SCHIZOPHRENIA Factsheet September 2020

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SCHIZOPHRENIA Factsheet September 2020 What is adenosine? Adenosine modulates dopamine and glutamine which are both implicated in schizophrenia’s pathophysiology; therefore adenosine NeuRA (Neuroscience Research Australia) is one of modulators may be useful adjunctive treatments for schizophrenia. the largest independent medical Allopurinol is used for the treatment of gout and hyperuricemia; it and clinical research institutes in Australia and an international inhibits purine degradation and subsequently increases adenosine leader in neurological research. levels. Dipyridamole and propentofylline inhibit cellular reuptake of Diseases of the brain and adenosine and increases extracellular adenosine concentration. nervous system pose the greatest health, economic and social burden of any disease group because they are chronic, What is the evidence for adenosine? debilitating and have no known cures. Moderate to low quality evidence suggests adjunctive adenosine Medical research is the modulators (particularly dipyridamole and propentofylline) may improve cornerstone of efforts to advance the health and symptoms, particularly positive symptoms, in people with schizophrenia. wellbeing of families and the community. Our dedicated scientists are focussed on transforming their research into significant and practical benefits for all patients. While we hope you find this information useful, it is always important to discuss any questions about schizophrenia or its treatment with your doctor or other health care provider. For more information see the technical table We are able to make significant advances due to the generosity of countless people. Your donation allows us HOW YOUR to continue to work towards transforming lives. For information on how you can support our research, phone SUPPORT HELPS 1300 888 019 or make a secure donation at neura.edu.au/donate/schizophrenia. NeuRA (Neuroscience Research Australia) Foundation Margarete Ainsworth Building T 1300 888 019 F +61 2 9399 1082 Barker Street, Randwick NSW 2031 ABN 57 008 429 961 PO Box 1165 Randwick Sydney NSW 2031 Australia neura.edu.au.

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Npp2013223.Pdf
Neuropsychopharmacology (2014) 39, 499–506 & 2014 American College of Neuropsychopharmacology. All rights reserved 0893-133X/14 www.neuropsychopharmacology.org Chronic Administration of the Methylxanthine Propentofylline Impairs Reinstatement to Cocaine by a GLT-1-Dependent Mechanism ,1 1,2 1 1 1 Kathryn J Reissner* , Robyn M Brown , Sade Spencer , Phuong K Tran , Charles A Thomas and 1 Peter W Kalivas 1 2 Department of Neurosciences, Medical University of South Carolina, Charleston, SC, USA; Florey Institute of Neuroscience and Mental Health, University of Melbourne, Parkville, Australia In recent years, interactions between neurons and glia have been evaluated as mediators of neuropsychiatric diseases, including drug addiction. In particular, compounds that increase expression of the astroglial glutamate transporter GLT-1 (N-acetylcysteine and ceftriaxone) can decrease measures of drug seeking. However, it is unknown whether the compounds that influence broad measures of glial physiology can influence behavioral measures of drug relapse, nor is it clear whether the upregulated GLT-1 is functionally important for suppressing of drug seeking. To address these questions, we sought to determine whether the glial modulator and neuroprotective agent propentofylline (PPF) modifies drug seeking in rats using a reinstatement model of cocaine relapse. We found that 7 days of chronic (but not acute) administration of PPF significantly decreased both cue- and cocaine-induced reinstatement of cocaine seeking. We next determined whether the effect of systemic PPF on reinstatement depended upon its ability to restore expression of GLT-1 in the nucleus accumbens. PPF restored the cocaine-induced decrease in GLT-1 in the accumbens core; then, using an antisense strategy against glutamate transporter GLT-1, we found that restored transporter expression was necessary for PPF to inhibit cue-primed cocaine seeking.
