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Trinity College Dublin

Personal Information
College Photo Name Harkin, Andrew
Main Department Pharmacy
College Title Associate Professor in Pharmacology
E-mail aharkin@tcd.ie
College Tel +353 1 896 2807
Web http://people.tcd.ie/aharkin
Fax +353 1 896 2810
 
Biography
Andrew Harkin is Associate Professor of Pharmacology in The School of Pharmacy & Pharmaceutical Sciences in Trinity College Dublin and a principle investigator in Trinity College Institute of Neuroscience. He leads a neuropsychopharmacology research group which is focused on bridging neuroscience to the pharmacological treatment of psychiatric and neurological disorders. Current research interests include- - bidirectional nervous system immune interactions, the role of inflammation in the pathogenesis, and potential of anti-inflammatory agents in treating, psychiatric disorders. - targeting the N-methyl-D-aspartic acid (NMDA) receptor and the NMDA-nitric oxide-cGMP intra-neuronal signalling in stress related psychiatric disorders. Professor Harkin’s research program is funded by the European Commission (Framework 7), Science Foundation Ireland, the Irish Health Research Board and the Irish Research Council for Science Engineering and Technology, His group collaborates widely with a variety of academic and industrial partners on fundamental and clinical projects.
 
Membership of Professional Institutions, Associations, Societies
Details Date From Date To
Psychoneuroimmunology Research Society 2010 present
Collegium Internationale Neuro-Psychopharmacologicum 2003 present
British Pharmacological Society 2003 present
British Association for Psychopharmacology 1997 present
Neuroscience Ireland 2012 Present
 
Awards and Honours
Award Date
Health Research Board career development fellowship 2002
CINP Young Investigator Award. 2004
Fellowship Trinity College Dublin 2011
 
Description of Research Interests
My research falls within the remit of Neuropsychopharmacology, a discipline that links basic neuroscience to the pharmacological treatment of psychiatric and neurological disease. Selected examples of projects in these areas are outlined below: 1. Marie Curie Initial Training Networks (ITN): FP7-PEOPLE-2012-ITN Brain Imaging Return to Health “reBIRTH” see http://www.rbirth.eu/). The r’BIRTH consortium is a Marie Curie Initial Training Network that gathers experts on molecular mechanisms of age-associated pathologies including neurodegeneration and depression. They work together to identify stress-regulated molecules provoking neuronal atrophy and hindering neurogenesis (birth of new neurons), and monitor the consequences of these processes in human brain that contribute to cognitive decline and increased depressive and anxiety disorders associated with ageing. The work is funded by the European Commission (FP7) under the sub-programme PEOPLE (Marie Curie Actions). 16 early stage researchers will be trained in the topics of the programme i.e. molecular imaging (MRI), proteomics, immunotechnology, high content screening, molecular neuroscience, neuropharmacology and patient studies. The training is provided by seven universities, two private companies and one non-profit research organisation from 7 European countries. 2. Early diagnosis, treatment and prevention of mood disorders targeting the activated inflammatory response system [Acronym: MOODINFLAME] Our research group is funded under EU FP7 as part of a collaborative, large-scale research project entitled “Early diagnosis, treatment and prevention of mood disorders targeting the activated inflammatory response system. [Acronym: MOODINFLAME]. A consortium of 14 European Universities/Research Institutes and 4 SMEs have come together for this project with the overall objective of developing biomarker tests for mood disorder patients based on an activated inflammatory response system (IRS) and inflammation-mediated disturbances in tryptophan metabolism. As part of this programme patients are treated with drugs to counteract the consequences of an activated IRS/disturbed metabolism of tryptophan. The project leads to an enhanced understanding of the pathogenesis of inflammation-related mood disorders, and of the mechanism of anti-inflammatory drugs and drugs targeting tryptophan metabolism in treating depressive behaviour. 3. Neuronal nitric oxide synthase (nNOS): a novel target for antidepressant action. Inhibition of NMDA-R has shown considerable promise as a drug target to produce new antidepressants that work faster, and are more effective than existing antidepressants. We hypothesise that targeting signalling events down-stream of NMDA-R may provide a more viable approach. nNOS is a down stream target of NMDA-R. We have published a number of original papers demonstrating that 1) NOS inhibitors have antidepressant properties 2) such properties are dependent on endogenous serotonin and 3) NOS inhibitors can augment the effects of conventional antidepressants in preclinical models. Currently our research is assessing the efficacy of nNOS inhibitors as novel antidepressant agents. A future aim is to determine if uncoupling the NMDA-R from nNOS can elicit antidepressant actions. This work is funded by the Health research board.
 
