# Neural Mechanisms of Mindfulness-Based Cognitive Therapy (MBCT) for Post-Traumatic Stress Disorder (PTSD)

> **NIH NIH R61** · UNIVERSITY OF MICHIGAN AT ANN ARBOR · 2020 · $70,578

## Abstract

There is growing evidence that MBCT and MBSR have efficacy for acute psychiatric conditions, including hard-
to-treat ones like posttraumatic stress disorder (PTSD), treatment-resistant depression, and generalized
anxiety disorder (GAD). However, specific mechanisms are not understood, nor is whether mechanisms are
shared with other therapies (e.g. exposure, behavioral activation), or are distinct and potentially
complementary. Elucidating MBCT mechanisms can enhance ongoing refinement and optimal targeting.
Psychological mechanisms of MBCT involve “decentering”, attentional training increases metacognitive
awareness, which can reduce over-personalization and negative reactivity, experiential avoidance, rumination,
and psychiatric symptoms. PTSD and depression are associated with aberrant intrinsic neural connectivity,
e.g. between default mode network (DMN), salience network (SN) and attentional control networks.
Converging evidence suggests that MBCT/MBSR can alter these connectivities to enhance mental and
physical health. For example, MBCT/MBSR increases connectivity of DMN with attention networks nodes (e.g.
DLPFC), with associated reductions in PTSD symptoms and plasma IL-6. MBCT/MBSR also decreases
functional connectivity between DMN (vmPFC, subgenual ACC) and SN (insula, amygdala). These findings
suggest MCBT may redirect attentional resources in ways that lead to a “de-automatization” or partial
uncoupling of aversive perceptual signals from rapid/automatic behavioral response systems that can be costly
and maladaptive when overused, and which may represent core transdiagnostic mechanisms underlying
mood, anxiety, and trauma disorders. We hypothesize that MBCT/MBSR leads to increased DMN-attention
network connectivity (e.g. PCC-DLPFC, vmPFC-DLPFC) and increased meta-cognitive attentional capacity,
contextualizing, and attention shifting (H1), and decreased DMN-SN connectivity (e.g. vmPFC-insula), leading
to increased ability to depersonalize potentially aversive cues and interoceptive signals, reducing negative
reactivity (H2). We will test these hypotheses in treatment of PTSD, which provides an useful model system,
since the networks known to be impacted by MBCT are also known to be involved in PTSD, and MBCT is
known to reduce PTSD symptoms. Our R61 will test network target engagement by MBCT (H1 or H2) in PTSD
patients (N=42), using pre-post MBCT seed-based and whole brain connectomics (a) in resting state functional
connectivity and (b) during self-referential processing. “Go-criteria” will be increased DMN-attention network or
decreased DMN-SN connectivity post MBCT. Our R33 will use an RCT of MBCT (N=53) vs a Prolonged
Exposure therapy in vivo exposure group (N=53) to validate target engagement by MBCT and mediation of
symptom improvement, and whether mechanisms are different from those engaged by PE in vivo exposure.
We will test for treatment group differences in network target engagement and its mediation of changes in
decenter...

## Key facts

- **NIH application ID:** 10175462
- **Project number:** 3R61AT009867-02S1
- **Recipient organization:** UNIVERSITY OF MICHIGAN AT ANN ARBOR
- **Principal Investigator:** ANTHONY P KING
- **Activity code:** R61 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $70,578
- **Award type:** 3
- **Project period:** 2018-09-21 → 2021-05-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10175462

## Citation

> US National Institutes of Health, RePORTER application 10175462, Neural Mechanisms of Mindfulness-Based Cognitive Therapy (MBCT) for Post-Traumatic Stress Disorder (PTSD) (3R61AT009867-02S1). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/10175462. Licensed CC0.

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