Abnormal resting-state functional connectivity of hippocampal subregions in type 2 diabetes mellitus-associated cognitive decline.

Objective: Type 2 diabetes mellitus (T2DM) over time predisposes to inflammatory responses and abnormalities in functional brain networks that damage learning, memory, or executive function. The hippocampus is a key region often reporting connectivity abnormalities in memory disorders. Here, we investigated peripheral inflammatory responses and resting-state functional connectivity (RSFC) changes characterized of hippocampal subregions in type 2 diabetes-associated cognitive decline (T2DACD). Methods: The study included 16 patients with T2DM, 16 patients with T2DACD and 25 healthy controls (HCs). Subjects were assessed for cognitive performance, tested for the expression of inflammatory factors IL-6, IL-10 and TNF-α in peripheral serum, underwent resting-state functional magnetic resonance imaging scans, and analyzed for RSFC using the hippocampal subregions as seeds. We also calculated the correlation between cognitive performance and RSFC of hippocampal subregion, and analyzed the significantly altered RSFC values of T2DACD for Receiver Operating Characteristic (ROC) analysis. Results: T2DACD patients showed a decline in their ability to complete cognitive assessment scales and experimental paradigms, and T2DM did not show abnormal cognitive performance. IL-6 expression was increased in peripheral serum in both T2DACD and T2DM. Compared with HCs, T2DACD showed abnormalities RSFC of the left anterior hippocampus with left precentral gyrus and left angular gyrus. T2DM showed abnormalities RSFC of the left middle hippocampus with right medial frontal gyrus, right anterior and middle hippocampus with left precuneus, left anterior hippocampus with right precuneus and right posterior middle temporal gyrus. Compared with T2DM, T2DACD showed abnormalities RSFC of the left posterior hippocampus and right middle hippocampus with left precuneus. In addition, RSFC in the left posterior hippocampus with left precuneus of T2DACD was positively correlated with Flanker conflict response time (r=0.766, P=0.001). In the ROC analysis, the significantly altered RSFC values of T2DACD achieved significant performance. Conclusions: T2DACD showed a significant decrease in attentional inhibition and working memory, peripheral pro-inflammatory response increased, and abnormalities RSFC of the hippocampal subregions with default mode network and sensory-motor network. T2DM did not show a significant cognitive decline, but peripheral pro-inflammatory response increased and abnormalities RSFC of the hippocampus subregions occurred in the brain. In addition, the left precuneus may be a key brain region in the conversion of T2DM to T2DACD. The results of this study may provide a basis for the preliminary diagnosis of T2DACD.

Association between childhood trauma and depressive symptoms in adolescents during the post COVID-19 pandemic: the mediating role of social peer rejection.

This study aimed to investigate the associations of childhood trauma and its facets with depressive symptoms in depressed adolescents during the post COVID-19 epidemic, and explore the potential mediating role of social peer rejection in these associations. A total of 413 adolescents with depressive disorders completed the Chinese version of the Child Trauma Questionnaire Short Form, the Social Peer Rejection, and the Children's Depression Inventory. Childhood trauma (ß = 0.42, p < 0.01) and social peer rejection (ß = 0.18, p < 0.01) were positively related to depressive symptoms, after adjustment for demographic factors. Furthermore, social peer rejection partly mediated the relationship between childhood trauma and depressive symptoms, and the mediation effect ratio was 17.0% (p < 0.001). This study found that childhood trauma and social peer rejection are both risk factors for depressive symptoms, and social peer rejection played a mediating role in the relationship between childhood trauma and depressive symptoms.

Self-concept mediates the relationships between childhood traumatic experiences and adolescent depression in both clinical and community samples.

