART. A low level viral replication in the central nervous system (CNS) may persist even in patients presenting with HIV-1 suppression in plasma, leading to local inflammation, neuronal damage and a poorer neuropsychological performance. A poor penetration of ARV drugs into the CNS may allow local HIV replication and may be associated with asymptomatic and even symptomatic HIV-related neurocognitive impairment or neurologic symptoms, which may be severe and present as HIV encephalitis in some occasions. For this reason we consider it extremely important to conduct research in order to improve the knowledge of the newer antiretroviral drugs penetration into the CNS and so to carry out a pilot study based on these results. HYPOTHESIS: 1. Maraviroc may reach pharmacological concentrations above the IC50 range in the CSF. 2. Maraviroc in combination with other antiretroviral drugs may help to maintain HIV viral suppression in the CSF. 3. Etravirine concentrations in CSF may be low but higher than the IC50. 4. Etravirine in combination with other antiretroviral drugs may help to maintain HIV viral suppression in the CSF. 5. Amprenavir concentrations in CSF may be above the IC50. 6. Fosamprenavir/ritonavir monotherapy may be sufficient to maintain HIV viral suppression in CSF. 7. A treatment switch from tenofovir, emtricitabine and efavirenz to abacavir, lamivudine and maravicoc in patients with neurocognitive impairment may be associated with a reduction on CSF inflammatory markers, CSF HIV RNA and an improvement in their neurocognitive performance. CONCLUSIONS: 1. Maraviroc concentrations in CSF in HIV-infected patients. -In all except 1 CSF sample, MVC concentrations exceeded the median serum- adjusted IC90. -Our data suggest that MVC may contribute to inhibit HIV-1 replication in CNS. -Maraviroc in combination with nucleoside-sparing regimens, including new ARV drugs, seems to be locally active. 2. Etravirine concentrations in CSF in HIV-infected patients -In all samples Etravirine concentrations exceeded the IC50 range. -Our data suggest that Etravirine may contribute to inhibiting HIV-1 replication in the CNS and that combined nucleoside sparing regimens, including new antiretroviral drugs, seem to be locally active. 3. Viral response in stable patients switching to fosamprenavir/ritonavir monotherapy. -Although the high percentage of viral failure with FPV/r monotherapy found in our study, this study is a proof of concept that boosted PI monotherapy could be enough to suppress HIV viral replication in CSF. 4. Viral and inflammatory markers in cerebrospinal fluid of patients with HIV-1-associated neurocognitive impairment during antiretroviral treatment switch. -There was a non-statistically significant reduction on the CSF HIV viral load after six months. -A significant reduction on TNF-α would suggest a reduction on local inflammatory reaction following treatment switch. This could be related to a reduction in CSF viral load, the anti-inflammatory effect of Maraviroc or both. -A trend towards an improvement in neurocognitive performance could be related to the above mentioned effects. - A switch to a regimen with a higher CPE score containing MVC was associated with a trend towards an improvement in neuropsychological performance and a reduction in TNF-α. In CSF. GENERAL CONCLUSION. The study of the concentrations and antiviral activity in CSF of the antiretroviral drugs will make possible the design for more effective combinations to be implemented in patients with NCI. A treatment switch can contribute to clinical and virological improvement as well as a reduction in the inflammatory markers.
INTRODUCCIÓN: En los últimos años diversos estudios han puesto en evidencia la persistencia de trastornos neurocognitivos (TNC) asociados al VIH, siendo en su mayoría formas asintomáticas o leves y moderadas. Si bien son múltiples los factores que favorecen la presencia de TNC en individuos infectados por el VIH (hepatopatía crónica, enfermedad cardiovascular, alcoholismo, uso de drogas, psicofármacos, etc), el virus –que ingresa en el SNC desde los primeros días de la infección- parece jugar un papel importante y ser causa de TNC incluso severos y/o enfermedad neurológica en forma de encefalitis aguda que puede llevar al coma y la muerte. En este contexto, la diferente penetración de los fármacos ARV podría jugar un papel en la prevención, y tratamiento de estas alteraciones. OBJETIVO GENERAL: Generar conocimiento sobre la penetración y actividad de diferentes fármacos antirretrovirales. Utilizar dicha información para poner en práctica una intervención destinada a mejorar la eficacia de una combinación antirretroviral en SNC. HIPÓTESIS: 1. Maraviroc alcanzaría niveles farmacológicos en LCR superiores a la CI50. 2. Maraviroc en combinación con otros fármacos antirretrovirales ayudaría a mantener la supresión viral en LCR. 3. Las concentraciones de Etravirina en LCR serían bajas aunque superiores a la CI50. 4. Etravirina en combinación con otros fármacos antirretrovirales contribuiría a mantener la supresión viral en LCR. 5. Las concentraciones de Amprenavir en LCR serían superiores a la CI50. 6. Fosamprenavir/ritonavir en monoterapia sería suficiente para mantener la supresión viral en LCR. 7. En pacientes que reciben una pauta de emtricitabina/tenofovir/ efavirenz y presentan deterioro neurocognitivo, el cambio a abacavir/lamivudina/maraviroc se asociaría a una disminución de marcadores inflamatorios, carga viral en LCR y a una mejoría en los TNC. CONCLUSIÓN: El estudio de las concentraciones de fármacos antirretrovirales y su actividad en LCR permitirá diseñar con mayor eficacia las pautas a utilizar en pacientes con TNC. Aunque hacen falta estudios más amplios, nuestros datos sugieren un posible beneficio clínico, virológico y de parámetros inflamatorios en pacientes con TNC que cambian a un TAR con mayor penetrabilidad en SNC.
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Jansson, Björn. "Models for the Transfer of Drugs from the Nasal Cavity to the Central Nervous System." Doctoral thesis, Uppsala University, Department of Pharmacy, 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-3905.

