Functional and structural abnormalities of thalamus in individuals at early stage of schizophrenia.

Thalamic abnormalities in schizophrenia are recognized, alongside cognitive deficits. However, the current findings about these abnormalities during the prodromal period remain relatively few and inconsistent. This study applied multimodal methods to explore the alterations in thalamic function and structure and their relationship with cognitive function in first-episode schizophrenia (FES) patients and ultra-high-risk (UHR) individuals, aiming to affirm the thalamus's role in schizophrenia development and cognitive deficits. 75 FES patients, 60 UHR individuals, and 60 healthy controls (HC) were recruited. Among the three groups, gray matter volume (GMV) and functional connectivity (FC) were evaluated to reflect the structural and functional abnormalities in the thalamus. Pearson correlation was used to calculate the association between these abnormalities and cognitive impairments. No significant difference in GMV of the thalamus was found among the abovementioned three groups. Compared with HC individuals, FES patients had decreased thalamocortical FC mostly in the thalamocortical triple network, including the default mode network (DMN), salience network (SN), and executive control network (ECN). UHR individuals had similar but milder dysconnectivity as the FES group. Furthermore, FC between the left thalamus and right putamen was significantly correlated with execution speed and attention in the FES group. Our findings revealed decreased thalamocortical FC associated with cognitive deficits in FES and UHR subjects. This improves our understanding of the functional alterations in thalamus in prodromal stage of schizophrenia and the related factors of the cognitive impairment of the disease. ClinicalTrials.govNCT03965598; https://clinicaltrials.gov/ct2/show/NCT03965598.

Wang Y ，Ouyang L ，Fan L ，Zheng W ，Li Z ，Tang J ，Yuan L ，Li C ，Jin K ，Liu W ，Chen X ，He Y ，Ma X ... -  《-》

Short-term antipsychotic treatment reduces functional connectivity of the striatum in first-episode drug-naïve early-onset schizophrenia.

The striatum is thought to play a critical role in the pathophysiology and antipsychotic treatment of schizophrenia. Previous studies have revealed abnormal functional connectivity (FC) of the striatum in early-onset schizophrenia (EOS) patients. However, no prior studies have examined post-treatment changes of striatal FC in EOS patients. We recruited 49 first-episode drug-naïve EOS patients to have resting-state functional magnetic resonance imaging scans at baseline and after 8 weeks of treatment with antipsychotics, along with baseline scanning of 34 healthy controls (HCs) for comparison purposes. We examined the FC values between each seed in striatal subregion and the rest of the brain. The Positive and Negative Syndrome Scale (PANSS) was applied to measure psychiatric symptoms in patients. Compared with HCs at baseline, EOS patients exhibited weaker FC of striatal subregions with several brain regions of the salience network and default mode network. Meanwhile, FC between the dorsal caudal putamen (DCP) and left supplementary motor area, as well as between the DCP and right postcentral gyrus, was negatively correlated with PANSS negative scores. Furthermore, after 8 weeks of treatment, EOS patients showed decreased FC between subregions of the putamen and the triangular part of inferior frontal gyrus, middle frontal gyrus, supramarginal gyrus and inferior parietal lobule. Decreased striatal FC is evident, even in the early stages of schizophrenia, and enhance our understanding of the neurodevelopmental abnormalities in schizophrenia. The findings also demonstrate that reduced striatal FC occurs after antipsychotic therapy, indicating that antipsychotic effects need to be accounted for when considering striatal FC abnormalities in schizophrenia.

Hu W ，Ran X ，Wu Z ，Zhu H ，Kou Y ，Zhang S ，Yang G ，Li W ，Yang Y ，Lv L ，Zhang Y ... -  《-》

Brain Network Localization of Gray Matter Atrophy and Neurocognitive and Social Cognitive Dysfunction in Schizophrenia.