BACKGROUND: Childhood trauma is a pivotal risk factor for adolescent depression. While the association between childhood trauma and depression is well-established, the mediating role of self-concept has not been acknowledged. Specifically, limited attention has been paid to how childhood maltreatment impacts adolescent depression through physical and social self-concept, both in clinical and community samples. This study aims to investigate how distinct and cumulative childhood trauma affects adolescent depression, as well as the potential mediating role of self-concept in their relationships. METHODS: We recruited 227 depressed adolescents (dataset 1, 45 males, age = 15.34 ± 1.96) and 574 community adolescents (dataset 2, 107 males, age = 16.79 ± 0.65). Each participant was assessed on five subtypes of childhood trauma severity, cumulative trauma index, physical and social self-concept, and depression. Mediation models were tested separately in the clinical and community samples. RESULTS: Clinically depressed adolescents experienced a higher level of trauma severity, a greater number of trauma subtypes, and had lower levels of physical and social self-concept compared to community adolescents. Analyses on childhood trauma severity and cumulative trauma index jointly indicated that physical and social self-concept played mediation roles in the relationships between childhood trauma experiences and depression. Moreover, the mediating effects of self-concept were stronger in depressed adolescents when compared to community samples. CONCLUSIONS: Our findings suggest that physical and social self-concept play mediating roles in the pathway linking childhood trauma and adolescent depression, particularly in clinically depressed individuals.

In vivo analyses reveal hippocampal subfield volume reductions in adolescents with schizophrenia, but not with major depressive disorder.

BACKGROUND: Adult studies have reported atypicalities in the hippocampus and subfields in patients with schizophrenia (SCZ) and major depressive disorder (MDD). Both affective and psychotic disorders typically onset in adolescence, when human brain develops rapidly and shows increased susceptibility to adverse environments. However, few in vivo studies have investigated whether hippocampus subfield abnormalities occur in adolescence and whether they differ between SCZ and MDD cases. METHODS: We recruited 150 adolescents (49 SCZ patients, 67 MDD patients, and 34 healthy controls) and obtained their structural images. We used FreeSurfer to automatically segment hippocampus into 12 subfields and analyzed subfield volumetric differences between groups by analysis of covariance, covarying for age, sex, and intracranial volume. Composite measures by summing subfield volumes were further compared across groups and analyzed in relation to clinical characteristic. RESULTS: SCZ adolescents showed significant volume reductions in subfields of CA1, molecular layer, subiculum, parasubiculum, dentate gyrus and CA4 than healthy controls, and almost significant reductions, as compared to the MDD group, in left molecular layer, dentate gyrus, CA2/3 and CA4. Composite analyses showed smaller volumes in SCZ group than in healthy controls in all bilateral composite measures, and reduced volumes in comparison to MDD group in all left composite measures only. CONCLUSIONS: SCZ adolescents exhibited both hippocampal subfield and composite volumes reduction, and also showed greater magnitude of deviance than those diagnosed with MDD, particularly in core CA regions. These results indicate a hippocampal disease process, suggesting a potential intervention marker of early psychotic patients and risk youths.

Network analysis links adolescent depression with childhood, peer, and family risk environment factors.

BACKGROUND: Adolescent mental health is influenced by various adverse environmental conditions. However, it remains unclear how these factors jointly affect adolescent depression. This study aimed to use network analysis to assess the associations between different environmental factors and depressive symptoms in adolescents and to identify key pathways between them. METHODS: This study included 610 adolescents with depression from inpatient and outpatient units recruited between March 2020 and November 2021. The mean age was 14.86 ± 1.96, with no significant difference between males (n = 155, 15.10 ± 2.19) and females (n = 455, 14.78 ± 1.88). Depressive symptoms were measured using the Children's Depression Inventory, and individual risk environment factors included childhood trauma, social peer and family risk factors. Network features, including network centrality, stability, and bridge centrality, were investigated. RESULTS: Anhedonia and self-esteem were found to be more central in depressive symptoms. Insult experiences from the social peer and emotional abuse experience from childhood were more central environmental factors. Childhood trauma experiences were more related to adolescent depressive symptoms compared to family and peer factors. Bridge analyses identified emotional abuse, emotional neglect and physical neglect as the main bridges linking environment risk to depressive symptoms. LIMITATIONS: This was a cross-sectionally designed study, which limited its ability to examine longitudinal dynamic interactions between environmental factors and adolescent depressive symptoms. CONCLUSIONS: Our findings suggested that childhood trauma experiences might have greater psychological impacts on adolescent depression than family and social peer environments, and should be considered as crucial targets for preventing severe depressive moods.

