Professor Paul Cumming, BSc, MSc, PhD
Department of Nuclear Medicine, University of Bern, Bern, Switzerland
School of Psychology and Counselling, Faculty of Health, Queensland University of Technology, Brisbane Australia
International Centre for Education and Research in Neuropsychiatry,
Samara State Medical University, Samara, Russia
The technology of molecular imaging of biomarkers in brain has attained considerable maturity as a tool for investigating the pathophysiological basis of schizophrenia. Since the early days of positron emission tomography, much emphasis was placed on positron emission tomography (PET) studies of dopamine synthesis capacity in brain using positron-emitting DOPA decarboxylase substrate such as fluorine-18 FDOPA. Meta-analysis of many such studies confirmed that a group of 300+ untreated patients with schizophrenia had significantly increased dopamine synthesis capacity in striatum. However, there two kinds of schizophrenia with respect to FDOPA-PET results; nearly one half of patients have entirely normal PET results. Other research suggests that high dopamine synthesis in prodromal individuals, and predicts for conversion to psychosis, especially regarding positive symptoms. Other molecular studies link reduced binding sites for muscarinic acetylcholine receptors in patients with schizophrenia, or specific patterns of reduced brain energy metabolism (i.e., glucose consumption) in relation to specific positive or negative symptomatologies. Schizophrenia is a heterogeneous disorder; molecular imaging across a range of markers may eventually support a biochemical typology of its variants, and guide individualized medical therapy.