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Carole Czudek

Other affiliations: University of Sheffield
Bio: Carole Czudek is an academic researcher from University of Nottingham. The author has contributed to research in topics: Neurotransmitter & Dopamine. The author has an hindex of 12, co-authored 13 publications receiving 871 citations. Previous affiliations of Carole Czudek include University of Sheffield.

Papers
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Journal ArticleDOI
TL;DR: The binding of this ligand to brain tissue taken at autopsy has demonstrated a decreased density of GABA uptake sites in the hippocampus in schizophrenia, providing a link between neuropathology, evidence of laterality, and the dopamine hypothesis of the disease.

197 citations

Journal ArticleDOI
TL;DR: Dopamine and HVA concentrations were both significantly reduced in the AIDS group, with 20 of 34 patients exhibiting dopamine concentrations below the control range, which is consistent with a loss of nigrostriatal dopaminergic neurones and indicates the potential value of antiparkinsonian therapy in such patients.
Abstract: We sought to determine whether the motor dysfunctions and neuroleptic sensitivity that can occur in patients with AIDS relates to a deficit of striatal dopamine innervation similar to that of Parkinson's disease. For this purpose we measured concentrations of dopamine and its major metabolite homovanillic acid (HVA) in caudate nucleus tissue taken post-mortem from patients with AIDS and from appropriate age-matched control subjects. Dopamine and HVA concentrations were both significantly reduced in the AIDS group, with 20 of 34 patients exhibiting dopamine concentrations below the control range. This finding is consistent with a loss of nigrostriatal dopaminergic neurones, and may underlie the motor dysfunction and neuroleptic sensitivity that can occur in AIDS patients, indicating the potential value of antiparkinsonian therapy in such patients.

120 citations

Journal ArticleDOI
TL;DR: The results indicate profound transmitter deficits and neuropathological abnormalities in adult patients with Down's syndrome, which closely resemble those of Alzheimer's disease.
Abstract: Brain tissue taken at necropsy from five cases of Down's syndrome and six controls was analysed for changes in neurotransmitter markers. Concentrations of noradrenaline (NA), dopamine (DA) and its major metabolite homovanillic acid (HVA), 5-hydroxytryptamine (5HT) and its metabolite 5-hydroxyindoleacetic acid (5HIAA) were determined by means of HPLC, whilst choline acetyltransferase (ChAT) was measured by a radiochemical technique. Significant reductions in NA, 5HT and ChAT were found in most cortical and subcortical regions of the Down's syndrome tissue investigated. The neuropathological lesions were assessed using a fluorescent stain for neuritic plaques and neurofibrillary tangles. These were present to varying extents in every Down's syndrome case except the youngest but were not found in control tissue of comparable age. The results indicate profound transmitter deficits and neuropathological abnormalities in adult patients with Down's syndrome, which closely resemble those of Alzheimer's disease.

109 citations

Journal ArticleDOI
TL;DR: 5-HT and 5-HIAA concentrations in putamen were significantly lower in drug-free suicides who death by non-violent means than in those who died by violent means.

78 citations


Cited by
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Journal ArticleDOI
TL;DR: The theory is proposed that the most dangerous form of suicidal desire is caused by the simultaneous presence of two interpersonal constructs-thwarted belongingness and perceived burdensomeness (and hopelessness about these states)-and further that the capability to engage in suicidal behavior is separate from the desire to engageIn suicidal behavior.
Abstract: Suicidal behavior is a major problem worldwide and, at the same time, has received relatively little empirical attention. This relative lack of empirical attention may be due in part to a relative absence of theory development regarding suicidal behavior. The current article presents the interpersonal theory of suicidal behavior. We propose that the most dangerous form of suicidal desire is caused by the simultaneous presence of two interpersonal constructs—thwarted belongingness and perceived burdensomeness (and hopelessness about these states)—and further that the capability to engage in suicidal behavior is separate from the desire to engage in suicidal behavior. According to the theory, the capability for suicidal behavior emerges, via habituation and opponent processes, in response to repeated exposure to physically painful and/or fear-inducing experiences. In the current article, the theory’s hypotheses are more precisely delineated than in previous presentations (Joiner, 2005), with the aim of inviting scientific inquiry and potential falsification of the theory’s hypotheses.

