학술논문

Multiscale neural gradients reflect transdiagnostic effects of major psychiatric conditions on cortical morphology
Document Type
article
Source
Communications Biology. 5(1)
Subject
Biological Sciences
Biomedical and Clinical Sciences
Depression
Neurosciences
Behavioral and Social Science
Serious Mental Illness
Mental Health
Brain Disorders
Schizophrenia
2.1 Biological and endogenous factors
Aetiology
Neurological
Mental health
Good Health and Well Being
Autism Spectrum Disorder
Connectome
Dopamine
Humans
Neural Pathways
Serotonin
Biological sciences
Biomedical and clinical sciences
Language
Abstract
It is increasingly recognized that multiple psychiatric conditions are underpinned by shared neural pathways, affecting similar brain systems. Here, we carried out a multiscale neural contextualization of shared alterations of cortical morphology across six major psychiatric conditions (autism spectrum disorder, attention deficit/hyperactivity disorder, major depression disorder, obsessive-compulsive disorder, bipolar disorder, and schizophrenia). Our framework cross-referenced shared morphological anomalies with respect to cortical myeloarchitecture and cytoarchitecture, as well as connectome and neurotransmitter organization. Pooling disease-related effects on MRI-based cortical thickness measures across six ENIGMA working groups, including a total of 28,546 participants (12,876 patients and 15,670 controls), we identified a cortex-wide dimension of morphological changes that described a sensory-fugal pattern, with paralimbic regions showing the most consistent alterations across conditions. The shared disease dimension was closely related to cortical gradients of microstructure as well as neurotransmitter axes, specifically cortex-wide variations in serotonin and dopamine. Multiple sensitivity analyses confirmed robustness with respect to slight variations in analytical choices. Our findings embed shared effects of common psychiatric conditions on brain structure in multiple scales of brain organization, and may provide insights into neural mechanisms of transdiagnostic vulnerability.