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The blood-brain barrier restricts the access of many compounds, including therapeutic agents, to the brain. Several human studies indicate that nasal administration of hydrophilic compounds, such as peptides, can bypass the blood-brain barrier. The aims of this thesis were to develop and refine models for this direct nose-to-brain transfer.

In a mouse model, [3H]-dopamine was given as a unilateral nasal dose. The resulting radioactivity in the ipsilateral olfactory bulb was significantly higher than that in the contralateral bulb and peaked at 4 h. Tape section autoradiography showed that the radioactivity was concentrated in the olfactory nerve layer and the glomerular layer of the olfactory bulb. The olfactory transfer of dopamine was also studied in vitro. At a lower donor concentration, the mucosal-to-serosal dopamine permeability was higher than the serosal-to-mucosal permeability, but at a higher concentration, the permeability coefficients were similar. Together, these results suggest that the olfactory transfer of dopamine has an active component.

Olfactory transfer of fluorescein-labeled dextran through the epithelium and deeper tissues was studied in a rat model, which enabled visualization of the transfer using fluorescence microscopy. Although the epithelial transfer appeared to be mainly intracellular, transfer in the following deeper tissues was extracellular. Without altering the route of uptake, a gellan gum formulation enhanced the uptake of fluorescein dextran. The enhancing effect was considered likely to be the result of an increased residence time in the nasal cavity.

In conclusion, dopamine and fluorescein-labeled dextran were identified as suitable model compounds for the study of olfactory drug transfer mechanisms and the influence of drug formulation. Two new in vitro models of olfactory transfer were compared. Also, a rat model, which enabled the visualization of the entire nose-to-brain transfer, was developed.

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Jansson, Björn. "Models for the transfer of drugs from the nasal cavity to the central nervous system /." Uppsala : Acta Universitatis Upsaliensis: Univ.-bibl. [distributör], 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-3905.

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Sinei, Kipruto Arap. "The effect of antidepressant drugs on the circadian rhythm of 5-hydroxytryptamine synthesis in the central nervous system." Thesis, University of Bath, 1987. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.375335.

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Berggård, Cecilia. "Transcription factor AP-2 in relation to personality and antidepressant drugs /." Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-4638.

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Dublin, Sascha. "Risk of epithelial ovarian cancer in relation to use of antidepressants, benzodiazepines, and other medications acting on the central nervous system /." Thesis, Connect to this title online; UW restricted, 1999. http://hdl.handle.net/1773/10861.

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Nightingale, Sam. "The role of the central nervous system as a sanctuary site for HIV due to limited penetration of antiretroviral drugs." Thesis, University of Liverpool, 2015. http://livrepository.liverpool.ac.uk/2013319/.