3,428 citations

Journal ArticleDOI
TL;DR: A model is proposed for integrating the neural and cognitive aspects of the positive symptoms of acute schizophrenia, using evidence from postmortem neuropathology and neurochemistry, clinical and preclinical studies of dopaminergic neurotransmission, anatomical connections between the limbic system and basal ganglia, attentional and other cognitive abnormalities underlying the positive Symptoms of schizophrenia.
Abstract: A model is proposed for integrating the neural and cognitive aspects of the positive symptoms of acute schizophrenia, using evidence from postmortem neuropathology and neurochemistry, clinical and preclinical studies of dopaminergic neurotransmission, anatomical connections between the limbic system and basal ganglia, attentional and other cognitive abnormalities underlying the positive symptoms of schizophrenia, specific animal models of some of these abnormalities, and previous attempts to model the cognitive functions of the septohippocampal system and the motor functions of the basal ganglia Anatomically, the model emphasises the projections from the septohippocampal system, via the subiculum, and the amygdala to nucleus accumbens, and their interaction with the ascending dopaminergic projection to the accumbens Psychologically, the model emphasises a failure in acute schizophrenia to integrate stored memories of past regularities of perceptual input with ongoing motor programs in the control of current perception A number of recent experiments that offer support for the model are briefly described, including anatomical studies of limbic-striatal connections, studies in the rat of the effects of damage to these connections, and of the effects of amphetamine and neuroleptics, on the partial reinforcement extinction effect, latent inhibition and the Kamin blocking effect; and studies of the latter two phenomena in acute and chronic schizophrenics

1,268 citations

Journal ArticleDOI
TL;DR: Investigation of the GABA system in rodent, primate and human brain and the characterization of changes in specific phenotypic subclasses of interneurons in schizophrenia and bipolar disorder will undoubtedly provide important new insights into how the integration of this transmitter system may be altered in neuropsychiatric disease.

1,063 citations

Journal ArticleDOI
TL;DR: Dysfunction of glutamatergic neurotransmission may play an important role in the pathophysiology of schizophrenia, especially of the negative symptoms and cognitive impairments associated with the disorder, and is a promising target for drug development.
Abstract: OBJECTIVE: Research has implicated dysfunction of glutamatergic neurotransmission in the pathophysiology of schizophrenia. This review evaluates evidence from preclinical and clinical studies that brain glutamatergic neurotransmission is altered in schizophrenia, may affect symptom expression, and is modulated by antipsychotic drugs. METHOD: A comprehensive review of scientific articles published over the last decade that address the role of glutamate in the pathophysiology of schizophrenia was carried out. RESULTS: Glutamatergic neurons are the major excitatory pathways linking the cortex, limbic system, and thalamus, regions that have been implicated in schizophrenia. Postmortem studies have revealed alterations in pre- and postsynaptic markers for glutamatergic neurons in several brain regions in schizophrenia. The N-methyl-d-aspartic acid (NMDA) subtype of glutamate receptor may be particularly important as blockade of this receptor by the dissociative anesthetics reproduces in normal subjects the sym...

885 citations

Journal ArticleDOI
TL;DR: In this paper, the authors measured the rates of synthesis of indolamine in the human brain using positron emission tomography (PET) and found that the mean rate of synthesis in normal males was 52% higher than in normal females, which may be a factor relevant to the lower incidence of major unipolar depression in males.
Abstract: Rates of serotonin synthesis were measured in the human brain using positron emission tomography. The sensitivity of the method is indicated by the fact that measurements are possible even after a substantial lowering of synthesis induced by acute tryptophan depletion. Unlike serotonin levels in human brain, which vary greatly in different brain areas, rates of synthesis of the indolamine are rather uniform throughout the brain. The mean rate of synthesis in normal males was found to be 52% higher than in normal females; this marked difference may be a factor relevant to the lower incidence of major unipolar depression in males.

878 citations