Interaction between TSPO-a neuroimmune marker-and redox status in clinical high risk for psychosis: a PET-MRS study

Altered neuroimmune response and oxidative stress have both been implicated in the pathophysiology of schizophrenia. While preclinical studies have proposed several pathways regarding potential interactions between oxidative stress and neuroimmune imbalance in the development of psychosis, the molec...

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Veröffentlicht in:Neuropsychopharmacology (New York, N.Y.) N.Y.), 2018-07, Vol.43 (8), p.1700-1705
Hauptverfasser: Hafizi, Sina, Da Silva, Tania, Meyer, Jeffrey H, Kiang, Michael, Houle, Sylvain, Remington, Gary, Prce, Ivana, Wilson, Alan A, Rusjan, Pablo M, Sailasuta, Napapon, Mizrahi, Romina
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Sprache:eng
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Zusammenfassung:Altered neuroimmune response and oxidative stress have both been implicated in the pathophysiology of schizophrenia. While preclinical studies have proposed several pathways regarding potential interactions between oxidative stress and neuroimmune imbalance in the development of psychosis, the molecular mechanisms underlying this interaction are not yet understood. To date, no study has investigated this link in vivo in the human brain. We conducted the first in vivo study linking translocator protein 18  kDa (TSPO) expression and glutathione (a major brain antioxidant and a marker for redox status) in the medial prefrontal cortex (mPFC) of a relatively large sample of participants (N = 48) including 27 antipsychotic-naïve individuals at clinical high risk for psychosis and 21 matched healthy volunteers using high-resolution PET with TSPO radioligand, [ F]FEPPA, and 3T proton magnetic resonance spectroscopy ( H MRS). The omnibus model (including TSPO genotype as covariate) was significant (F  = 10.01, p 
ISSN:0893-133X
1740-634X
DOI:10.1038/s41386-018-0061-5