![]() Likewise, studies also found overlapped genetic loci of schizophrenia and cortical morphometry to be enriched in immunologic gene sets. Studies of inflammation indicated that genetically predicted IL-6 was associated with brain volume in the middle temporal gyrus and may potentially be involved in the pathology of schizophrenia. Supporting this hypothesis, therapeutic studies indicated a beneficial effect of using anti-inflammatory medications as an add-on treatment in the early stage of schizophrenia. The vulnerability-stress-inflammation model proposes that genetic risks and early life exposures, such as stress or infection, may promote a chronic pro-inflammatory state and subsequently lead to neurotransmission disturbances and brain structural changes that are relevant for schizophrenia. The suggestion that immune dysfunction may contribute to the pathophysiology of schizophrenia has a long history. In recent years, imaging genetics analysis has been increasingly applied to schizophrenia to reveal its potential pathological pathway. Imaging genetics study provides an opportunity to quantify disease-related neuroanatomical deviations and to elucidate the potential biological mechanism underlying these changes. ![]() Yet, the pathological mechanism of schizophrenia remains to be unclear. The prolonged illness course and impaired cognitive functioning are the main reasons contributing to the disease burden. Schizophrenia is a severe mental disorder ranked among the top 20 causes of disability worldwide. Our findings suggest that the immunity-brain-behavior association may play a crucial role in the pathogenesis of schizophrenia. Inflammation may be an important factor contributing to cortical thinning in first-episode schizophrenia. Patients with schizophrenia exhibit regional-specific cortical thickness changes in the prefrontal and parietooccipital cortices, which is related to their cognitive impairment. In addition, cortical thickness change in the left superior parietal lobule positively correlated with changes in digital span-backward test scores in patients. 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). 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. Furthermore, we examined the brain structural changes and peripheral inflammation markers in association with behavioral symptoms and cognitive functioning in patients. Transcriptional data were retrieved from the Allen Human Brain Atlas. 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. High-resolution T1-weighted magnetic resonance imaging (MRI) and clinical assessments were performed at baseline and 2 ~ 6 months follow-up for all subjects. Thirty-eight patients with first-episode schizophrenia and 51 healthy controls were included. ![]() We aim to address this question, by relating brain structural changes with the transcriptional profile of inflammation markers in the early stage of schizophrenia. Neuroimaging studies have highlighted longitudinal brain structural changes in patients with schizophrenia, yet it is unclear whether this is related to inflammation. Inflammation has been implicated in the pathology of schizophrenia and may cause neuronal cell death and dendrite loss.
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