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    PET imaging of putative microglial activation in individuals at ultra-high risk for psychosis, recently diagnosed and chronically ill with schizophrenia

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    Author
    Di Biase, MA; Zalesky, A; O'keefe, G; Laskaris, L; Baune, BT; Weickert, CS; Olver, J; McGorry, PD; Amminger, GP; Nelson, B; ...
    Date
    2017-08-29
    Source Title
    Translational Psychiatry
    Publisher
    NATURE PUBLISHING GROUP
    University of Melbourne Author/s
    Pantelis, Christos; Zalesky, Andrew; Shannon Weickert, Cynthia; Olver, James; McGorry, Patrick; Amminger, Guenter; Everall, Ian; Cropley, Vanessa; Scott, Andrew; Nelson, Christopher; ...
    Affiliation
    Medicine and Radiology
    Psychiatry
    Centre for Youth Mental Health
    Metadata
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    Document Type
    Journal Article
    Citations
    Di Biase, M. A., Zalesky, A., O'keefe, G., Laskaris, L., Baune, B. T., Weickert, C. S., Olver, J., McGorry, P. D., Amminger, G. P., Nelson, B., Scott, A. M., Hickie, I., Banati, R., Turkheimer, F., Yaqub, M., Everall, I. P., Pantelis, C. & Cropley, V. (2017). PET imaging of putative microglial activation in individuals at ultra-high risk for psychosis, recently diagnosed and chronically ill with schizophrenia. TRANSLATIONAL PSYCHIATRY, 7 (8), https://doi.org/10.1038/tp.2017.193.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/256836
    DOI
    10.1038/tp.2017.193
    Abstract
    We examined putative microglial activation as a function of illness course in schizophrenia. Microglial activity was quantified using [11C](R)-(1-[2-chrorophynyl]-N-methyl-N-[1-methylpropyl]-3 isoquinoline carboxamide (11C-(R)-PK11195) positron emission tomography (PET) in: (i) 10 individuals at ultra-high risk (UHR) of psychosis; (ii) 18 patients recently diagnosed with schizophrenia; (iii) 15 patients chronically ill with schizophrenia; and, (iv) 27 age-matched healthy controls. Regional-binding potential (BPND) was calculated using the simplified reference-tissue model with four alternative reference inputs. The UHR, recent-onset and chronic patient groups were compared to age-matched healthy control groups to examine between-group BPND differences in 6 regions: dorsal frontal, orbital frontal, anterior cingulate, medial temporal, thalamus and insula. Correlation analysis tested for BPND associations with gray matter volume, peripheral cytokines and clinical variables. The null hypothesis of equality in BPND between patients (UHR, recent-onset and chronic) and respective healthy control groups (younger and older) was not rejected for any group comparison or region. Across all subjects, BPND was positively correlated to age in the thalamus (r=0.43, P=0.008, false discovery rate). No correlations with regional gray matter, peripheral cytokine levels or clinical symptoms were detected. We therefore found no evidence of microglial activation in groups of individuals at high risk, recently diagnosed or chronically ill with schizophrenia. While the possibility of 11C-(R)-PK11195-binding differences in certain patient subgroups remains, the patient cohorts in our study, who also displayed normal peripheral cytokine profiles, do not substantiate the assumption of microglial activation in schizophrenia as a regular and defining feature, as measured by 11C-(R)-PK11195 BPND.

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