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Introduction. HIV-associated neurocognitive disorders appear to remain common despite access to antiretroviral therapy (ART). Penetration of ART into the central nervous system (CNS) is highly variable between drugs and between individuals. Cerebrospinal fluid (CSF) concentrations of many antiretroviral medications fall below the minimum inhibitory concentration for wild type virus. HIV-1 RNA can be detected in the CSF at greater levels than in plasma (CSF/plasma discordance), however the clinical significance of this is unclear, and the degree of difference considered pathological varies. Whether the CNS can act as a sanctuary site leading to persistent HIV detection in plasma is not known. Methods. The PARTITION study recruited HIV positive adults from 13 UK clinical sites. Paired CSF and plasma was collected from patients undergoing LP for clinical indication (group A) and subjects with unexplained viraemia despite ART (group B). The study aimed to determine a) the prevalence of CSF/plasma discordance and factors associated with this occurrence, and b) the prevalence of HIV-1 RNA detection in CSF in those with HIV-1 RNA persistence in plasma. A sensitive assay detected HIV-1 RNA below 50 copies/ml in a subgroup and a cytometric bead array determined CSF biomarkers. A matrix of clinical features and CSF/plasma biomarkers was related to cognitive decline in subjects from the CHARTER study. Drug concentrations in CSF and plasma were measured by mass spectrometry assays and related to host genetic factors in subjects in the PARTITION study and a Vietnamese cohort with tuberculous meningitis. Results. CSF/plasma HIV discordance occurred in 13% of this cohort and was associated with nadir, but not current, CD4 cell count. CSF/plasma discordance occurred in 7 of 40 (18%) of subjects with ongoing viral detection in plasma vs. 0 of 39 of those without. Residual HIV-1 RNA detection below 50 copies/ml was also associated with CSF HIV-1 RNA detection. Resistance associated HIV mutations were detected in CSF of subjects with CSF/plasma discordance. CSF/plasma discordance above 0.5log10 was associated with raised profiles of inflammatory CSF proteomic biomarkers compared to those without discordance. In the CHARTER cohort, cognitive decline over 18 months was associated with lower concentrations of CSF TNFa and plasma IGF1/2. CSF concentrations of efavirenz were associated with the CYP2B6 c.516G>T single nucleotide polymorphism. Efavirenz metabolites were mainly glucuronidated in CSF, were present at neurotoxic levels, and were related to degree of blood brain barrier permeability. Host genetic factors were did not relate to CSF DRV concentrations. Conclusions. CSF/plasma discordance is a frequent occurrence, likely related to processes established during advanced immunosuppression not fully reversed by ART. It is associated with CSF HIV resistance and raised CSF biomarkers, even at levels 0.5-1log10 which have been considered non-significant in some studies. Potentially neurotoxic CSF concentrations of efavirenz relate to host genetic factors.
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Books on the topic "Drugs acting on the central nervous system"

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Drug action in the central nervous system. New York: Oxford University Press, 1998.

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Zhong yao ying xiang shen jing xi tong huo xing cheng fen: Active components on nervous system in TCM. Beijing: Ke xue chu ban she, 2012.

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Welling, Peter G. Pharmacokinetics of cardiovascular, central nervous system, and antimicrobial drugs. London: The Royal Society of Chemistry, 1985.

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Miller, Richard Lawrence. The encyclopedia of addictive drugs. Westport, Conn. USA: Greenwood Press, 2002.

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The encyclopedia of addictive drugs. Westport, Conn: Greenwood Press, 2002.

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J, Whalley Lawrence, ed. ACE inhibitors: Central actions. New York: Raven Press, 1994.

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E, Bloom Floyd, and Roth Robert H. 1939-, eds. The biochemical basis of neuropharmacology. 8th ed. Oxford: Oxford University Press, 2003.

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E, Bloom Floyd, ed. The biochemical basis of neuropharmacology. 7th ed. New York: Oxford University Press, 1996.

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E, Bloom Floyd, and Roth Robert H. 1939-, eds. The biochemical basis of neuropharmacology. 5th ed. New York: Oxford University Press, 1986.

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E, Bloom Floyd, and Roth Robert H. 1939-, eds. The biochemical basis of neuropharmacology. 6th ed. New York: Oxford University Press, 1991.

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Book chapters on the topic "Drugs acting on the central nervous system"

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Moore, Joanne I. "Drugs Acting on the Central Nervous System." In Oklahoma Notes, 90–119. New York, NY: Springer New York, 1995. http://dx.doi.org/10.1007/978-1-4612-2514-0_6.

