Publications
698 results found
Beck K, Arumuham A, Brugger S, et al., 2022, The association between <i>N</i>-methyl-d-aspartate receptor availability and glutamate levels: A multi-modal PET-MR brain imaging study in first-episode psychosis and healthy controls, JOURNAL OF PSYCHOPHARMACOLOGY, Vol: 36, Pages: 1051-1060, ISSN: 0269-8811
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- Citations: 1
Harvey PD, Bosia M, Cavallaro R, et al., 2022, Cognitive dysfunction in schizophrenia: An expert group paper on the current state of the art, SCHIZOPHRENIA RESEARCH-COGNITION, Vol: 29, ISSN: 2215-0013
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- Citations: 14
Correll CU, Agid O, Crespo-Facorro B, et al., 2022, A Guideline and Checklist for Initiating and Managing Clozapine Treatment in Patients with Treatment-Resistant Schizophrenia (vol 36, pg 659, 2022), CNS DRUGS, Vol: 36, Pages: 1015-1015, ISSN: 1172-7047
Zahid U, McCutcheon RA, Borgan F, et al., 2022, The effect of antipsychotics on glutamate levels in the anterior cingulate cortex and clinical response: A <sup>1</sup>H-MRS study in first-episode psychosis patients, Frontiers in Psychiatry, Vol: 13
Introduction: Glutamatergic dysfunction is implicated in the pathophysiology of schizophrenia. It is unclear whether glutamatergic dysfunction predicts response to treatment or if antipsychotic treatment influences glutamate levels. We investigated the effect of antipsychotic treatment on glutamatergic levels in the anterior cingulate cortex (ACC), and whether there is a relationship between baseline glutamatergic levels and clinical response after antipsychotic treatment in people with first episode psychosis (FEP). Materials and methods: The sample comprised 25 FEP patients; 22 completed magnetic resonance spectroscopy scans at both timepoints. Symptoms were assessed using the Positive and Negative Syndrome Scale (PANSS). Results: There was no significant change in glutamate [baseline 13.23 ± 2.33; follow-up 13.89 ± 1.74; t(21) = −1.158, p = 0.260], or Glx levels [baseline 19.64 ± 3.26; follow-up 19.66 ± 2.65; t(21) = −0.034, p = 0.973]. There was no significant association between glutamate or Glx levels at baseline and the change in PANSS positive (Glu r = 0.061, p = 0.777, Glx r = −0.152, p = 0.477), negative (Glu r = 0.144, p = 0.502, Glx r = 0.052, p = 0.811), general (Glu r = 0.110, p = 0.607, Glx r = −0.212, p = 0.320), or total scores (Glu r = 0.078, p = 0.719 Glx r = −0.155, p = 0.470). Conclusion: These findings indicate that treatment response is unlikely to be associated with baseline glutamatergic metabolites prior to antipsychotic treatment, and there is no major effect of antipsychotic treatment on glutamatergic metabolites in the ACC.