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Structure-Activity Relationship and Mechanistic Studies on The
University of Tennessee Health Science Center UTHSC Digital Commons Theses and Dissertations (ETD) College of Graduate Health Sciences 12-2008 Structure-Activity Relationship and Mechanistic Studies on the Chemopreventive Activity of Dipyridamole and Its Analogues Ja’Wanda Shavon Grant University of Tennessee Health Science Center Follow this and additional works at: https://dc.uthsc.edu/dissertations Part of the Pharmacy and Pharmaceutical Sciences Commons Recommended Citation Grant, Ja’Wanda Shavon , "Structure-Activity Relationship and Mechanistic Studies on the Chemopreventive Activity of Dipyridamole and Its Analogues" (2008). Theses and Dissertations (ETD). Paper 100. http://dx.doi.org/10.21007/ etd.cghs.2008.0114. This Dissertation is brought to you for free and open access by the College of Graduate Health Sciences at UTHSC Digital Commons. It has been accepted for inclusion in Theses and Dissertations (ETD) by an authorized administrator of UTHSC Digital Commons. For more information, please contact [email protected]. Structure-Activity Relationship and Mechanistic Studies on the Chemopreventive Activity of Dipyridamole and Its Analogues Document Type Dissertation Degree Name Doctor of Philosophy (PhD) Program Pharmaceutical Sciences Research Advisor John K. Buolamwini, Ph.D. Committee Richard E. Lee, Ph.D. Duane Miller, Ph.D. David Nelson, Ph.D. Jie Zheng, Ph.D. DOI 10.21007/etd.cghs.2008.0114 This dissertation is available at UTHSC Digital Commons: https://dc.uthsc.edu/dissertations/100 STRUCTURE-ACTIVITY RELATIONSHIP AND
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Exploring the Glial Mechanisms Underlying Central Neuropathic Pain in a Novel Rat Model of Spinal Cord Injury
i Exploring the Glial Mechanisms Underlying Central Neuropathic Pain in a Novel Rat Model of Spinal Cord Injury by Amanda Lynne Ellis B.A., University of Colorado, 2006 M.A., University of Colorado, 2011 A thesis submitted to the Faculty of the Graduate School of the University of Colorado in partial fulfillment of the requirement of the degree of Doctor of Philosophy Department of Psychology and Neuroscience 2014 ii This thesis entitled: Exploring the Glial Mechanisms Underlying Central Neuropathic Pain in a Novel Rat Model of Spinal Cord Injury written by Amanda Lynne Ellis has been approved for the Department of Psychology and Neuroscience ___________________________________ Dr. Linda Watkins ______________________________________________ Dr. Steven Maier ___________________________________________ Dr. Serge Campeau _______________________________________________ Dr. Benjamin Greenwood _______________________________________________ Dr. Michael Stallings Date____________ The final copy of this thesis has been examined by the signatories, and we Find that both the content and the form meet acceptable presentation standards Of scholarly work in the above mentioned discipline iii Abstract Ellis, Amanda Lynne (Ph.D., Psychology and Neuroscience) Glial Mechanisms of Central Neuropathic Pain Thesis directed by Distinguished Professor Linda Watkins Neuropathic pain is a debilitating condition that is usually intractable to treatment. Spinal cord injury (SCI) is the leading cause of central neuropathic pain (CNP), and patients often describe their pain as severe and intolerable. Although most of the focus in the pain literature has been on neurons, it is now well known that non-neuronal cells of the central nervous system called microglia and astrocytes (herein referred to as “glial cells” or “glia”) play a key role in the induction and maintenance of neuropathic pain.
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Methylxanthines and Neurodegenerative Diseases: an Update
nutrients Review Methylxanthines and Neurodegenerative Diseases: An Update Daniel Janitschke 1,† , Anna A. Lauer 1,†, Cornel M. Bachmann 1, Heike S. Grimm 1, Tobias Hartmann 1,2 and Marcus O. W. Grimm 1,2,* 1 Experimental Neurology, Saarland University, 66421 Homburg/Saar, Germany; [email protected] (D.J.); [email protected] (A.A.L.); [email protected] (C.M.B.); [email protected] (H.S.G.); [email protected] (T.H.) 2 Deutsches Institut für DemenzPrävention (DIDP), Saarland University, 66421 Homburg/Saar, Germany * Correspondence: [email protected] † These authors contributed equally to this work. Abstract: Methylxanthines (MTX) are purine derived xanthine derivatives. Whereas naturally occurring methylxanthines like caffeine, theophylline or theobromine are widely consumed in food, several synthetic but also non-synthetic methylxanthines are used as pharmaceuticals, in particular in treating airway constrictions. Besides the well-established bronchoprotective effects, methylxanthines are also known to have anti-inﬂammatory and anti-oxidative properties, mediate changes in lipid homeostasis and have neuroprotective effects. Known molecular mechanisms include adenosine receptor antagonism, phosphodiesterase inhibition, effects on the cholinergic system, wnt signaling, histone deacetylase activation and gene regulation. By affecting several pathways associated with neurodegenerative diseases via different pleiotropic mechanisms and due to its moderate side effects, intake of methylxanthines have been suggested to be an interesting approach in dealing with neurodegeneration. Especially in the past years, the impact of methylxanthines in neurodegenerative diseases has been extensively studied and several new aspects have been elucidated. In this review Citation: Janitschke, D.; Lauer, A.A.; Bachmann, C.M.; Grimm, H.S.; we summarize the ﬁndings of methylxanthines linked to Alzheimer´s disease, Parkinson’s disease Hartmann, T.; Grimm, M.O.W.