Brain structural abnormalities in adult major depressive disorder revealed by voxel- and source-based morphometry: evidence from the REST-meta-MDD Consortium.

BACKGROUND: Neuroimaging studies on major depressive disorder (MDD) have identified an extensive range of brain structural abnormalities, but the exact neural mechanisms associated with MDD remain elusive. Most previous studies were performed with voxel- or surface-based morphometry which were univariate methods without considering spatial information across voxels/vertices. METHODS: Brain morphology was investigated using voxel-based morphometry (VBM) and source-based morphometry (SBM) in 1082 MDD patients and 990 healthy controls (HCs) from the REST-meta-MDD Consortium. We first examined group differences in regional grey matter (GM) volumes and structural covariance networks between patients and HCs. We then compared first-episode, drug-naïve (FEDN) patients, and recurrent patients. Additionally, we assessed the effects of symptom severity and illness duration on brain alterations. RESULTS: VBM showed decreased GM volume in various regions in MDD patients including the superior temporal cortex, anterior and middle cingulate cortex, inferior frontal cortex, and precuneus. SBM returned differences only in the prefrontal network. Comparisons between FEDN and recurrent MDD patients showed no significant differences by VBM, but SBM showed greater decreases in prefrontal, basal ganglia, visual, and cerebellar networks in the recurrent group. Moreover, depression severity was associated with volumes in the inferior frontal gyrus and precuneus, as well as the prefrontal network. CONCLUSIONS: Simultaneous application of VBM and SBM methods revealed brain alterations in MDD patients and specified differences between recurrent and FEDN patients, which tentatively provide an effective multivariate method to identify potential neurobiological markers for depression.

Segmental abnormalities of superior longitudinal fasciculus microstructure in patients with schizophrenia, bipolar disorder, and attention-deficit/hyperactivity disorder: An automated fiber quantification tractography study.

Introduction: Superior longitudinal fasciculus (SLF) is a white matter (WM) tract that connects the frontal, parietal and temporal lobes. SLF integrity has been widely assessed in neuroimaging studies of psychiatric disorders, such as schizophrenia (SZ), bipolar disorder (BD), and attention-deficit/hyperactivity disorder (ADHD). However, prior studies have revealed inconsistent findings and comparisons across disorders have not been fully examined. Methods: Here, we obtained data for 113 patients (38 patients with SZ, 40 with BD, 35 with ADHD) and 94 healthy controls from the UCLA Consortium for Neuropsychiatric Phenomic LA5c dataset. We assessed the integrity of 20 major WM tracts with a novel segmentation method by automating fiber tract quantification (AFQ). The AFQ divides each tract into 100 equal parts along the direction of travel, with fractional anisotropy (FA) of each part taken as a characteristic. Differences in FA among the four groups were examined. Results: Compared to healthy controls, patients with SZ showed significantly lower FA in the second half (51-100 parts) of the SLF. No differences were found between BD and healthy controls, nor between ADHD and healthy controls. Results also demonstrated that patients with SZ showed FA reduction in the second half of the SLF relative to patients with BP. Moreover, greater FA in patients in SLF was positively correlated with the manic-hostility score of the Brief Psychiatry Rating scale. Discussion: These findings indicated that differences in focal changes in SLF might be a key neurobiological abnormality contributing to characterization of these psychiatric disorders.

Resting-state BOLD signal variability is associated with individual differences in metacontrol.