Numerous studies have established the presence of gray matter atrophy and brain activation abnormalities during neurocognitive and social cognitive tasks in schizophrenia. Despite a growing consensus that diseases localize better to distributed brain networks than individual anatomical regions, relatively few studies have examined brain network localization of gray matter atrophy and neurocognitive and social cognitive dysfunction in schizophrenia. To address this gap, we initially identified brain locations of structural and functional abnormalities in schizophrenia from 301 published neuroimaging studies with 8712 individuals with schizophrenia and 9275 healthy control participants. By applying novel functional connectivity network mapping to large-scale resting-state functional magnetic resonance imaging datasets, we mapped these affected brain locations to 3 brain abnormality networks of schizophrenia. The gray matter atrophy network of schizophrenia comprised a broadly distributed set of brain areas predominantly implicating the ventral attention, somatomotor, and default networks. The neurocognitive dysfunction network was also composed of widespread brain areas primarily involving the frontoparietal and default networks. By contrast, the social cognitive dysfunction network consisted of circumscribed brain regions mainly implicating the default, subcortical, and visual networks. Our findings suggest shared and unique brain network substrates of gray matter atrophy and neurocognitive and social cognitive dysfunction in schizophrenia, which may not only refine the understanding of disease neuropathology from a network perspective but may also contribute to more targeted and effective treatments for impairments in different cognitive domains in schizophrenia.

Cheng Y ，Cai H ，Liu S ，Yang Y ，Pan S ，Zhang Y ，Mo F ，Yu Y ，Zhu J ... -  《-》

Tract-Specific White Matter Hyperintensities Disrupt Brain Networks and Associated With Cognitive Impairment in Mild Traumatic Brain Injury.

Traumatic brain injury (TBI) is considered to initiate cerebrovascular pathology, involving in the development of multiple forms of neurodegeneration. However, it is unknown the relationships between imaging marker of cerebrovascular injury (white matter hyperintensity, WMH), its load on white matter tract and disrupted brain dynamics with cognitive function in mild TBI (mTBI). MRI data and neuropsychological assessments were collected from 85 mTBI patients and 52 healthy controls. Between-group difference was conducted for the tract-specific WMH volumes, white matter integrity, and dynamic brain connectivity (i.e., fractional occupancies [%], dwell times [seconds], and state transitions). Regression analysis was used to examine associations between white matter damage, brain dynamics, and cognitive function. Increased WMH volumes induced by mTBI within the thalamic radiation and corpus callosum were highest among all tract fibers, and related with altered fractional anisotropy (FA) within the same tracts. Clustering identified two brain states, segregated state characterized by the sparse inter-independent component connections, and default mode network (DMN)-centered integrated state with strongly internetwork connections between DMN and other networks. In mTBI, higher WMH loads contributed to the longer dwell time and larger fractional occupancies in DMN-centered integrated state. Every 1 mL increase in WMH volume within the left thalamic radiation was associated with a 47% increase fractional occupancies, and contributed to 65.6 s delay in completion of cognitive processing speed test. Our study provided the first evidence for the structural determinants (i.e., small vessel lesions) that mediate the spatiotemporal brain dynamics to cognitive impairments in mTBI.

Li X ，Wang Z ，Zhang H ，Zhao W ，Ji Q ，Zhang X ，Jia X ，Bai G ，Pan Y ，Wu T ，Yin B ，Shi L ，Li Z ，Ding J ，Zhang J ，Salat DH ，Bai L ... -  《-》

Brain structural and functional abnormalities in affective network are associated with anxious depression.

Anxious depression (AD) is a common subtype of major depressive disorder (MDD). Neuroimaging studies of AD have revealed inconsistent and heterogeneous brain alterations with the use of single-model methods. Therefore, it is necessary to explore the pathogenesis of AD using multi-model imaging analyses to obtain more homogeneous and robust results. One hundred and eighty-two patients with MDD and 64 matched healthy controls (HCs) were recruited. Voxel-based morphometry (VBM) was used to estimate the gray matter volume (GMV) of all subjects. The GMV differences between the AD and non-anxious depression (NAD) participants were used as regions of interest (ROIs) for subsequent resting state functional connectivity (rs-FC) analyses. Correlation analysis was used to evaluate the associations between clinical symptoms and abnormal function in specific brain areas. Decreased GMV in the medial frontal gyrus (MFG) and the superior frontal gyrus (SFG) was observed in the AD group compared to the NAD group. Taking the MFG and SFG as ROIs, the rs-FC analysis revealed decreased FC between the left SFG and left temporal pole and between the left SFG and right MFG in the AD group compared to the NAD group. Finally, the FC between the left SFG and left temporal pole was negatively correlated with HAMD-17 scores in the AD group. By combining the GMV and rs-FC models, this study revealed that structural and functional disruption of the affective network may be an important pathophysiology underlying AD. The structural impairment may serve as the foundation of the functional impairment.

Juan Q ，Shiwan T ，Yurong S ，Jiabo S ，Yu C ，Shui T ，Zhijian Y ，Qing L ... -  《BMC Psychiatry》