Novel therapy development in psychiatry is at an impasse, with a significant lull since the 1980s and 1990s when most of the monoamine-targeted therapies that form the foundation of modern practice were first launched. The monoaminergic targets of such therapies have failed to deliver novel treatments. Instead, some of the most promising novel therapies have arisen from the twin biomarker findings of increased inflammation and oxidative stress across the major psychiatric disorders, including depression, schizophrenia, and bipolar disorder. Research on inflammation and oxidative stress has led to the identification of promising repurposed therapeutic options, which include celecoxib, minocycline, N-acetylcysteine, statins, aspirin, and infliximab.1 The logical next step, and a long-term goal of precision psychiatry, is to use hypothesized biomarkers to guide treatment choices and enhance therapy responses. Theoretically, people stratified to have higher or lower levels of the biomarker of interest should be more likely to respond to therapy with an agent that engages that target, which is a premise of the Research Domain Criteria philosophy.2
Berk M, Walker AJ, Nierenberg AA. Biomarker-Guided Anti-inflammatory Therapies: From Promise to Reality Check. JAMA Psychiatry. 2019;76(8):779–780. doi:10.1001/jamapsychiatry.2019.0673
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