Numerous studies demonstrate that moment-to-moment neural variability is behaviorally relevant and beneficial for tasks and behaviors requiring cognitive flexibility. However, it remains unclear whether the positive effect of neural variability also holds for cognitive persistence. Moreover, different brain variability measures have been used in previous studies, yet comparisons between them are lacking. In the current study, we examined the association between resting-state BOLD signal variability and two metacontrol policies (i.e., persistence vs. flexibility). Brain variability was estimated from resting-state fMRI (rsfMRI) data using two different approaches (i.e., Standard Deviation (SD), and Mean Square Successive Difference (MSSD)) and metacontrol biases were assessed by three metacontrol-sensitive tasks. Results showed that brain variability measured by SD and MSSD was highly positively related. Critically, higher variability measured by MSSD in the attention network, parietal and frontal network, frontal and ACC network, parietal and motor network, and higher variability measured by SD in the parietal and motor network, parietal and frontal network were associated with reduced persistence (or greater flexibility) of metacontrol (i.e., larger Stroop effect or worse RAT performance). These results show that the beneficial effect of brain signal variability on cognitive control depends on the metacontrol states involved. Our study highlights the importance of temporal variability of rsfMRI activity in understanding the neural underpinnings of cognitive control.

Smaller putamen volumes are associated with greater problems in external emotional regulation in depressed adolescents with nonsuicidal self-injury.

The functions of nonsuicidal self-injury (NSSI) consist of social and emotional aspects (Social influence, Sensation seeking, Internal and External emotion regulation). Previous studies have indicated that dysfunction in reward-related brain structures especially the striatum might drive this habitual behavior. However, no studies to date have investigated the associations between striatum and different functions for adolescents engaging in NSSI behaviors. Here, we recruited 35 depressed adolescents with recent NSSI behaviors and 36 healthy controls and acquired structural brain images, depressive symptoms, social, academic and family environments assessments, in addition to NSSI functions in patients only. Subcortical volumes and cortical thickness were estimated with FreeSurfer. Mixed linear regressions were performed to examine associations between striatal structures (caudate, putamen, nucleus accumbens, pallidum) and NSSI functions, with age, sex, total intracranial volume, hemisphere and depression severity included as covariates. Effect of environmental factors and potential associations with cortical thickness and other subcortical volumes were also tested. We found that, among the four functions, external emotional regulation represented the main function for NSSI engagement. Increased external emotion regulation was significantly associated with smaller putamen volume. No environmental factors biased the association with putamen. No associations with other cortical or subcortical regions were observed. Our findings suggested that smaller putamen might be a biomarker of NSSI engagement for depressed adolescents when they regulated frustrated or angry emotions. The results have potentially clinical implications in early identification and brain intervention of NSSI in youth.

Cortical thickness distinguishes between major depression and schizophrenia in adolescents.

BACKGROUND: Early diagnosis of adolescent psychiatric disorder is crucial for early intervention. However, there is extensive comorbidity between affective and psychotic disorders, which increases the difficulty of precise diagnoses among adolescents. METHODS: We obtained structural magnetic resonance imaging scans from 150 adolescents, including 67 and 47 patients with major depressive disorder (MDD) and schizophrenia (SCZ), as well as 34 healthy controls (HC) to explore whether psychiatric disorders could be identified using a machine learning technique. Specifically, we used the support vector machine and the leave-one-out cross-validation method to distinguish among adolescents with MDD and SCZ and healthy controls. RESULTS: We found that cortical thickness was a classification feature of a) MDD and HC with 79.21% accuracy where the temporal pole had the highest weight; b) SCZ and HC with 69.88% accuracy where the left superior temporal sulcus had the highest weight. Notably, adolescents with MDD and SCZ could be classified with 62.93% accuracy where the right pars triangularis had the highest weight. CONCLUSIONS: Our findings suggest that cortical thickness may be a critical biological feature in the diagnosis of adolescent psychiatric disorders. These findings might be helpful to establish an early prediction model for adolescents to better diagnose psychiatric disorders.

Morphometry of the Hippocampus Across the Adult Life-Span in Patients with Depressive Disorders: Association with Neuroticism.

