Linking Brain Entropy to Molecular and Cellular Architecture in Psychosis
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Brain entropy reflects the complexity of intrinsic activity and has been associated with cognitive function and psychiatric disorders. However, its relationship with neurochemical and cellular architecture in the brain remains poorly understood. By integrating molecular imaging, and neuroimaging datasets, we provide converging evidence that the spatial distribution of diverse cell types, neurotransmitter systems, and mitochondrial phenotypes is systematically associated with brain entropy. We found significant differences in entropy correlations between normal controls and individuals with schizophrenia for the muopioid receptor and dopamine receptor (D1), and between normal controls and bipolar disorder for the norepinephrine transporter (NAT) and N-methyl-D-aspartate receptor (NMDA). No significant differences were observed between schizophrenia and bipolar disorder in the neurotransmitter domain. In terms of cellular and metabolic features, both the normal controls vs. schizophrenia and normal controls vs. bipolar disorder comparisons revealed widespread differences associated with most mitochondrial markers, as well as glial cells and inhibitory neurons. These findings suggest disruptions in energy metabolism, neuroinflammatory activity, and inhibitory neuronal regulation in the clinical groups. Furthermore, these results indicate that brain entropy is not randomly distributed but is systematically linked to specific neurochemical systems and cellular characteristics. This systems-level perspective offers valuable insights into how the complexity of brain activity emerges from the underlying molecular architecture and how it is altered in psychiatric disorders. Moreover, it provides a biological foundation for understanding brain entropy in the context of psychosis.
