A recent study revealed that altered retinal structures and electrophysiological responses in schizophrenia patients were significantly associated with disease severity and individual genetic risk.
Published in the Biological Psychiatry Journal, the study investigated the correlations between retinal microstructures and electrophysiological alterations in individuals with schizophrenia spectrum disorders (SSD), highlighting their associations with disease severity and polygenic risk for schizophrenia.
Researchers utilized optical coherence tomography, electroretinography, and brain magnetic resonance imaging to examine 103 patients with SSD and 130 healthy controls. Employing a sparse partial least squares algorithm, the team identified a multivariate phenotype-eye-brain signature that connected clinical disease features with biological changes in the visual system.
Key findings from the research included:
- Retinal Thinning: Patients with SSD exhibited significant microstructural thinning across most retinal layers, including reduced macular thickness and thinner retinal nerve fiber and inner plexiform layers.
- Electrophysiological Alterations: SSD patients demonstrated altered electrophysiological responses, characterized by less negative a-wave amplitude and lower b-wave amplitude, indicating compromised retinal function.
- Disease Severity Correlation: The severity of retinal alterations was correlated with the clinical severity of SSD, encompassing longer illness duration and impaired cognitive function.
- Genetic Association: Higher individual loadings on the disease-relevant visual system signature were significantly associated with elevated polygenic risk for schizophrenia, indicating a genetic underpinning for the observed retinal changes.
The study provided evidence that microstructural and functional alterations of the retina in SSD were associated with disease duration and severity, as well as with individual genetic risk. These findings suggest that retinal imaging and electrophysiology may serve as valuable tools for understanding the neurobiological mechanisms of SSD and could potentially complement established clinical investigations.
Conflict of interest disclosures can be found in the study.