Rogeau A, Nordio G, Veronese M, et al., 2022, The relationship between glutamate, dopamine, and cortical gray matter: A simultaneous PET-MR study, MOLECULAR PSYCHIATRY, Vol: 27, Pages: 3493-3500, ISSN: 1359-4184
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- Citations: 2
Lally J, Ajnakina O, Stubbs B, et al., 2022, Vitamin D and cardiometabolic outcomes in first episode psychosis (FEP): A prospective cohort study, SCHIZOPHRENIA RESEARCH, Vol: 246, Pages: 26-29, ISSN: 0920-9964
D'Ambrosio E, Pergola G, Pardinas AF, et al., 2022, A polygenic score indexing a <i>DRD2</i>-related co-expression network is associated with striatal dopamine function, SCIENTIFIC REPORTS, Vol: 12, ISSN: 2045-2322
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- Citations: 2
Griffiths K, Egerton A, Millgate E, et al., 2022, Impaired verbal memory function is related to anterior cingulate glutamate levels in schizophrenia: findings from the STRATA study, SCHIZOPHRENIA, Vol: 8
Wong SMY, Suen YN, Wong CWC, et al., 2022, Striatal dopamine synthesis capacity and its association with negative symptoms upon resolution of positive symptoms in first-episode schizophrenia and delusional disorder, PSYCHOPHARMACOLOGY, Vol: 239, Pages: 2133-2141, ISSN: 0033-3158
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- Citations: 1
Correll CU, Agid O, Crespo-Facorro B, et al., 2022, A Guideline and Checklist for Initiating and Managing Clozapine Treatment in Patients with Treatment-Resistant Schizophrenia, CNS DRUGS, Vol: 36, Pages: 659-679, ISSN: 1172-7047
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- Citations: 18
Shin S, Jung WH, McCutcheon R, et al., 2022, The Relationship Between Frontostriatal Connectivity and Striatal Dopamine Function in Schizophrenia: An 18F-DOPA PET and Diffusion Tensor Imaging Study in Treatment Responsive and Resistant Patients, PSYCHIATRY INVESTIGATION, Vol: 19, Pages: 570-579, ISSN: 1738-3684
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- Citations: 3
Wall MB, Freeman TP, Hindocha C, et al., 2022, Individual and combined effects of cannabidiol and Δ<SUP>9</SUP>-tetrahydrocannabinol on striato-cortical connectivity in the human brain, JOURNAL OF PSYCHOPHARMACOLOGY, Vol: 36, Pages: 732-744, ISSN: 0269-8811
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- Citations: 7
McCutcheon RA, Pillinger T, Efthimiou O, et al., 2022, Reappraising the variability of effects of antipsychotic medication in schizophrenia: a meta-analysis, WORLD PSYCHIATRY, Vol: 21, Pages: 287-294, ISSN: 1723-8617
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- Citations: 12
Nordio G, Easmin R, Giacomel A, et al., 2022, An automated framework for FDOPA PET imaging analysis, 30th International Symposium on Cerebral Blood Flow, Metabolism and Function (BRAIN) in conjunction with the 15th International Conference on Quantification of Brain Function with PET (BRAIN PET), Publisher: SAGE PUBLICATIONS INC, Pages: 6-7, ISSN: 0271-678X
Osimo EF, Perry B, Mallikarjun P, et al., 2022, Predicting treatment resistance in people with a first-episode of psychosis using commonly recorded clinical information, Publisher: CAMBRIDGE UNIV PRESS, Pages: S107-S107, ISSN: 0924-9338
Figueiredo IC, Borgan F, Pasternak O, et al., 2022, White-matter free-water diffusion MRI in schizophrenia: a systematic review and meta-analysis, NEUROPSYCHOPHARMACOLOGY, Vol: 47, Pages: 1413-1420, ISSN: 0893-133X
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- Citations: 8
Sportelli L, Eisenberg D, D'Ambrosio E, et al., 2022, Tensor-Based Decomposition Associates Striatal Gene Co-Expression With Increased Dopamine Signaling in Individuals at Genetic Risk for Schizophrenia, 77th Annual Scientific Convention and Meeting of the Society-of-Biological-Psychiatry (SOBP), Publisher: ELSEVIER SCIENCE INC, Pages: S294-S294, ISSN: 0006-3223
Baumeister D, Peters E, Pruessner J, et al., 2022, The effects of voice content on stress reactivity: A simulation paradigm of auditory verbal hallucinations, SCHIZOPHRENIA RESEARCH, Vol: 243, Pages: 225-231, ISSN: 0920-9964
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- Citations: 3
Bloomfield MAP, Yamamori Y, Hindocha C, et al., 2022, The acute effects of cannabidiol on emotional processing and anxiety: a neurocognitive imaging study, PSYCHOPHARMACOLOGY, Vol: 239, Pages: 1539-1549, ISSN: 0033-3158
