Publications by authors named "Oswald J N Bloemen"

Glutamatergic dysfunction is implicated in schizophrenia pathoaetiology, but this may vary in extent between patients. It is unclear whether inter-individual variability in glutamate is greater in schizophrenia than the general population. We conducted meta-analyses to assess (1) variability of glutamate measures in patients relative to controls (log coefficient of variation ratio: CVR); (2) standardised mean differences (SMD) using Hedges g; (3) modal distribution of individual-level glutamate data (Hartigan's unimodality dip test).

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Importance: Proton magnetic resonance spectroscopy (1H-MRS) studies indicate that altered brain glutamatergic function may be associated with the pathophysiology of schizophrenia and the response to antipsychotic treatment. However, the association of altered glutamatergic function with clinical and demographic factors is unclear.

Objective: To assess the associations of age, symptom severity, level of functioning, and antipsychotic treatment with brain glutamatergic metabolites.

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Article Synopsis
  • - The study investigates the relationship between M receptor signaling deficits and associative learning and memory impairments in individuals with psychotic disorders, supported by previous findings linking these issues to fronto-temporal activation deficits.
  • - Twenty-six patients with psychotic disorders and 29 matched healthy controls underwent fMRI while performing learning tasks, with one session under placebo and another under an M antagonist (biperiden).
  • - Results indicated that patients showed DLPFC hypoactivation during memory tasks and greater hyperactivation in other brain regions after biperiden, suggesting that M receptor signaling may play a significant role in their cognitive deficits related to learning and memory.
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Article Synopsis
  • The study investigates the role of the muscarinic cholinergic system in cognitive dysfunction related to psychosis, specifically looking at choline concentrations in the anterior cingulate cortex (ACC) and striatum.
  • It involved 30 subjects with psychosis and 30 healthy controls, using H-MRS and functional MRI to assess the effects of the M receptor antagonist biperiden on cognitive performance and brain connectivity.
  • Results showed no significant differences in choline levels or cognitive performance between groups after placebo or biperiden, suggesting no major cholinergic abnormalities were present in the studied sample.
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Background: 22q11.2 deletion syndrome (22q11DS), one of the most common recurrent copy number variant disorders, is associated with dopaminergic abnormalities and increased risk for psychotic disorders.

Aims: Given the elevated prevalence of substance use and dopaminergic abnormalities in non-deleted patients with psychosis, we investigated the prevalence of substance use in 22q11DS, compared with that in non-deleted patients with psychosis and matched healthy controls.

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Striatal dopamine (DA) dysfunction has been consistently reported in psychotic disorders. Differences and similarities in the pathogenesis between populations at clinical and genetic risk for developing psychosis are yet to be established. Here we explored markers of dopamine (DA) function in subjects meeting clinically ultra-high risk criteria for psychosis (UHR) and in subjects with 22q11.

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The acetylcholine muscarinic M receptor has been implicated in both psychosis and cognition. Post-mortem research has shown reduced muscarinic M receptor density in 25% of chronic patients with schizophrenia. It is unknown whether reduced M receptor density is related to cognitive symptoms of psychosis.

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Rationale: 22q11 deletion syndrome (22q11DS) is associated with an increased risk for psychotic disorders, suggesting a relationship between genotypes and the pathophysiology of psychotic disorders. Two genes in the deleted region, catechol-O-methyl-transferase (COMT) and proline dehydrogenase (oxidase) 1 (PRODH), contain polymorphisms associated with neuropsychiatric phenotypes.

Objectives: Here, we explored the association between polymorphisms and full-scale intelligence (FSIQ), startle reactivity (SR) and prepulse inhibition (PPI) in adults with 22q11DS.

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Schizophrenia is a disabling, chronic psychiatric disorder with a prevalence rate of 0.5-1% in the general population. Symptoms include positive (e.

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22q11 deletion syndrome (22q11DS) is a genetic disorder caused by a microdeletion on chromosome 22, which includes the gene coding for catechol-O-methyl-transferase (COMT). High dopamine (DA) levels due to COMT haplo-insufficiency may be associated with the increased risk of developing schizophrenia in adults with 22q11DS. Reduced prepulse inhibition (PPI) of the acoustic startle response has been associated with schizophrenia and with disrupted DAergic transmission in the prefrontal cortex (PFC).

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Altered striatal dopaminergic neurotransmission is thought to be fundamental to schizophrenia. Increased presynaptic dopaminergic activity ([18F]-DOPA PET) may predate the onset of psychotic symptoms and correlates to clinical symptoms in subjects at Ultra High Risk (UHR) for developing psychosis. Postsynaptic dopaminergic neurotransmission has not been investigated yet in UHR patients.

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Background: Autistic Spectrum Disorder (ASD), including Asperger syndrome and autism, is a highly genetic neurodevelopmental disorder. There is a consensus that ASD has a biological basis, and it has been proposed that it is a "connectivity" disorder. Diffusion Tensor Magnetic Resonance Imaging (DT-MRI) allows measurement of the microstructural integrity of white matter (a proxy measure of "connectivity").

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Young people with 22q11 Deletion Syndrome (22q11DS) are at substantial risk for developing psychosis and have significant differences in white matter (WM) volume. However, there are few in vivo studies of both WM microstructural integrity (as measured using Diffusion Tensor (DT)-MRI) and WM volume in the same individual. We used DT-MRI and structural MRI (sMRI) with voxel based morphometry (VBM) to compare, respectively, the fractional anisotropy (FA) and WM volume of 11 children and adolescents with 22q11DS and 12 controls.

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Background: Autism-spectrum disorder is increasingly recognised, with recent studies estimating that 1% of children in South London are affected. However, the biology of comorbid mental health problems in people with autism-spectrum disorder is poorly understood.

Aims: To investigate the brain anatomy of people with autism-spectrum disorder with and without psychosis.

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