Introduction: Early recognition of bipolar disorder improves the prognosis and decreases the burden of the disease. However, there is a significant delay in diagnosis. Multiple risk factors for bipolar disorder have been identified and a population at high-risk for the disorder has been more precisely defined. These advances have allowed the development of risk calculators to predict individual risk of conversion to bipolar disorder. This review aims to identify the risk calculators for bipolar disorder and assess their clinical applicability. Methods: A systematic review of original studies on the development of risk calculators in bipolar disorder was performed. The studies’ quality was evaluated with the Newcastle-Ottawa Quality Assessment Form for Cohort Studies and according to recommendations of the Transparent Reporting of a multivariable prediction model for Individual Prognosis or Diagnosis Initiative. Results: Three studies met the inclusion criteria; one developed a risk calculator of conversion from major depressive episode to bipolar disorder; one of conversion to new-onset bipolar spectrum disorders in offspring of parents with bipolar disorder; and the last one of conversion in youths with bipolar disorder not-otherwise-specified. Conclusions: The calculators reviewed in this article present good discrimination power for bipolar disorder, although future replication and validation of the models is needed.

Mass spectrometry (MS)-based techniques can be a powerful tool to identify neuropsychiatric disorder biomarkers, improving prediction and diagnosis ability. Here, we evaluate the efficacy of MS proteomics applied to human peripheral fluids of schizophrenia (SCZ) patients to identify disease biomarkers and relevant networks of biological pathways. Following PRISMA guidelines, a search was performed for studies that used MS proteomics approaches to identify proteomic differences between SCZ patients and healthy control groups (PROSPERO database: CRD42021274183). Nineteen articles fulfilled the inclusion criteria, allowing the identification of 217 differentially expressed proteins. Gene ontology analysis identified lipid metabolism, complement and coagulation cascades, and immune response as the main enriched biological pathways. Meta-analysis results suggest the upregulation of FCN3 and downregulation of APO1, APOA2, APOC1, and APOC3 in SCZ patients. Despite the proven ability of MS proteomics to characterize SCZ, several confounding factors contribute to the heterogeneity of the findings. In the future, we encourage the scientific community to perform studies with more extensive sampling and validation cohorts, integrating omics with bioinformatics tools to provide additional comprehension of differentially expressed proteins. The produced information could harbor potential proteomic biomarkers of SCZ, contributing to individualized prognosis and stratification strategies, besides aiding in the differential diagnosis.