Neuroimaging Biomarker for Striatal Dysfunction Distinguishes Schizophrenia with 80% Accuracy
A new functional striatal abnormalities biomarker, validated across seven independent scanning sites with 1,100 participants, distinguished schizophrenia from healthy controls with over 80% accuracy. Baseline scores predicted antipsychotic treatment response in two longitudinal cohorts, and the biomarker revealed a severity spectrum across neuropsychiatric disorders. The spatial distribution of striatal hyperactivity recapitulated dopaminergic function and schizophrenia polygenic risk expression profiles, providing biological validation for the imaging metric.
The original study
A neuroimaging biomarker for striatal dysfunction in schizophrenia.
- Authors
- Li A, Zalesky A, Yue W, Howes O, Yan H, Liu Y, et al.
- Journal
- Nature medicine
- Type
- Journal Article, Research Support, Non-U.S. Gov't, Validation Study
- PMID
- 32251404
Original abstract
Mounting evidence suggests that function and connectivity of the striatum is disrupted in schizophrenia1-5. We have developed a new hypothesis-driven neuroimaging biomarker for schizophrenia identification, prognosis and subtyping based on functional striatal abnormalities (FSA). FSA scores provide a personalized index of striatal dysfunction, ranging from normal to highly pathological. Using inter-site cross-validation on functional magnetic resonance images acquired from seven independent scanners (n = 1,100), FSA distinguished individuals with schizophrenia from healthy controls with an accuracy exceeding 80% (sensitivity, 79.3%; specificity, 81.5%). In two longitudinal cohorts, inter-individual variation in baseline FSA scores was significantly associated with antipsychotic treatment response. FSA revealed a spectrum of severity in striatal dysfunction across neuropsychiatric disorders, where dysfunction was most severe in schizophrenia, milder in bipolar disorder, and indistinguishable from healthy individuals in depression, obsessive-compulsive disorder and attention-deficit hyperactivity disorder. Loci of striatal hyperactivity recapitulated the spatial distribution of dopaminergic function and the expression profiles of polygenic risk for schizophrenia. In conclusion, we have developed a new biomarker to index striatal dysfunction and established its utility in predicting antipsychotic treatment response, clinical stratification and elucidating striatal dysfunction in neuropsychiatric disorders.