Neuroticism is one of the main endophenotypes of major depressive disorder (MDD) and is closely related to the negative effect systems of Research Domain Criteria (RDoC) domains. The relationship between neuroticism and aging is dynamic and complex. Moreover, reduced hippocampal volumes are probably the most frequently reported structural neuroimaging finding associated with MDD. However, it remains unclear to what extent hippocampal abnormalities are linked with age and neuroticism changes in people with depression through the adult life span. This study aimed to examine the interplay between aging and neuroticism on hippocampal morphometric across the adult life-span in a relative large sample of patients with depressive disorders (114 patients, 73 females, age range: 18-74 years) and healthy control (HC) subjects (112 healthy controls, 72 females, age range: 19-72 years). MDD patients showed reduced bilateral hippocampal volumes. The effect of aging on the left hippocampal showed linear and the right hippocampal volume non-linear trajectories throughout the adult life span in healthy groups and MDD groups respectively. The hippocampal atrophy was dynamically impacted by depression at the early stages of adult life. Furthermore, we observed that right hippocampal volume reduction was associated with higher neuroticism in depressive patients younger than 30.65 years old. Our results suggest that the age-related atrophy in the right hippocampal volume was more affected by individual differences in neuroticism among younger depressive patients. Hippocampal volume reduction as a vulnerability factor for early-onset and major geriatric depression may have a distinct endophenotype.

Alteration of Resting-state Functional Connectivity in the Sensorimotor Network in Patients with Thalamic Infarction.

PURPOSE: To explore changes in functional connectivity (FC) within the sensorimotor network (SMN) and the relationship between the SMN and bilateral thalamus in patients with thalamic infarction (TI) using resting state functional magnetic resonance imaging (rs-fMRI). Also determined was whether those measures are useful for monitoring the functional recovery of somatosensory deficits. METHODS: The study included 31 patients with TI presenting somatosensory dysfunction and 31 controls who underwent clinical assessments and MRI scanning at 6 months after a stroke. An independent component analysis was used to identify the SMN. The mean time courses of SMN activity were extracted for each subject, and FC with the bilateral thalamus was assessed. Differences in connectivity strength were compared between groups. Finally, we correlated the altered FC values with clinical data from patients with TI. RESULTS: Compared to controls, patients with TI showed decreases in FC within SMN in the ipsilesional posterior central gyrus (PCG) (Z-score = -4.581, cluster size = 171), but presented increased FC within the SMN in the ipsilesional supplementary motor area (SMA) (Z-score = 4.648, cluster size = 46). The FC values of the ipsilesional SMA correlated with the somatosensory function score of patients with TI (r = 0.426, P = 0.027). Increased FC was observed between the SMN and bilateral thalamus in patients with TI. The region exhibiting increased FC was adjacent to the lesion in the affected thalamus, while the area with increased FC overlapped the location of the lesion when the lesion was mirrored onto the unaffected thalamus. CONCLUSION: The increased FC in the ipsilesional SMA and between the SMN and perilesional thalamus might reflect functional reorganization in patients with TI presenting somatosensory deficits.

Rostral middle frontal gyrus thickness mediates the relationship between genetic risk and neuroticism trait.

Neuroticism is a robust personality trait associated with multiple mental disorders. Heretofore, research on the relationship among genes, brain, and behavior to explore individual differences in neuroticism is scarce. Hence, in this study (N = 630), genetic data, self-reported neuroticism, and brain structural data were combined to explore whether the cortical thickness (CT) of brain regions mediated the relationship between the polygenic risk score (PRS) of neuroticism and NEO neuroticism (NEO-N), and the enrichment analysis was performed to reveal the underlying mechanism of their relationship. Results showed that the PRSs were significantly associated with NEO-N scores (p < .05). The CT of left rostral middle frontal gyrus was negatively related to the best PRS in PRSice (PRSbest ) or the PRS at 0.05 threshold (PRS0.05 ) (corrected p < .05), which was also found to mediate the association between the PRS and NEO-N (PRSbest : ab = .012, p < .05; PRS0.05 : ab = .012, p < .05). Enrichment analysis revealed that these genes were mainly involved in biological adhesion, cell adhesion, neuron part, and synapse part, which were associated with the abnormal thickness of frontal cortex. By integrating genetic, brain imaging, and behavioral data, our research initially revealed the neurogenetic underpinnings of neuroticism, which is helpful for understanding individual differences in neuroticism.