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Federal Register / Vol. 60, No. 80 / Wednesday, April 26, 1995 / Notices DIX to the HTSUS—Continued
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(12) Patent Application Publication (10) Pub. No.: US 2003/0068365A1 Suvanprakorn Et Al
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Stembook 2018.Pdf
The use of stems in the selection of International Nonproprietary Names (INN) for pharmaceutical substances FORMER DOCUMENT NUMBER: WHO/PHARM S/NOM 15 WHO/EMP/RHT/TSN/2018.1 © World Health Organization 2018 Some rights reserved. This work is available under the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 IGO licence (CC BY-NC-SA 3.0 IGO; https://creativecommons.org/licenses/by-nc-sa/3.0/igo). Under the terms of this licence, you may copy, redistribute and adapt the work for non-commercial purposes, provided the work is appropriately cited, as indicated below. In any use of this work, there should be no suggestion that WHO endorses any specific organization, products or services. The use of the WHO logo is not permitted. If you adapt the work, then you must license your work under the same or equivalent Creative Commons licence. If you create a translation of this work, you should add the following disclaimer along with the suggested citation: “This translation was not created by the World Health Organization (WHO). WHO is not responsible for the content or accuracy of this translation. The original English edition shall be the binding and authentic edition”. Any mediation relating to disputes arising under the licence shall be conducted in accordance with the mediation rules of the World Intellectual Property Organization. Suggested citation. The use of stems in the selection of International Nonproprietary Names (INN) for pharmaceutical substances. Geneva: World Health Organization; 2018 (WHO/EMP/RHT/TSN/2018.1). Licence: CC BY-NC-SA 3.0 IGO. Cataloguing-in-Publication (CIP) data.
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Technical Commentary
TECHNICAL COMMENTARY Adenosine modulators Introduction less stringent reporting checklists than the PRISMA, and that some reviews may have Adenosine modulates dopamine and glutamine been limited by journal guidelines. which are both implicated in schizophrenia’s pathophysiology; therefore adenosine Evidence was graded using the Grading of modulators may be useful adjunctive Recommendations Assessment, Development treatments for schizophrenia. Allopurinol is and Evaluation (GRADE) Working Group used for the treatment of gout and approach where high quality evidence such as hyperuricemia; it inhibits purine degradation that gained from randomised controlled trials and subsequently increases adenosine levels. (RCTs) may be downgraded to moderate or low Dipyridamole and propentofylline inhibit cellular if review and study quality is limited, if there is reuptake of adenosine and increases inconsistency in results, indirect comparisons, extracellular adenosine concentration. imprecise or sparse data and high probability of reporting bias. It may also be downgraded if Method risks associated with the intervention or other We have included only systematic reviews matter under review are high. Conversely, low (systematic literature search, detailed quality evidence such as that gained from methodology with inclusion/exclusion criteria) observational studies may be upgraded if effect published in full text, in English, from the year sizes are large or if there is a dose dependent 2000 that report results separately for people response. We have also taken into account with a diagnosis of schizophrenia, sample size and whether results are consistent, schizoaffective disorder, schizophreniform precise and direct with low associated risks disorder or first episode schizophrenia. (see end of table for an explanation of these Reviews were identified by searching the terms)2.
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A Placebo Controlled Study of the Propentofylline Added to Risperidone in Chronic Schizophrenia
Available online at www.sciencedirect.com Progress in Neuro-Psychopharmacology & Biological Psychiatry 32 (2008) 726–732 www.elsevier.com/locate/pnpbp A placebo controlled study of the propentofylline added to risperidone in chronic schizophrenia Samarand Salimi a, Akbar Fotouhi b, Abolfazl Ghoreishi c, Mohammad-Kamran Derakhshan d, Mohammad-Reza Khodaie-Ardakani d, Mohammad-Reza Mohammadi a, Ahmad-Ali Noorbala a, Seyed-Ali Ahmadi-Abhari a, Mohammad Hajiazim e, ⁎ Seyed-Hesameddin Abbasi f, Shahin Akhondzadeh a, a Psychiatric Research Center, Roozbeh Psychiatric Hospital, Tehran University of Medical Sciences, Tehran, Iran b Department of Epidemiology and Biostatistics, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran c Departement of Psychiatry, Zanjan University of Medical Sciences, Zanjan, Iran d Razi Psychiatric Hospital, Welfare Sciences University, Iran e Semnan University of Medical Sciences, Garmsar, Iran f National Iranian Oil Company, Central Hospital, Tehran, Iran Received 10 August 2007; received in revised form 9 November 2007; accepted 17 November 2007 Available online 23 November 2007 Abstract Impaired activity of the purinergic system is a plausible common factor that could be responsible for many aspects of schizophrenia. Based on purinegic hypothesis of schizophrenia, pharmacological treatments enhancing adenosine activity could be effective treatment in schizophrenia. Propentofylline is a novel xantine derivative which is being developed for treatment of degenerative and vascular dementia. It enhances extracellular adenosine level via inhibition of adenosine uptake. The purpose of the present investigation was to assess the efficacy of propentofylline as an adjuvant agent in the treatment of chronic schizophrenia in an 8-week double blind and placebo controlled trial.
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Wo 2007/120485 A2
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