Background and PurposeThe proportion of patients with somatic diseases associated with anxiety is increasing each year, and pulmonary nodules have become a non-negligible cause of anxiety, the mechanism of which is unclear. The study focus on the cerebral blood flow (CBF) of anxiety in patients with pulmonary nodules to explore the cerebral perfusion pattern of anxiety associated with pulmonary nodules, blood perfusion status and mode of pulmonary nodule induced anxiety state.Materials and MethodsPatients with unconfirmed pulmonary nodules were evaluated by Hamilton Anxiety Scale (HAMA). The total score > 14 was defined as anxiety group, and the total score ≤ 14 points was defined as non-anxiety group. A total of 38 patients were enrolled, of which 19 patients were the anxiety group and 19 were the non-anxiety group. All subjects underwent arterial spin labeling imaging using a 3.0 T MRI. A two-sample t-test was performed to compare the CBF between the two groups. The CBF was extracted in brain regions with difference, and Spearman correlation was used to analyze the correlation between CBF and HAMA scores; ROC was used to analyze the performance of CBF to distinguish between the anxiety group and the non-anxiety group.ResultsThe CBF in the right insula/Heschl’s cortex of the anxiety group decreased (cluster = 109, peak t = 4.124, and P < 0.001), and the CBF in the right postcentral gyrus increased (cluster = 53, peak t = −3.912, and P < 0.001) in the anxiety group. But there was no correlation between CBF and HAMA score. The ROC analysis of the CBF of the right insula/Heschl’s cortex showed that the AUC was 0.856 (95%CI, 0.729, 0.983; P < 0.001), the optimal cutoff value of the CBF was 50.899, with the sensitivity of 0.895, and specificity of 0.789. The ROC analysis of CBF in the right postcentral gyrus showed that the AUC was 0.845 (95%CI, 0.718, 0.972; P < 0.001), the optimal cutoff value of CBF was 43.595, with the sensitivity of 0.737, and specificity of 0.842.ConclusionThe CBF of the right insula/Heschl’s cortex decreased and the CBF of the right postcentral gyrus increased in patients with pulmonary nodules under anxiety state, and the CBF of the aforementioned brain regions can accurately distinguish the anxiety group from the non-anxiety group.

Background Inflammation has been implicated in the pathology of schizophrenia and may cause neuronal cell death and dendrite loss. Neuroimaging studies have highlighted longitudinal brain structural changes in patients with schizophrenia, yet it is unclear whether this is related to inflammation. We aim to address this question, by relating brain structural changes with the transcriptional profile of inflammation markers in the early stage of schizophrenia. Methods Thirty-eight patients with first-episode schizophrenia and 51 healthy controls were included. High-resolution T1-weighted magnetic resonance imaging (MRI) and clinical assessments were performed at baseline and 2 ~ 6 months follow-up for all subjects. Changes in the brain structure were analyzed using surface-based morphological analysis and correlated with the expression of immune cells-related gene sets of interest reported by previous reviews. Transcriptional data were retrieved from the Allen Human Brain Atlas. Furthermore, we examined the brain structural changes and peripheral inflammation markers in association with behavioral symptoms and cognitive functioning in patients. Results Patients exhibited accelerated cortical thickness decrease in the left frontal cortices, less decrease or an increase in the superior parietal lobule and right lateral occipital lobe, and increased volume in the bilateral pallidum, compared with controls. Changes in cortical thickness correlated with the transcriptional level of monocyte across cortical regions in patients (r = 0.54, p < 0.01), but not in controls (r =  − 0.05, p = 0.76). In addition, cortical thickness change in the left superior parietal lobule positively correlated with changes in digital span-backward test scores in patients. Conclusions Patients with schizophrenia exhibit regional-specific cortical thickness changes in the prefrontal and parietooccipital cortices, which is related to their cognitive impairment. Inflammation may be an important factor contributing to cortical thinning in first-episode schizophrenia. Our findings suggest that the immunity-brain-behavior association may play a crucial role in the pathogenesis of schizophrenia.

Major psychiatric disorders create a significant public health burden, and mental disorders such as major depressive disorder, bipolar disorder, and schizophrenia are major contributors to the national disease burden. The search for biomarkers has been a leading endeavor in the field of biological psychiatry in recent decades. And the application of cross-scale and multi-omics approaches combining genes and imaging in major psychiatric studies has facilitated the elucidation of gene-related pathogenesis and the exploration of potential biomarkers. In this article, we summarize the results of using combined transcriptomics and magnetic resonance imaging to understand structural and functional brain changes associated with major psychiatric disorders in the last decade, demonstrating the neurobiological mechanisms of genetically related structural and functional brain alterations in multiple directions, and providing new avenues for the development of quantifiable objective biomarkers, as well as clinical diagnostic and prognostic indicators.

How genetic risk variants may relate to brain abnormalities is crucial for understanding cross-scale pathophysiological mechanisms underlying schizophrenia. The present study identifies brain structural correlates of variation in gene expression in schizophrenia and its clinical significance. Of 43 patients with schizophrenia, RNA-seq data from blood samples, MRI, and clinical assessments were collected, together with data from 60 healthy controls. Gene expression differentiation between schizophrenia and health controls was assessed and cross-referenced to schizophrenia-related genomic variations (GWAS on 76,755 patients and 243,649 controls and GWAS on 22,778 East Asian patients) and brain gene expressions (samples from 559 patients and 175 individuals). Multivariate correlation analysis was employed to examine associations across gene expression, brain volume, and clinical assessments. Differentially expressed genes in blood samples from patients with schizophrenia were significantly enriched for genes previously reported in genome-wide association studies on schizophrenia (P = 0.002, false discovery rate corrected) and were associated with gene expression differentiation in the brain (P = 0.016, 5,000 permutations). Transcriptional levels of differentially expressed genes were found to significantly correlate with gray matter volume in the frontal and temporal regions of cognitive brain networks in schizophrenia (q < 0.05, false discovery rate corrected). A significant correlation was further observed between gene expression, gray matter volume, and performance in the Wechsler Adult Intelligence Scale test (P = 0.031). Our findings suggest that genomic variations in schizophrenia are associated with differentiation in the blood transcriptome, which further plays a role in individual variations in macroscale brain structure and cognition.