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Dunlap, Norma, and Donna M. Huryn. "Drugs acting on the central nervous system." In Medicinal Chemistry, 395–436. New York, NY : Garland Science, Taylor & Francis Group, LLC, [2018]: Garland Science, 2018. http://dx.doi.org/10.1201/9781315100470-13.

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Locatelli, Vittorio, Elena Bresciani, Laura Tamiazzo, and Antonio Torsello. "Central Nervous System-Acting Drugs Influencing Hypothalamic-Pituitary-Adrenal Axis Function." In Pediatric Neuroendocrinology, 108–20. Basel: KARGER, 2009. http://dx.doi.org/10.1159/000262533.

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Kaminska, Bozena, Magdalena Tyburczy, Konrad Gabrusiewicz, and Malgorzata Sielska. "Glioblastoma: Anti-tumor Action of Cyclosporin A and Functionally Related Drugs." In Tumors of the Central Nervous System, Volume 2, 241–53. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-0618-7_25.

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Ishibashi, S., T. Kurokawa, T. Dan’ura, and A. Yamashita. "Changes in Apparent Functions of Component Proteins of Adenylate Cyclase System in Rat Brain by Drugs Acting on the Central Nervous System." In Neuroreceptors and Signal Transduction, 287–99. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4757-5971-6_23.

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Carney, J. M., H. D. Christensen, L. A. Reinke, and L. E. Rikans. "Central Nervous System Drugs." In Oklahoma Notes, 58–97. New York, NY: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-0280-3_3.

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Christensen, H. D., L. A. Reinke, and L. E. Rikans. "Central Nervous System Drugs." In Oklahoma Notes, 60–97. New York, NY: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-0353-4_3.

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Baumann, Pierre, and Christoph Hiemke. "Central Nervous System Drugs." In Metabolism of Drugs and Other Xenobiotics, 301–29. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2012. http://dx.doi.org/10.1002/9783527630905.ch11.

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Al-Zidan, Radhwan Nidal. "Drugs Affecting the Central Nervous System." In Drugs in Pregnancy, 223–83. Includes bibliographical references and index.: Apple Academic Press, 2020. http://dx.doi.org/10.1201/9781003019107-7.

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Pawlowski, John. "Drugs Acting on the Autonomic Nervous System." In Essentials of Pharmacology for Anesthesia, Pain Medicine, and Critical Care, 219–33. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-8948-1_14.

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Conference papers on the topic "Drugs acting on the central nervous system"

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Moreira, Lorrane de Moura, Bruna Stefany Alves Françozo, Bruno Barcelos Pereira, Camila Almeida Sardinha, Débora Pimenta Alves, Filipe Henrique Almeida Barbosa Godoi, Katherine Oliveira Ferreira, and Silvia Oliveira Dourado. "Diagnosis and treatment of Multiple sclerosis: Brazilian and global overview." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.490.

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Introduction: Multiple sclerosis (MS) is a neurodegenerative autoimmune disease of the central nervous system with a chronic, progressive and inflammatory character. In addition, it presents itself in a heterogeneous way, and can be as an isolated syndrome or as a recurrent remitter, in the first stage, or as progressive, in the second stage. The present work was developed with the objective of determining which is the best form of diagnosis and therapy for multiple sclerosis in Brazil. Methods: The review was performed in PubMed platform, with the descriptors: “multiple sclerosis”, “diagnosis”, “therapy” and “research”. Results: The research result in 148 articles. After a criterious reading and the application of the used criteria, was selected 20 articles. Conclusion: For the diagnosis of this chronic neurological disease, magnetic resonance imaging is used to assess myelination of the different regions of the central nervous system, which is the most suitable for the diagnosis of MS. Μoreover, as a complement, cerebrospinal fluid extraction and blood tests are performed in order to ascertain the concentration of B cells. Regarding therapeutics, this is diversified, including drugs, diets and therapies that stimulate cognition and motor action, such as the use of virtual reality programs and motor images. In relation to drugs, it is of importance that SUS makes natalizumab and ocrelizumab available because they are more efficient and enable users to have a better quality of life. Finally, nutritional monitoring is also suggested to establish a ketogenic or fasting diet in a balanced way
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Elói, Daniel Vinicius, Daniel Lopes Marques de Araújo, Gabriela Fonseca Marçal, Luana Soares Vargas, Matheus Garcia Ribeiro, and Nicollas Nunes Rabelo. "Canabinoids as a therapeutic alternative in refractory epilepsy." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.554.