Functional connectivity underpinnings of electroconvulsive therapy-induced memory impairments in patients with depression.

Electroconvulsive therapy (ECT) is an effective treatment for severe medication-resistant depression. However, ECT frequently results in episodic memory impairments, causing many patients to discontinue treatment. The objective of this study was to explore the functional connectivity underpinnings of ECT-induced episodic memory impairments. We investigated verbal episodic memory and intrinsic functional connectivity in 24 patients with depression (13F, 11M) before and after ECT, and 1 month after treatment. We used a novel individual-oriented approach to examine functional connectivity, and trained a linear support vector regression model to estimate verbal memory performance based on connectivity. The model identified a set of brain connections that can predict baseline verbal memory performance (r = 0.535, p = 0.026). Importantly, we found a nonoverlapping set of brain connections whose changes after ECT can track patients' verbal memory impairments (r = 0.613, p = 0.008). These connections mainly involve the frontoparietal control, default mode, and hippocampal networks, suggesting that ECT affects broad functional networks that are involved in memory performance. In contrast, functional connectivity defined using traditional group-level analyses was unable to estimate either baseline memory performance or post-ECT verbal memory impairments. A parallel analysis using the same strategy did not identify a connectivity marker for overall mood improvement, suggesting that functional connectivity changes related to depressive symptoms may be highly heterogenous. Our findings shed light on the mechanism through which ECT impairs episodic memory, and additionally underline the importance of accounting for interindividual variability in the investigation of functional brain organization in patients with depression.

Personality traits and negative affect mediate the relationship between cortical thickness of superior frontal cortex and aggressive behavior.

Aggression reflects the psychological and physical behavior that perpetrator intends to harm victim. Initiation of aggression is influenced by the distal factors (e.g. personality) and proximate causes (e.g. affect) of perpetrator. However, few studies explored the brain structural basis of relationship between these traits and aggressive behavior. In this study, we first explored the association between cortical thickness and aggression in a large young adult sample from the Human Connectome Project. Results found aggressive behavior assessed by the Adult Self-Report was positively correlated with cortical thickness in left superior frontal gyrus (SFG), which was implicated in emotion regulation and executive function. Then, mediation analyses with distal and proximate factors separately showcased that the association between the left SFG thickness and aggressive behavior was partially mediated by negative affect (anger and sadness), and fully mediated by personality traits (agreeableness and neuroticism). Taken together, these experimental findings established dorsal prefrontal cortex as the key region in generating aggressive behavior, and gave a neutral explanation for why individuals with high negative affect and neuroticism exhibit more aggression. This study implicated the possible targeted brain region and behavioral intervention for such at-risk individuals initiating violence.

The reductions in the subcallosal region cortical volume and surface area in major depressive disorder across the adult life span.

BACKGROUND: Imaging studies have shown that the subcallosal region (SCR) volume was decreased in patients with major depressive disorder (MDD). However, whether the volumetric reductions in the SCR are due to thinning of the cortex or a loss of surface area (SA) remains unclear. In addition, the relationship between cortical measurements of the SCR and age through the adult life span in MDD remains unclear. METHODS: We used a cross-sectional design from 114 individuals with MDD and 112 matched healthy control (HC) individuals across the adult life span (range: 18-74 years). The mean cortical volume (CV), SA and cortical thickness (CT) of the SCR were computed using cortical parcellation based on FreeSurfer software. Multivariate analyses of covariance models were performed to compare differences between the MDD and HC groups on cortical measurements of the SCR. Multiple linear regression models were used to test age-by-group interaction effects on these cortical measurements of the SCR. RESULTS: The MDD had significant reductions in the CV and SA of the left SCR compared with HC individuals after controlling of other variables. The left SCR CV and SA reductions compared with matched controls were observed only in early adulthood patients. We also found a significant age-related CT reduction in the SCR both in the MDD and HC participants. CONCLUSIONS: The SCR volume reduction was mainly driven by SA in MDD. The different trajectories between the CT and SA of the SCR with age may provide valuable information to distinguish pathological processes and normal ageing in MDD.

