Wednesday, April 2, 2025
4/2/2025
Using latent cause modeling and neurofeedback to understand fear relapse and its relationship to anxiety - PROJECT SUMMARY/ABSTRACT Exposure therapy is the most effective evidence-based treatment for a variety of anxiety disorders, but relapse is common. Failures of exposure therapy can be explained in part by laboratory studies using aversive conditioning and extinction, where the extinction phase can be viewed as a model of exposure therapy. These studies show that the “safe” association learned during extinction is tenuous, and the original negative association can sometimes return – a process known as spontaneous recovery. Recent work from our group shows that during extinction, some participants update the original association from fear to safety while others remember the fear association. The latter participants show spontaneous recovery (relapse) of fear at a later test. The overall goal of this fellowship is to understand these individual differences in spontaneous recovery, their relationship to transdiagnostic mental health symptoms of anxiety, and their neural underpinnings. To accomplish this goal, I will leverage the computational framework of latent cause inference; according to this framework, spontaneous recovery arises when an old latent cause associated with an aversive outcome is inferred to be active in a harmless situation, a form of overgeneralization. I will fit a model to behavior of individual participants to precisely quantify individual differences in the computational process underlying spontaneous recovery and correlate these to symptoms. We will also identify the neurocognitive systems that are implicated in this overgeneralization: we hypothesize that participants show spontaneous recovery because of deficient memory-control processes – these participants are failing to suppress retrieval of the original memory, even in the presence of evidence that the situation is now “safe”. We will relate this to clinical symptoms: based on prior work, we hypothesize that spontaneous recovery will be associated with low memory-control ability and high clinical symptoms of anxiety. Aim 1 will test for relationships between memory control, spontaneous recovery, anxiety symptoms, and parameters of latent cause inference, taking a dimensional approach in a large-scale online study. Aim 2 will causally test our hypotheses about brain networks that mediate spontaneous recovery by intervening on these networks with real-time fMRI neurofeedback, with the goal of reducing spontaneous recovery in individuals who are prone to it. Taken together, these studies will substantially advance our understanding of why spontaneous recovery occurs and how it relates to clinical symptoms; this, in turn, can inform our treatment of anxiety disorders by helping us identify who is most likely to relapse after exposure therapy, and how we might intervene to prevent relapse.
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