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Impaired prosodic discrimination in patients with schizophrenia
Tracy Derek
Annals of General Psychiatry , 2006, DOI: 10.1186/1744-859x-5-s1-s209
Neuroimaging of prosodic comprehension
Tracy Derek,Shergill Sukhwinder
Annals of General Psychiatry , 2006, DOI: 10.1186/1744-859x-5-s1-s131
Mechanisms Underlying Auditory Hallucinations—Understanding Perception without Stimulus
Derek K. Tracy,Sukhwinder S. Shergill
Brain Sciences , 2013, DOI: 10.3390/brainsci3020642
Abstract: Auditory verbal hallucinations (AVH) are a common phenomenon, occurring in the “healthy” population as well as in several mental illnesses, most notably schizophrenia. Current thinking supports a spectrum conceptualisation of AVH: several neurocognitive hypotheses of AVH have been proposed, including the “feed-forward” model of failure to provide appropriate information to somatosensory cortices so that stimuli appear unbidden, and an “aberrant memory model” implicating deficient memory processes. Neuroimaging and connectivity studies are in broad agreement with these with a general dysconnectivity between frontotemporal regions involved in language, memory and salience properties. Disappointingly many AVH remain resistant to standard treatments and persist for many years. There is a need to develop novel therapies to augment existing pharmacological and psychological therapies: transcranial magnetic stimulation has emerged as a potential treatment, though more recent clinical data has been less encouraging. Our understanding of AVH remains incomplete though much progress has been made in recent years. We herein provide a broad overview and review of this.
Passive processing of visual and auditory stimuli in the young and elderly: a neuroimaging study
Joyce Dan,Tracy Derek,Dannhauser Thomas,Shergill Sukhwinder
Annals of General Psychiatry , 2006, DOI: 10.1186/1744-859x-5-s1-s87
Beyond Dopamine: Glutamate as a Target for Future Antipsychotics
Kyra-Verena Sendt,Giovanni Giaroli,Derek K. Tracy
ISRN Pharmacology , 2012, DOI: 10.5402/2012/427267
Beyond Dopamine: Glutamate as a Target for Future Antipsychotics
Kyra-Verena Sendt,Giovanni Giaroli,Derek K. Tracy
ISRN Pharmacology , 2012, DOI: 10.5402/2012/427267
Abstract: The dopamine hypothesis of schizophrenia remains the primary theoretical framework for the pharmacological treatment of the disorder. Despite various lines of evidence of dopaminergic abnormalities and reasonable efficacy of current antipsychotic medication, a significant proportion of patients show suboptimal treatment responses, poor tolerability, and a subsequent lack of treatment concordance. In recent decades, intriguing evidence for the critical involvement of other neurotransmitter systems in the pathophysiology of schizophrenia has emerged, most notably of dysfunctions within the glutamate pathways. Consequently, the glutamate synapse has arisen as a promising target for urgently needed novel antipsychotic compounds—particularly in regards to debilitating negative and cognitive symptoms poorly controlled by currently available drugs. In this paper, recent findings integrating glutamatergic and dopaminergic abnormalities in schizophrenia and their implications for novel pharmacological targets are discussed. An overview of compounds in various stages of development is given: drugs enhancing NMDA receptor function as well as metabotropic glutamate receptor (mGluR) agonist and positive allosteric modulators (PAMs) are emphasised. Together with other agents more indirectly affecting glutamatergic neurotransmission, their potential future role in the pharmacotherapy of schizophrenia is critically evaluated. 1. Introduction Since the development of chlorpromazine in the 1950s antipsychotic drugs have been the primary treatment choice for schizophrenia [1]. The common pharmacological antagonism of dopamine (DA) D2 receptors by all antipsychotics and direct link with clinical improvement led to the theory of excess dopaminergic neurotransmission precipitating psychotic states [2–4]. Later, advances in animal, postmortem, and neuroimaging studies led to refinements of the dopamine hypothesis and a regional specificity of abnormal DA signalling was proposed. Negative symptoms of schizophrenia (such as anhedonia, flat or blunted affect, alogia, and avolition) as well as cognitive impairments (including deficits in executive functions, attention, and working memory) were postulated to be caused by deficiencies in DA transmission at D1 receptors in mesocortical projections to the prefrontal cortex (PFC). This dysregulation in cortical DA pathways, through a reciprocal relationship with subcortical DA projections, was hypothesised to cause a hyperdopaminergic state at D2 receptors in mesolimbic DA projections, resulting in positive symptoms of the disorder
Protein Tyrosine Phosphatase PTP1B Is Involved in Hippocampal Synapse Formation and Learning
Federico Fuentes, Derek Zimmer, Marybless Atienza, Jamie Schottenfeld, Ian Penkala, Tracy Bale, Kendra K. Bence, Carlos O. Arregui
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0041536
