Psychiatric research is often confronted with complex abstractions and dynamics that are not readily accessible or well-defined to our perception and measurements, making data-driven methods an appealing approach. Deep neural networks (DNNs) are capable of automatically learning abstractions in the data that can be entirely novel and have demonstrated superior performance over classical machine learning models across a range of tasks and, therefore, serve as a promising tool for making new discoveries in psychiatry. A key concern for the wider application of DNNs is their reputation as a "black box" approach-i.e., they are said to lack transparency or interpretability of how input data are transformed to model outputs. In fact, several existing and emerging tools are providing improvements in interpretability. However, most reviews of interpretability for DNNs focus on theoretical and/or engineering perspectives. This article reviews approaches to DNN interpretability issues that may be relevant to their application in psychiatric research and practice. It describes a framework for understanding these methods, reviews the conceptual basis of specific methods and their potential limitations, and discusses prospects for their implementation and future directions.
Metformin, a diabetes drug with anti-aging cellular responses, has complex actions that may alter dementia onset. Mixed results are emerging from prior observational studies. To address this complexity, we deploy a causal inference approach accounting for the competing risk of death in emulated clinical trials using two distinct electronic health record systems. In intention-to-treat analyses, metformin use associates with lower hazard of all-cause mortality and lower cause-specific hazard of dementia onset, after accounting for prolonged survival, relative to sulfonylureas. In parallel systems pharmacology studies, the expression of two AD-related proteins, APOE and SPP1, was suppressed by pharmacologic concentrations of metformin in differentiated human neural cells, relative to a sulfonylurea. Together, our findings suggest that metformin might reduce the risk of dementia in diabetes patients through mechanisms beyond glycemic control, and that SPP1 is a candidate biomarker for metformin’s action in the brain.
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