Hierarchical Structured Sparse Learning for Schizophrenia Identification.

Fractional amplitude of low-frequency fluctuation (fALFF) has been widely used for resting-state functional magnetic resonance imaging (rs-fMRI) based schizophrenia (SZ) diagnosis. However, previous studies usually measure the fALFF within low-frequency fluctuation (from 0.01 to 0.08Hz), which cannot fully cover the complex neural activity pattern in the resting-state brain. In addition, existing studies usually ignore the fact that each specific frequency band can delineate the unique spontaneous fluctuations of neural activities in the brain. Accordingly, in this paper, we propose a novel hierarchical structured sparse learning method to sufficiently utilize the specificity and complementary structure information across four different frequency bands (from 0.01Hz to 0.25Hz) for SZ diagnosis. The proposed method can help preserve the partial group structures among multiple frequency bands and the specific characters in each frequency band. We further develop an efficient optimization algorithm to solve the proposed objective function. We validate the efficacy of our proposed method on a real SZ dataset. Also, to demonstrate the generality of the method, we apply our proposed method on a subset of Alzheimer's Disease Neuroimaging Initiative (ADNI) database. Experimental results on both datasets demonstrate that our proposed method achieves promising performance in brain disease classification, compared with several state-of-the-art methods.

Cortical Thinning in the Medial Temporal Lobe and Precuneus Is Related to Cognitive Deficits in Patients With Subcortical Ischemic Vascular Disease.

Subcortical ischemic vascular disease (SIVD) is a major cause of vascular cognitive impairment (CI) and features extensive atrophy in the cerebral cortex. We aimed to test the hypothesis that cognitive deficits in SIVD are linked to decreased cortical thickness in specific brain regions, which may constitute neuroimaging biomarkers of CI. Sixty-seven SIVD patients without (SIVD-NC, n = 35) and with (SIVD-CI, n = 32) CI and a group of healthy controls (HCs, n = 36) underwent structural magnetic resonance imaging (MRI) and cognitive functional assessments. FreeSurfer was used to preprocess structural MRI data and to calculate and compare cortical thickness. The correlation between cortical thickness and cognitive scores was examined in SIVD patients. Significantly altered cortical thickness in the bilateral insula, middle and inferior temporal lobes, precuneus, and medial temporal lobe (MTL) was identified among the three groups (p < 0.05, Monte Carlo simulation corrected). Post hoc results showed significantly decreased thickness in the bilateral insula and temporal lobe in SIVD-NC and SIVD-CI patients compared with HCs. However, the areas with reduced cortical thickness were larger in SIVD-CI than SIVD-NC patients. SIVD-CI patients had significantly reduced thickness in the bilateral precuneus and left MTL (Bonferroni corrected) compared with SIVD-NC patients when we extracted the mean thickness for each region of interest. In SIVD patients, the thicknesses of the left MTL and bilateral precuneus were positively correlated with immediate recall in the memory test. SIVD might lead to extensive cerebral cortical atrophy, while atrophy in the MTL and precuneus might be associated with memory deficits.

Prefrontal sensitivity to changes in language form and semantic content during speech production.

In bilingual speakers, language switching might involve a change in language form, meaning, or both. However, the neural substrates of language control in the three switching conditions have not been specified. We examined bilingual speech production using a picture-naming paradigm that teased apart language and semantic switching. Bilingual participants named two serially presented pictures, which show the same or different object, with one or two languages. The three switching conditions showed distinct neural activation patterns within the prefrontal cortex. Moreover, neural substrates shared by all switching conditions were primarily found in fronto-parietal regions. Besides, forward switching (L1-to-L2) activated a more widespread neural network than backward switching (L2-to-L1). We discuss differential engagement of the cognitive control system as a function of switching type during bilingual speech production.