Research Interests
Addiction and substance abuse Depression Emotional, behavioural and cognitive disorders Imaging Techniques
In vitro testing, trial methods Neurobiology Neurochemistry and neuropharmacology Neuropharmacology
Neuroscience Psychiatry
 
Research Projects
Project title Brain Imaging Return to Health
Summary Marie Curie Initial Training Networks (ITN): FP7-PEOPLE-2012-ITN Brain Imaging Return to Health “reBIRTH” (see http://www.rbirth.eu/) The r’BIRTH consortium is a Marie Curie Initial Training Network that gathers experts on molecular mechanisms of age-associated pathologies including neurodegeneration and depression. They work together to identify stress-regulated molecules provoking neuronal atrophy and hindering neurogenesis, and monitor the consequences of these processes in human brain. At the cellular level, diminished birth of new neurons (neurogenesis) contributes to cognitive decline and increased depressive and anxiety disorders that are associated with ageing. The work is funded by the European Commission (FP7) under the sub-programme PEOPLE (Marie Curie Actions). 16 early stage researchers will be trained in the topics of the programme i.e. molecular imaging (MRI), proteomics, immunotechnology, high content screening, molecular neuroscience, neuropharmacology and patient studies. The training is provided by seven universities, two private companies and one non-profit research organisation from 7 European countries.
Funding Agency European Commission
Programme Marie Curie Initial Training Network
Type of Project Research
Date from 2014
Date to 2018
Person Months 48


Project title Early diagnosis, treatment and prevention of mood disorders targeting the activated inflammatory response system.
Summary [Acronym: MOODINFLAME] 2008-2013. A collaborative, large-scale focused research project entitled “Early diagnosis, treatment and prevention of mood disorders targeting the activated inflammatory response system. [Acronym: MOODINFLAME]. A consortium of 14 European Universities/Research Institutes and 4 SMEs have come together for this project with the overall objective of developing biomarker tests for mood disorder patients based on an activated inflammatory response system (IRS) and inflammation-mediated disturbances in tryptophan metabolism. As part of this programme patients are treated with drugs to counteract the consequences of an activated IRS/disturbed metabolism of tryptophan. The project leads to an enhanced understanding of the pathogenesis of inflammation-related mood disorders, and of the mechanism of anti-inflammatory drugs and drugs targeting tryptophan metabolism in treating depressive behaviour.
Funding Agency EU 7th Framework
Programme FP7- HEALTH-2007-2.2.1-8: From mood disorders to experimental models
Type of Project Research
Date from 2008
Date to 2012
Person Months 48


Project title Neuronal nitric oxide synthase: A novel target for antidepressant activity
Summary Inhibition of N-methyl-D-aspartic acid receptors (NMDA-R) has shown considerable promise as a drug target to produce new antidepressants that work faster, and are more effective than existing antidepressants. However, targeting NMDA-R directly is problematic due to adverse effects. We hypothesise that targeting signalling events down-stream of NMDA-R may provide a more viable approach. nNOS is a down stream target of NMDA-R. We have published a number of original papers demonstrating that 1) NOS inhibitors have antidepressant properties 2) such properties are dependent on endogenous serotonin and 3) NOS inhibitors can augment the effects of conventional antidepressants in preclinical models. Currently our research is assessing the efficacy of nNOS inhibitors as novel antidepressant agents. A future aim is to determine if uncoupling the NMDA-R from nNOS can elicit antidepressant actions.
Funding Agency Health Research Board
Programme Research Project Grant
Type of Project
Date from 2008
Date to 2012
Person Months 48


Project title Caffeine exacerbates the acute toxicity of 3,4 methylenedioxymethamphetamine (MDMA; “Ecstasy”): A role for dopamine ?
Summary Co-administration of caffeine profoundly enhances the acute toxicity of MDMA. This project will elucidate the mechanism underlying a potentially serious drug interaction between caffeine and MDMA and clarify risks associated with the concurrent consumption of caffeine with other drugs which increase dopaminergic transmission.
Funding Agency Health Research Board
Programme Research Project Grant
Type of Project
Date from 2006
Date to 2009
Person Months 36


 
Publications and Other Research Outputs
Peer Reviewed
Doucet MV, Harkin A, Dev KK, The PSD-95/nNOS Complex: New Drugs for Depression?, Pharmacology & Therapeutics, 133, 2012, p218 - 229
TARA - Full Text
Vanattou-Saifoudine N, McNamara R, Harkin A, Caffeine provokes adverse interactions with MDMA ("Ecstasy") and related psychostimulants: mechanisms and mediators, British Journal of Pharmacology, 2012, pEpub ahead of print
E.N. McNamee, K.M. Ryan, E.W. Griffin, R.E. González-Reyes, K.J. Ryan, A. Harkin and T.J. Connor, Noradrenaline acting at central beta-adrenoceptors induces interleukin-10 and suppressor of cytokine signaling-3 expression in rat brain: Implications for neurodegeneration, Brain Behavior and Immunity, 24, (4), 2010, p660 - 671
Notes: [PubMed ID: 20193756]
DOI
L.C. Gleeson, K.J. Ryan, E.W. Griffin, T.J. Connor and A. Harkin, The beta2-adrenoceptor agonist clenbuterol elicits neuroprotective, anti-inflammatory and neurotrophic actions in the kainic acid model of excitotoxicity , Brain Behavior and Immunity, 24, (8), 2010, p1354 - 1361
DOI
Vanattou-Saifoudine N, McNamara R, Harkin A., Mechanisms mediating the ability of caffeine to influence MDMA ("Ecstasy")-induced hyperthermia in rats. , British Journal of Pharmacology, 160, 2010, p860 - 877
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Last Updated:23-SEP-2014