Abstract: ER-bound PTP1B is expressed in hippocampal neurons, and accumulates among neurite contacts. PTP1B dephosphorylates ?-catenin in N-cadherin complexes ensuring cell-cell adhesion. Here we show that endogenous PTP1B, as well as expressed GFP-PTP1B, are present in dendritic spines of hippocampal neurons in culture. GFP-PTP1B overexpression does not affect filopodial density or length. In contrast, impairment of PTP1B function or genetic PTP1B-deficiency leads to increased filopodia-like dendritic spines and a reduction in mushroom-like spines, while spine density is unaffected. These morphological alterations are accompanied by a disorganization of pre- and post-synapses, as judged by decreased clustering of synapsin-1 and PSD-95, and suggest a dynamic synaptic phenotype. Notably, levels of ?-catenin-Tyr-654 phosphorylation increased ~5-fold in the hippocampus of adult PTP1B?/? (KO) mice compared to wild type (WT) mice and this was accompanied by a reduction in the amount of ?-catenin associated with N-cadherin. To determine whether PTP1B-deficiency alters learning and memory, we generated mice lacking PTP1B in the hippocampus and cortex (PTP1Bfl/fl–Emx1-Cre). PTP1Bfl/fl–Emx1-Cre mice displayed improved performance in the Barnes maze (decreased time to find and enter target hole), utilized a more efficient strategy (cued), and had better recall compared to WT controls. Our results implicate PTP1B in structural plasticity within the hippocampus, likely through modulation of N-cadherin function by ensuring dephosphorylation of ?-catenin on Tyr-654. Disruption of hippocampal PTP1B function or expression leads to elongation of dendritic filopodia and improved learning and memory, demonstrating an exciting novel role for this phosphatase.
Amphetamine Sensitization Alters Reward Processing in the Human Striatum and Amygdala
Owen G. O’Daly, Daniel Joyce, Derek K. Tracy, Adnan Azim, Klaas E. Stephan, Robin M. Murray, Sukhwinder S. Shergill
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0093955
Abstract: Dysregulation of mesolimbic dopamine transmission is implicated in a number of psychiatric illnesses characterised by disruption of reward processing and goal-directed behaviour, including schizophrenia, drug addiction and impulse control disorders associated with chronic use of dopamine agonists. Amphetamine sensitization (AS) has been proposed to model the development of this aberrant dopamine signalling and the subsequent dysregulation of incentive motivational processes. However, in humans the effects of AS on the dopamine-sensitive neural circuitry associated with reward processing remains unclear. Here we describe the effects of acute amphetamine administration, following a sensitising dosage regime, on blood oxygen level dependent (BOLD) signal in dopaminoceptive brain regions during a rewarded gambling task performed by healthy volunteers. Using a randomised, double-blind, parallel-groups design, we found clear evidence for sensitization to the subjective effects of the drug, while rewarded reaction times were unchanged. Repeated amphetamine exposure was associated with reduced dorsal striatal BOLD signal during decision making, but enhanced ventromedial caudate activity during reward anticipation. The amygdala BOLD response to reward outcomes was blunted following repeated amphetamine exposure. Positive correlations between subjective sensitization and changes in anticipation- and outcome-related BOLD signal were seen for the caudate nucleus and amygdala, respectively. These data show for the first time in humans that AS changes the functional impact of acute stimulant exposure on the processing of reward-related information within dopaminoceptive regions. Our findings accord with pathophysiological models which implicate aberrant dopaminergic modulation of striatal and amygdala activity in psychosis and drug-related compulsive disorders.
Circling the Blood in the Water: The Difficulties in Endangered Species Protections for the Great White Shark  [PDF]
Derek Julio
Natural Resources (NR) , 2014, DOI: 10.4236/nr.2014.511058
The purpose of legislation like the Endangered Species Act is to provide a means to conserve the ecosystems of endangered and threatened species, but not all species that may appear to need conservation are granted protection. An estimated 100 million sharks are killed each year largely due to exploitation, yet few shark species are ever granted protection under state or federal endangered species acts. The Northeastern Pacific population of the Great White Shark is no exception. Despite the numerous threats facing the white shark, NOAA denied a petition to list it as an endangered or threatened species under the federal Endangered Species Act. In light of the pending California decision to list the white shark under its state endangered species act, this paper considers whether or not such extreme protections are necessary. This paper first discusses the threats facing the white shark, the listing processes of both the federal and the California endangered species acts, and NOAA’s 12-month negative finding. Finally, this paper concludes that endangered species protections are not warranted in the case of the Northeastern Pacific white shark because of prior government intervention and conservation efforts already in place.
A New Method of Estimating the Asset Rate of Return  [PDF]
Moawia Alghalith, Tracy Polius
Theoretical Economics Letters (TEL) , 2011, DOI: 10.4236/tel.2011.11001
Abstract: We present a new consumption-based method of estimating the asset rate of return.
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