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Introduction: Epilepsy is characterized by abnormal electrical discharges in the brain that generate neuronal hyperexcitability and hypersynchrony. In the last years, pharmacological strategies have been efficient in the control of epileptic seizures of approximately 80% of patients, however, there are still refractory cases. Objective: To elucidate new forms of epilepsy treatment with cannabinoids. Design: Systematic Review performed at Centro Universitário Atenas – Paracatu – Minas Gerais. Methods: Literature review performed in the SciELO and PubMed databases, with the following terms: epilepsy and cannabidiol. Five papers, published from 2017 to 2020, written in English or Portuguese, were selected. Review: Epileptic seizures affect conscience, motor, sensory, and cognitive functions. The treatment with available antiepileptic drugs does not display a complete therapeutic efficiency, as it is still observed the presence of refractory patients. In this context, the cannabidiol (CBD), by interfering in the information flow between neurons, acts therapeutically preventing overload. In the central nervous system, CBD acts in the CB1 receptors, present in GABAergic inhibitory neurons and glutamatergic excitatory neurons. Evidence from an electronic research performed in 2015, with 117 parents of children with refractory epilepsy that used cannabidiol, displayed that seizures were reduced by 85%, including 14% with total suppression. Conclusion: The studies show that CBD, by acting with specific neuronal receptors, decreases cerebral hyperexcitability. Therefore, this therapeutic alternative may improve the physical and emotional well-being of refractory epileptics.
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Myllylä, T., A. Popov, L. Surażyński, J. Oinas, O. Bibikova, A. Bykov, M. S. Wróbel, et al. "Optical properties of the chemotherapy drugs used in the central nervous system lymphoma therapy: monitoring drug delivery." In European Conference on Biomedical Optics. Washington, D.C.: OSA, 2015. http://dx.doi.org/10.1364/ecbo.2015.95400q.

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Myllylä, T., A. Popov, L. Surazyński, J. Oinas, O. Bibikova, A. Bykov, M. S. Wróbel, et al. "Optical properties of the chemotherapy drugs used in the central nervous system lymphoma therapy: monitoring drug delivery." In European Conferences on Biomedical Optics, edited by Arjen Amelink and I. Alex Vitkin. SPIE, 2015. http://dx.doi.org/10.1117/12.2183765.

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Lueshen, Eric, Indu Venugopal, and Andreas Linninger. "Intrathecal Magnetic Drug Targeting: A New Approach to Treating Diseases of the Central Nervous System." In ASME 2013 2nd Global Congress on NanoEngineering for Medicine and Biology. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/nemb2013-93117.

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Intrathecal (IT) drug delivery is a standard technique which involves direct injection of drugs into the cerebrospinal fluid (CSF)-filled space within the spinal canal to treat many diseases of the central nervous system. Currently, in order to reach the therapeutic drug concentration at certain locations within the spinal canal, high drug doses are used. With no method to deliver the large drug doses locally, current IT drug delivery treatments are hindered with wide drug distributions throughout the central nervous system (CNS) which cause harmful side effects. In order to overcome the current limitations of IT drug delivery, we have developed the novel method of intrathecal magnetic drug targeting (IT-MDT). Gold-coated magnetite nanoparticles are infused into a physiologically and anatomically relevant in vitro human spine model and then targeted to a specific site using external magnetic fields, resulting in a substantial increase in therapeutic nanoparticle localization at the site of interest. Experiments aiming to determine the effect of key parameters such as magnet strength, duration of magnetic field exposure, location of magnetic field, and ferrous implants on the collection efficiency of our superparamagnetic nanoparticles in the targeting region were performed. Our experiments indicate that intrathecal magnetic drug targeting and implant-assisted IT-MDT are promising techniques for concentrating and localizing drug-functionalized nanoparticles at required target sites within the spinal canal for potential treatment of diseases affecting the central nervous system.
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Jiang, WG, MD Mason, and RE Mansel. "Abstract P5-06-07: Artemisinin Disrupts the Barrier Function in Vascular Endothelial Cells, a Potential Implication in Improving Penetration of Therapeutic Drugs in the Central Nervous System." In Abstracts: Thirty-Third Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 8‐12, 2010; San Antonio, TX. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/0008-5472.sabcs10-p5-06-07.