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- Citations: 4
Arumuham A, O'Brien O, Ahmad Z, et al., 2022, Low COVID-19 vaccination rates in people with severe mental illness and reasons for this: An out-patient study, ACTA PSYCHIATRICA SCANDINAVICA, Vol: 145, Pages: 416-418, ISSN: 0001-690X
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- Citations: 5
Osugo M, Whitehurst T, Shatalina E, et al., 2022, Dopamine partial agonists and prodopaminergic drugs for schizophrenia: Systematic review and meta-analysis of randomized controlled trials, NEUROSCIENCE AND BIOBEHAVIORAL REVIEWS, Vol: 135, ISSN: 0149-7634
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- Citations: 5
Osimo E, Brugger S, Thomas EL, et al., 2022, A cross-sectional MR study of body fat volumes and distribution in chronic schizophrenia, npj Schizophrenia, Vol: 8, ISSN: 2334-265X
People with schizophrenia show higher risk for abdominal obesity than the general population, which could contribute to excess mortality. However, it is unclear whether this is driven by alterations in abdominal fat partitioning. Here, we test the hypothesis that individuals with schizophrenia show a higher proportion of visceral to total body fat measured using magnetic resonance imaging (MRI). We recruited 38 participants with schizophrenia and 38 healthy controls matched on age, sex, ethnicity and body mass index. We found no significant differences in body fat distribution between groups, suggesting that increased abdominal obesity in schizophrenia is not associated with altered fat distribution.
Penzel N, Sanfelici R, Antonucci LA, et al., 2022, Pattern of predictive features of continued cannabis use in patients with recent-onset psychosis and clinical high-risk for psychosis, SCHIZOPHRENIA, Vol: 8
Krajner F, Hadaya L, McQueen G, et al., 2022, Subcortical volume reduction and cortical thinning 3 months after switching to clozapine in treatment resistant schizophrenia, SCHIZOPHRENIA, Vol: 8
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- Citations: 1
Ribeiro D, Hallett W, Howes O, et al., 2022, Assessing the impact of different penalty factors of the Bayesian reconstruction algorithm Q.Clear on in vivo low count kinetic analysis of [<SUP>11</SUP>C]PHNO brain PET-MR studies, EJNMMI RESEARCH, Vol: 12, ISSN: 2191-219X
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- Citations: 2
Correll CU, Abi-Dargham A, Howes O, 2022, Emerging Treatments in Schizophrenia., J Clin Psychiatry, Vol: 83
Although antipsychotics have been available for almost 70 years and greatly improved outcomes for individuals with schizophrenia, all currently available options derive their efficacy from blockade of dopaminergic receptors. However, this mechanism of action leaves many symptoms unresolved and is associated with a significant side effect burden. The mechanisms underlying schizophrenia, which were initially thought to be related to excessive presynaptic dopamine in specific areas of the brain, are now understood to be much more complex and involve structural and molecular changes throughout brain circuits. Consequently, drug discovery efforts have sought new targets in the search for safer and more effective medications that can improve symptoms of schizophrenia and psychosis, including trace amine-associated receptors (TAARs), muscarinic receptors, and serotonergic receptors. Positive phase 2 trial results indicating efficacy and safety of the TAAR1 agonist ulotaront (SEP-363856) and of the muscarinic M1/M4 agonist KarXT (xanomeline plus trospium) for total, positive, and negative symptoms in patients with acute exacerbation of schizophrenia, and of the serotonin 5-HT2A agonist/antagonist pimavanserin in patients with schizophrenia and predominant negative symptoms for negative symptom control are encouraging. Taken together, these data indicate in the context of ongoing phase 3 trial programs that patients with schizophrenia may soon have access to the first non-D2 blocking medication, which could drastically change the treatment landscape and improve outcomes for many of the individuals with schizophrenia who do not fully respond to or cannot tolerate currently available antipsychotic agents that currently all act via postsynaptic dopamine D2 receptor blockade.
