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Decoding Early Psychoses: Unraveling Stable Microstructural Features Associated With Psychopathology Across

Haley R Wang1, Zhen-Qi Liu2, Hajer Nakua3

  • 1Department of Psychology, University of California, Los Angeles, Los Angeles, California; Department of Psychiatry and Biobehavioral Sciences, Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles, Los Angeles, California.

Biological Psychiatry
|June 22, 2024
PubMed
Summary

Early psychosis (EP) patients show a stable neurobiological signature linking white matter changes to negative and somatic symptoms. This data-driven approach aids early intervention development by identifying shared neural underpinnings across diagnoses.

Keywords:
Clinical heterogeneityDiffusion-weighted imagingEarly psychosisNegative symptomsPLSPartial least squaresPsychopathologyWhite matter microstructure

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Area of Science:

  • Neuroscience
  • Psychiatry
  • Medical Imaging

Background:

  • Early psychosis (EP) presents significant patient variability, complicating outcome prediction.
  • Limited evidence exists for stable links between neural microstructural properties and symptom profiles in EP.
  • This gap hinders the development of targeted early interventions.

Purpose of the Study:

  • To identify stable and generalizable neurobiological signatures in early psychosis (EP) using a data-driven approach.
  • To examine multivariate relationships between white matter properties and symptomatology across independent EP cohorts.
  • To explore transdiagnostic neurobiological underpinnings of symptom profiles in EP.

Main Methods:

  • Utilized partial least squares correlation across two independent datasets (n=124 and n=78) of EP patients.
  • Included individuals with schizophrenia, schizoaffective disorder, and psychotic mood disorders.
  • Examined relationships between white matter microstructural properties and symptom profiles.

Main Results:

  • A significant latent component linked negative symptoms (diminished expression) and somatic symptoms with white matter disruption in subcortical and frontal association fibers.
  • The model trained on one cohort accurately predicted features in the replication cohort.
  • Findings were consistent across diagnoses and unaffected by medication or substance use.

Conclusions:

  • A stable, replicable neurobiological signature of white matter alterations in EP was identified across diagnoses and datasets.
  • These alterations strongly covary with a specific profile of negative and somatic symptoms.
  • Data-driven approaches can reveal shared neurobiological underpinnings for symptom domains in EP, suggesting clinical utility.