Search bioRxiv⌕ Search

bioRxiv · 10.1101/2025.07.09.663978

Emotion Regulation in the Gradient Framework: Large-Scale Brain Organization Shapes Individual Differences in Reappraisal Success

Abstract

Emotion regulation is essential for well-being and mental health, yet individuals vary widely in their emotion regulation success. Why? Traditional neuroimaging studies of emotion regulation often focus on localized neural activity or isolated networks, overlooking how large-scale brain organization may shape the integration of distributed systems and sub-processes supporting regulatory success. Here, we applied a novel system-level framework based on spatial gradients of macroscale brain organization to study variance in emotion regulation success. Using two large fMRI datasets (n=358, n=263), we projected global activation patterns from a laboratory emotion regulation task onto principal gradients derived from independent resting-state fMRI data from the Human Connectome Project. These gradients capture low-dimensional patterns of neural variation, providing a topographical framework within which complex mental phenomena, such as emotion regulation, emerge. In both datasets, individual differences in regulation success were predicted by systematic reconfiguration along Gradient 1--a principal axis differentiating unimodal and heteromodal brain areas. This gradient-based neural reconfiguration also predicted lower negative affect in daily life, as measured via smartphone-based experience sampling in a subset of participants (n=55). Meta-analytic decoding via Neurosynth revealed that Gradient 1 and regulation success align with multiple psychological processes, including social cognition, memory, attention, and negative emotion, suggesting this gradient reflects diverse, integrative demands during effective emotion regulation. These findings advance a network-level account of regulatory success, offering a biologically grounded, ecologically valid framework for understanding adaptive emotional functioning. Such gradient-based dynamics may serve as predictive biomarkers of regulatory success and inform targeted interventions in clinical populations. Significance StatementWhy are some people better than others at regulating their emotional experiences? This study employs a novel systems neuroscience framework to demonstrate that successful emotion regulation relies not only on localized brain activity, but also on how large-scale neural activation patterns systematically shift along principal axes of the brains intrinsic, large-scale spatial architecture. We demonstrate that variance in emotion regulation success--both in the laboratory (assessed using an established emotion regulation task) and in daily life (captured using phone-based experience sampling)--is associated with dynamic transitions along a principal neural gradient from sensory to transmodal association regions in the brain. This insight may lead to the development of new brain-based markers for predicting emotional resilience and tailoring mental health interventions.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Wang, R., Janet, R., Morawetz, C., Tusche, A.. 2025-07-15. Emotion Regulation in the Gradient Framework: Large-Scale Brain Organization Shapes Individual Differences in Reappraisal Success. https://doi.org/10.1101/2025.07.09.663978

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Rab10 and Arhgef7 interact to promote axon extension by linking vesicle supply and exocytosis

The formation of functional neural circuits begins with the extension of a single axon by immature neurons. Axon elongation requires an expansion of the plasma membrane that depends on the polarization of vesicle trafficking and exocytosis. It is not completely understood how the increased transport of vesicles into the growing axon is linked to their subsequent insertion into the plasma membrane. An analysis of early stages of neuronal differentiation indicates that an asymmetry in neurite length precedes axon specification and the accumulation of PPVs in the nascent axon. We show that increasing the transport of vesicles in unpolarized neurons is sufficient to promote the extension of additional axons. This effect indicates that an increased supply of vesicles stimulates their subsequent insertion into the membrane to allow neurite growth. The link between vesicle transport and exocytosis is mediated by the interaction of Rab10 with Arhgef7. Rab10 stimulates Arhgef7 activity on PPVs as a GEF for Cdc42b to promote axon extension through exocyst-dependent exocytosis, suggesting that their interaction links the increased supply of PPVs to their exocytosis.

neuroscience↗

Subcellular Spatial Profiling Unveils Links Between Neuritic Plaques with Selective Tau Vulnerability in Alzheimer's Disease

Alzheimer's disease (AD) features widespread extracellular amyloid-{beta} plaques but selective intraneuronal tau accumulation in cortical layers II/III and V, while layer IV remains relatively resistant. Here, we combined subcellular spatial transcriptomics with co-registered A{beta} and pTau immunohistochemistry to determine why neurons exposed to comparable plaque-associated pathology differ in somatic pTau accumulation. Plaque-associated neuritic stress occurred similarly across layers, but layer IV neurons showed attenuated pTau accumulation and reduced somatic expression of a shared neurite-soma stress program involving DCTN1, CALM3, NORAD, and PIN1. Trajectory analysis within layers identified tau-vulnerable and resistant neuronal states implicating calcium signaling, retrograde transport, and lysosomal function. Notably, astrocytic APOE-neuronal LRP1 co-expression increased significantly along the pTau-vulnerable trajectory, and APOE {epsilon}4 was associated with stronger coupling of local plaque pathology to pTau-associated molecular programs. These findings reveal neuronal programs and neuron-glia interactions underlying selective tau vulnerability and resistance in AD, highlighting potential tau-targeting therapeutics.

neuroscience↗

Widespread oscillatory suppression in autism persists in the absence of psychotropic medication.

Purpose: Investigate the neural oscillatory activity associated with autism spectrum disorder (ASD) using electroencephalographic (EEG) recordings in children and adolescents. Compare the corresponding oscillatory power between ASD patients taking psychotropic medication with a drug-naive group. Methods: ASD diagnosis was done using DSM-IV and CARS (Childhood Autism Rating Scale). EEG recordings employed 22 scalp electrodes (10/20 system). ASD vs. neurotypical groups were matched for sex and age (5 females; average age: ~10 years old). We analyzed the resting state (eyes open) EEG power spectrum during ~2-minute recordings. The multitaper FFT method was used to estimate spectral power for the delta, theta, alpha, beta and gamma frequency bands. We pooled together data from several electrodes to compute comprehensive power spectra and assess the oscillatory behavior of macro brain regions. Results: We observed widespread (~4Hz - 20Hz) oscillatory suppression comprising the theta, alpha and beta frequency bands. The most widespread and robust ASD-associated power suppression was in the high theta and alpha bands. Delta and gamma bands showed no significant power change for any of the brain regions studied. Results from a subgroup of patients (N = 9) who never used psychotropics confirmed these findings, indicating that they are not an artifact of medication. Conclusion: Suppression in theta, alpha and beta oscillations may offer insights into the neurophysiological underpinnings of autism and could be used as an accessible and comprehensive tool in ASD diagnosis, regardless of the patients being or not on medication.

neuroscience↗