Correll CU, Abi-Dargham A, Howes O, 2022, Emerging Treatments in Schizophrenia, JOURNAL OF CLINICAL PSYCHIATRY, Vol: 83, ISSN: 0160-6689
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- Citations: 2
Manchia M, Gathier AW, Yapici-Eser H, et al., 2022, The impact of the prolonged COVID-19 pandemic on stress resilience and mental health: A critical review across waves, EUROPEAN NEUROPSYCHOPHARMACOLOGY, Vol: 55, Pages: 22-83, ISSN: 0924-977X
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- Citations: 112
Nour MM, Beck K, Liu Y, et al., 2022, Relationship Between Replay-Associated Ripples and Hippocampal N-Methyl-D-Aspartate Receptors: Preliminary Evidence From a PET-MEG Study in Schizophrenia, Schizophrenia Bulletin Open, Vol: 3
Background and Hypotheses: Hippocampal replay and associated high-frequency ripple oscillations are among the best-characterized phenomena in resting brain activity. Replay/ripples support memory consolidation and relational inference, and are regulated by N-methyl-D-aspartate receptors (NMDARs). Schizophrenia has been associated with both replay/ripple abnormalities and NMDAR hypofunction in both clinical samples and genetic mouse models, although the relationship between these 2 facets of hippocampal function has not been tested in humans. Study Design: Here, we avail of a unique multimodal human neuroimaging data set to investigate the relationship between the availability of (intrachannel) NMDAR binding sites in hippocampus, and replay-associated ripple power, in 16 participants (7 nonclinical participants and 9 people with a diagnosis of schizophrenia, PScz). Each participant had both a [18F]GE-179 positron emission tomography (PET) scan (to measure NMDAR availability, VT) and a magnetoencephalography (MEG) scan (to measure offline neural replay and associated high-frequency ripple oscillations, using Temporally Delayed Linear Modeling). Study Results: We show a positive relationship between hippocampal NMDAR availability and replay-associated ripple power. This linkage was evident across control participants (r(5)=.94, P=.002) and PScz (r(7)=.70, P=.04), with no group difference. Conclusions: Our findings provide preliminary evidence for a relationship between hippocampal NMDAR availability and replay-associated ripple power in humans, and haverelevance for NMDAR hypofunction theories of schizophrenia.
Reid MJ, Rogdaki M, Dutan L, et al., 2022, Cell line specific alterations in genes associated with dopamine metabolism and signaling in midbrain dopaminergic neurons derived from 22q11.2 deletion carriers with elevated dopamine synthesis capacity, Schizophrenia Research, ISSN: 0920-9964
Microdeletions at the 22q11.2 locus are associated with increased risk for schizophrenia. Recent work has demonstrated that antipsychotic naïve 22q11.2 carriers display elevated levels of dopamine synthesis capacity (DSC) as assessed by 18F-DOPA PET imaging. While this is consistent with a role for abnormal dopamine function in schizophrenia, it is unclear what molecular changes may be associated with this neuro-imaging endophenotype, and moreover, if these alterations occur independently of clinical presentation. We therefore conducted a pilot study in which we generated human induced pluripotent stem cells (hiPSCs) from two 22q11.2 deletion carriers with elevated DSC in vivo, but distinct clinical presentations. From these and neurotypical control lines we were able to robustly generate midbrain dopaminergic neurons (mDA-neurons). We then assessed whether genes associated with dopamine synthesis, metabolism or signaling show altered expression between genotypes and further between the 22q11.2 deletion lines. Our data showed alterations in expression of genes associated with dopamine metabolism and signaling that differed between the two 22q11.2 hiPSC lines with distinct clinical presentations. This reinforces the importance of considering clinical, genetic and molecular information, when possible, when choosing which donors to generate hiPSCs from, to carry out mechanistic studies.
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