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B.Sc. M.Sc. D.Phil.
Royal Society Research Fellow
- Associate Professor
- Supernumerary Fellow, University College
Understanding links between genes and brain dysfunction in psychiatric illness
My group's research aims to understand how individual genes impact on the complex brain functions that are altered in psychiatric disorders. I believe that understanding these links will help to explain why some people respond well to treatments, whilst others do not, and will ultimately lead to new and improved therapies.
My research focuses on genes that affect the function of dopamine, a chemical messenger which is implicated in a number of psychiatric disorders and is critical to many different aspects of brain function in healthy people. In order to do this I use a wide range of experimental techniques, which allows me to study the function of these genes at all levels - from individual cells to the whole person. In order to achieve this, I collaborate with many other researchers within the Department, elsewhere in Oxford, and internationally.
Most of my group’s research to date has focussed on the COMT gene. We have shown that a drug that inhibits COMT increases dopamine levels in the brain and improve memory and attention. Most recently, we showed that a person’s genetic make-up determines whether the drug will improve memory or not. These findings show that inhibiting COMT could be beneficial for disorders in which patients suffer from problems with memory and attention, such as schizophrenia. They also emphasise that genetic factors can dramatically influence the response to a drug and suggest that in the future successful therapies may need to take a person’s individual genetic make-up into account.
Our current research focusses on how COMT and other dopamine genes regulate brain functions beyond memory and attention, looking in particular their effect on peoples’ emotions and responses to rewards. In addition, we are also investigating how these links are altered by environmental factors, such as exposure to cannabis and stress. My long-term goal is to use this knowledge to improve the lives of patients living with psychiatric disorders.
Key Publications5 False False
The role of catechol-O-methyltransferase in reward processing and addiction.
Tunbridge EM. et al, (2012), CNS Neurol Disord Drug Targets, 11, 306 - 323
COMT Val(158)Met genotype determines the direction of cognitive effects produced by catechol-O-methyltransferase inhibition.
Farrell SM. et al, (2012), Biol Psychiatry, 71, 538 - 544
Catechol-O-methyltransferase (COMT) influences the connectivity of the prefrontal cortex at rest.
Tunbridge EM. et al, (2013), Neuroimage, 68, 49 - 54
Human plasma homocysteine levels are associated with the catechol-O-methyltransferase Val158Met polymorphism
Tunbridge EM. et al, (2007), BIOLOGICAL PSYCHIATRY, 61, 191S - 191S
Catechol-o-methyltransferase, cognition, and psychosis: Val158Met and beyond.
Tunbridge EM. et al, (2006), Biol Psychiatry, 60, 141 - 151
Reduced cerebrovascular reactivity in young adults carrying the APOE ε4 allele.
Suri S. et al, (2015), Alzheimers Dement, 11, 648 - 57.e1
Modulation of hippocampal theta and hippocampal-prefrontal cortex function by a schizophrenia risk gene.
Cousijn H. et al, (2015), Hum Brain Mapp, 36, 2387 - 2395
How cannabis causes paranoia: using the intravenous administration of ∆9-tetrahydrocannabinol (THC) to identify key cognitive mechanisms leading to paranoia.
Freeman D. et al, (2015), Schizophr Bull, 41, 391 - 399
Modulation of hippocampal theta and hippocampal-prefrontal cortex function by a schizophrenia risk gene
Cousijn H. et al, (2015), Human Brain Mapping, 36, 2387 - 2395
Decreased striatal dopamine in group II metabotropic glutamate receptor (mGlu2/mGlu3) double knockout mice
Lane TA. et al, (2013), BMC NEUROSCIENCE, 14