ORCID Profile
0000-0001-8257-1517
Current Organisation
University of Cambridge
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Publisher: Elsevier
Date: 2009
Publisher: Royal College of Psychiatrists
Date: 08-2006
DOI: 10.1192/BJP.BP.105.015263
Abstract: The psychosis-inducing effect of ketamine is important evidence supporting the glutamate hypothesis of schizophrenia. However, the symptoms the drug produces have not been described systematically. To examine the effects of ketamine in healthy people using a structured psychiatric interview. Ketamine (200 ng/ml) or placebo was administered by continuous infusion to 15 healthy volunteers. Symptoms were rated using the Present State Examination, the Thought, Language and Communication Scale and the Scale for Assessment of Negative Symptoms. Ketamine induced a range of perceptual distortions, but not hallucinations. Referential ideas were seen in nearly half the s le. There were only mild and infrequent ratings on the thought disorder scale. Affective flattening and alogia were seen in some volunteers. Ketamine does not reproduce the full picture of schizophrenia. The main point of similarity concerns referential thinking. Phenomena resembling negative symptoms are also seen, but the distinction of these from the drug's sedative effects requires further elucidation.
Publisher: Elsevier BV
Date: 2016
Publisher: Frontiers Media SA
Date: 26-08-2015
Publisher: Elsevier BV
Date: 06-2011
DOI: 10.1016/J.NEUROPSYCHOLOGIA.2011.03.037
Abstract: Mild cognitive impairment (MCI) patients report memory problems greater than those normally expected with ageing, but do not fulfil criteria for clinically probable Alzheimer's disease. Accumulating evidence demonstrates that impaired performance on the Paired Associates Learning (PAL) test from the Cambridge Neuropsychological Test Automated Battery (CANTAB) may be sensitive and specific for early and differential diagnosis of Alzheimer's disease. We adapted the basic CANTAB PAL task for functional magnetic resonance imaging (fMRI) in order to examine the functional brain deficits, at encoding and retrieval separately, in patients with MCI compared to healthy matched volunteers. As well as investigating the main effects of encoding and retrieval, we characterized neural responses in the two groups to increasing memory load. We focused on changes in BOLD response in the hippoc us and related structures, as an a priori region of interest based on what is known about the neuropathology of the early stages of Alzheimer's disease and previous information on the neural substrates of the PAL task. We also used structural MRI in the same patients to assess accompanying structural brain abnormalities associated with MCI. In terms of the BOLD response, the bilateral hippoc al activation in the MCI and control groups depended upon load, the MCI patients activating significantly more than controls at low loads and significantly less at higher loads. There were no other differences between MCI patients and controls in terms of the neural networks activated during either encoding or retrieval of the PAL task, including the prefrontal, cingulate and temporal cortex. The functional deficit in hippoc al activation in the MCI patients was accompanied by structural differences in the same location, suggesting that the decrease in hippoc al activation may be caused by a decrease in the amount of grey matter. This is one of the first studies to have used both encoding and retrieval phases of a memory paradigm for fMRI in MCI patients, and to have shown that the BOLD response in MCI patients can show both hyperactivation and hypoactivation in the same in iduals as a function of memory load and encoding/retrieval. The findings suggest that performance on PAL might be a useful cognitive biomarker for early detection of Alzheimer's disease, especially when used in conjunction with neuroimaging.
Publisher: Springer Science and Business Media LLC
Date: 07-08-2007
Publisher: Springer Science and Business Media LLC
Date: 19-02-2008
Publisher: Oxford University Press (OUP)
Date: 31-10-2014
DOI: 10.1093/IJNP/PYU010
Publisher: Frontiers Media SA
Date: 2009
Publisher: Society for Neuroscience
Date: 18-06-2008
Publisher: Elsevier BV
Date: 2016
Publisher: Springer Science and Business Media LLC
Date: 21-08-2014
DOI: 10.1038/NPP.2014.210
Publisher: Elsevier BV
Date: 11-1999
Publisher: Elsevier BV
Date: 03-2000
Publisher: Oxford University Press (OUP)
Date: 21-07-2008
Publisher: Oxford University Press (OUP)
Date: 12-02-2010
Publisher: Oxford University Press (OUP)
Date: 09-2007
DOI: 10.1093/BRAIN/AWM173
Publisher: Proceedings of the National Academy of Sciences
Date: 18-02-2014
Abstract: Many influential models in economics, finance, and neurobiology assume risk preferences are a stable trait. In this study we find they are not. We examine the effects of chronic stress on financial risk taking by raising cortisol levels in volunteers over an 8-d period using in idually tailored hydrocortisone regimens. We find that they become more risk-averse and that the overweighting of small probabilities becomes more exaggerated among men relative to women. We designed our protocol to maintain ecological validity: The increase in cortisol among participants replicated levels we had previously observed in real traders when faced with uncertainty and market volatility. Physiology-induced shifts in risk preferences may thus be a cause of market instability that has been hitherto overlooked by economists, risk managers, and central bankers.
Publisher: Springer Science and Business Media LLC
Date: 28-12-2015
DOI: 10.1038/NPP.2015.370
Location: United Kingdom of Great Britain and Northern Ireland
No related grants have been discovered for Paul Fletcher.