A neuroimaging biomarker for treatment stratification in psychosis

Psychotic disorders affect 1 in every 100 people and are amongst the top causes of disease burden in working-age adults1. Treating psychosis is possible but almost a third of patients show limited or no response to first-line antipsychotic treatments2. Poor response is associated with increased health burden and higher costs3. There is an urgent clinical need for a biomarker to identify non- responders early to guide treatment choice. 

Several lines of evidence suggest that brain dopamine synthesis represents a neurochemical basis to stratify psychosis and predict non-response to antipsychotic treatment. Brain dopamine synthesis can be measured safely by a neuroimaging technique called Positron Emission Tomography (PET) following the injection of a radiotracer called FDOPA. The inclusion of an FDOPA-based test in clinical practice for first-episode psychosis would allow patients who are unlikely to benefit from conventional antipsychotic medication to be offered clozapine or novel alternative treatments years earlier than currently possible.4,5

Our innovation aims to develop a healthcare technology to transfer the FDOPA PET imaging from experimental medicine into clinical use. The technology comprises a simplified FDOPA PET imaging protocol, a unique FDOPA PET data repository in an open-source imaging informatics database (XNAT, Washington University), automated analytical protocols, and artificial intelligence (AI) prediction models for treatment stratification in psychosis.  This has the potential to become a screening test and generate informed, individualised treatment plans, to deliver precision medicine in psychosis and more in general across different brain disorders.


  1. A. Barbato, W. H. O. N. for Mental Health Initiative, W. H. O. D. of Mental Health, and P. of Substance Abuse, “Schizophrenia and public health / Angelo Barbato.” World Health Organization, p. DC.HQ, 1997.
  2. B. J. Kinon et al., “Early response to antipsychotic drug therapy as a clinical marker of subsequent  response in the treatment of schizophrenia.,” Neuropsychopharmacol.  Off. Publ. Am. Coll. Neuropsychopharmacol., vol. 35, no. 2, pp. 581–590, Jan. 2010, doi: 10.1038/npp.2009.164.
  3. J. L. Kennedy, C. A. Altar, D. L. Taylor, I. Degtiar, and J. C. Hornberger, “The social and economic burden of treatment-resistant schizophrenia: a systematic  literature review.,” Int. Clin. Psychopharmacol., vol. 29, no. 2, pp. 63–76, Mar. 2014, doi: 10.1097/YIC.0b013e32836508e6.
  4. M. J. Kempton and P. McGuire, “How can neuroimaging facilitate the diagnosis and stratification of patients with  psychosis?,” Eur. Neuropsychopharmacol.  J. Eur. Coll.  Neuropsychopharmacol., vol. 25, no. 5, pp. 725–732, May 2015, doi: 10.1016/j.euroneuro.2014.07.006.
  5. P. McGuire and P. Dazzan, “Does neuroimaging have a role in predicting outcomes in psychosis?,” World Psychiatry, vol. 16, no. 2, pp. 209–210, Jun. 2017, doi: 10.1002/wps.20426.