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Elizabeth M. Tunbridge

Researcher at University of Oxford

Publications -  80
Citations -  4759

Elizabeth M. Tunbridge is an academic researcher from University of Oxford. The author has contributed to research in topics: Catechol-O-methyl transferase & Bipolar disorder. The author has an hindex of 31, co-authored 72 publications receiving 4153 citations. Previous affiliations of Elizabeth M. Tunbridge include Oxford Health NHS Foundation Trust & United States Department of Health and Human Services.

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Journal ArticleDOI

Catechol-o-methyltransferase, cognition, and psychosis: Val158Met and beyond.

TL;DR: Preliminary data indicating that catechol-o-methyltransferase is a promising therapeutic target for ameliorating the cognitive deficits associated with schizophrenia are outlined.
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Catechol-o-methyltransferase inhibition improves set-shifting performance and elevates stimulated dopamine release in the rat prefrontal cortex.

TL;DR: It is concluded that COMT activity specifically affects ED set shifting and is a significant modulator of mPFC DA but not NE under conditions of increased catecholaminergic transmission, suggesting that the links between COMTActivity and PFC function can be modeled in rats and may be specifically mediated by DA.
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Tau protein is required for amyloid {beta}-induced impairment of hippocampal long-term potentiation

TL;DR: Results show that tau protein is required for Aβ to impair synaptic plasticity in the hippocampus and suggest that the Aβ-induced impairment of LTP is mediated by tau phosphorylation, and conclude that preventing the interaction between Aβ and tau could be a promising strategy for treating cognitive impairment in MCI and early AD.
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Catechol-O-Methyltransferase (COMT): A Gene Contributing to Sex Differences in Brain Function, and to Sexual Dimorphism in the Predisposition to Psychiatric Disorders

TL;DR: There are accumulating and in places compelling data showing that COMT differentially impacts on brain function and dysfunction in men and women, and it is anticipated that additional evidence will emerge for sexual dimorphisms not only in COMT but also in many other autosomal genes.
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Tryptophan depletion alters the decision-making of healthy volunteers through altered processing of reward cues.

TL;DR: The results suggest that serotonin mediates decision-making in healthy volunteers by modulating the processing of reward cues, perhaps represented within the orbitofrontal cortex.