Finally, we present an overlap of a molecular genetic signature and a clinical symptom between BP and SCZ. For the first time, we correlate a BP polygenic signal with a manic symptom dimension in SCZ individuals. This suggests that clinical dimensions of SCZ might be modified by risk variants for other disorders (i.e., “modifier” genes), which might thereby provide treatment targets for these dimensions. It provides further evidence that clinical heterogeneity in schizophrenia is in part due to genetic factors (24). More specifically, it suggests the existence of a mood spectrum that has distinct genetic substrates, and exists to a variable degree in multiple disorders. Evidence such as this could one day help identify individuals who might benefit from a specific course of treatment.