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Kim, Jung Hwan, Garrett W. Astary, Thomas H. Mareci, and Malisa Sarntinoranont. "A Computational Model of Direct Infusion Into the Rat Brain: Corpus Callosum and Hippocampus." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-205945.

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Despite the high therapeutic potential of many macromolecular drugs, it has proven difficult to apply them to treatment of cancer and other degenerative diseases of the central nervous system (CNS) due to low capillary permeability and low diffusivity. To overcome these barriers, recent experimental studies have shown local infusion, i.e., convection-enhanced delivery (CED), to be a promising delivery technique in the brain and spinal cord [1–3]. Predictive models of extracellular fluid flow and transport during CED would be useful for treatment optimization and planning.
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Smith, Joshua H., and Jose Jaime García. "A Nonlinear Biphasic Model for Fluid Transport and Tissue Deformation During Constant Flow Rate Infusion Into Brain Tissue." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-204506.

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The delivery of therapeutic agents into the brain is impeded by the blood-brain barrier, preventing adequate treatment of diseases of the central nervous system. Convection enhanced delivery was developed as a means to deliver therapeutic agents directly into brain tissue and to transport the drugs in the extracellular space using convective flow. Poroelastic or biphasic models have been used to study the concomitant fluid transport and tissue deformation that occurs during infusion, however previous studies have been limited by the assumption of linear elasticity of the solid phase [1].
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Soares, Mariana, Ana Clara Mota Gonçalo, Kaline dos Santos Kishishita Castro, and Victoria de Menezes Sá Lazera. "Use of cannabidiol as a therapeutic method in epilepsy." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.388.

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Introduction: Cannabis sativa has several therapeutic properties and has been used for millennials for healing purposes. Among its benefits are analgesic, antiemetic and tranquilizing effects, acting strongly on the nervous system. Objective: This study aims to emphasize the importance of Cannabidiol as a therapeutic purpose for epilepsy, especially in Brazil, where its use is still controlled. Method: A systematic literature review, using bibliographic searches carried out in the electronic databases LILACS, PubMed and SciELO with the descriptors “cannabidiol” and “epilepsy”. Of 1645 searches found, 06 were used in the study. Results: Epileptic seizures can be generalized or partial and are determined by the affected area. The treatment for epilepsy are drugs that decrease the arousal capacity of neural tissue and a significant percentage of individuals cannot control them with traditional drugs alone. Endocannabinoids work in response to epileptiform activity, to activate CB1 receptors for excitatory neurons, to contain excess neuronal activity, which occurs during seizures. It is proven that patients who use it do not have toxic adverse effects. Conclusions: In Brazil, Cannabis is a controlled drug and the fact that it is imported, interfere in the treatment, who is interrupted while patient waits the new dosage. The importance of cannabidiol as a target for research and studies is verified, as it has ample potential in the treatment of epilepsy and reduces brain damage caused by it. In order that patients with epilepsy, have improvements in their quality of life.
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Shah, Vrutangkumar V., Sachin Goyal, and Harish Palanthandalam-Madapusi. "A Biomechanical Approach to Diagnosis and Monitoring of Parkinson’s Disease." In ASME 2015 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. American Society of Mechanical Engineers, 2015. http://dx.doi.org/10.1115/detc2015-46781.

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Parkinson’s disease is an idiopathic and degenerative disorder of the central nervous system. Among the symptoms, the tremor at rest is one of the prominent symptoms. The challenge however is that there are no definitive diagnostic test that can confirm the presence or severity of Parkinson’s disease. This is a serious handicap especially since the drugs usually prescribed to control these symptoms have serious side effects and their dosages have to be tuned extensively. Also, the exact origin of tremor is unknown. There have been recent efforts [19] to understand the mechanism behind the Parkinsonian tremor, from a control-system perspectives. From these efforts, it appears that increased sensorimotor loop delay may be a cause for Parkinsonian tremor and thus serve as a key distinguishing feature. In the current work, we adopted this hypothesis and with the help of a relatively straightforward analysis of the motor control loop along with the help of some simulation and experimental examples, we first attempt to explain several qualitative observations relating to Parkinson’s Disease. Further, we explore the possibilities of for progress tracking, diagnosis, and early diagnosis before onset of tremor using biomechanical means.
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