A longitudinal investigation of structural brain changes during second language learning

ObjectiveWe aimed to investigate changes in whole-brain gray matter volumes (GMVs) before and after electroconvulsive therapy (ECT) in adolescents with major depressive disorder (MDD) and suicidal ideation (SI).MethodsThirty adolescents with MDD and SI were observed, and structural magnetic resonance imaging (sMRI) was performed at baseline and after ECT for each patient. But Twenty-five healthy controls (HCs) were scanned only at baseline. The voxel-based morphometry (VBM) techniques were used to examine GMVs.ResultsCompared with HCs, MDDs at baseline showed decreased GMVs in the left middle temporal gyrus, right superior temporal gyrus, right middle temporal gyrus, left precuneus, right precuneus, and left superior frontal gyrus. After ECT, MDDs showed increased GMVs in the right superior frontal gyrus and right superior temporal gyrus. Pearson’s correlation found that Beck Scale for Suicide Ideation (BSSI) scores at baseline were negatively correlated with GMVs in the left superior frontal gyrus and HAMD and BSSI scores after ECT were negatively correlated with GMVs in the right superior temporal gyrus.ConclusionFrontal–temporal–precuneus structure changes may be a potential cause of depressive and suicidal symptoms in adolescents. ECT may improve depressive and suicidal symptoms in adolescents by regulating brain structures to compensate original defects.

Introduction Changes in grey matter volume (GMV) and cortical thickness (CT) have been previously documented in adult Crohn’s Disease (CD) patients in remission, however data is inconsistent and not explored in patients with active CD. Here, we investigate alterations in GMV and CT in patients with active CD, and their correlation with disease activity biomarkers such as faecal calprotectin (FCP), C-reactive protein (CRP), Interleukin-6 (IL-6), Interleukin-1β (IL-1β) and TNFα Methods 25 active ileal/colonic CD patients and 25 healthy controls (HC) age-, BMI- and gender-matched were scanned. Active CD was defined as Harvey Bradshaw index >5 and CRP >5 mg/dl, or FCP >250 µg/g or assessed through ileocolonoscopy or magnetic resonance enterography. Cytokine levels were measured from serum samples using colorimetric ELISA. FCP were acquired at inclusion. Anatomical T1-weighted brain images were acquired on a 3T Philips Achieva scanner using a 32-channel receive coil. GMV was measured using voxel based morphometry and cortical thickness was determined using computational anatomy toolbox (CAT12) in Statistical Parametric Mapping (SPM) software. Results In CD patients, significant cortical thinning in the right rostral middle-frontal area (involved in attention and working memory) was found compared with HCs. A significant decrease in GMV was found in CD compared with HC in pre-central gyrus (motor cortex) and post-central gyrus (somatosensory cortex). Correlating IL-6 with CT in CD showed cortical thinning in the right superior-frontal area (involved in self-awareness) and right lingual regions (involved in vision processing) with increasing IL-6 levels. IL-6 was negatively correlated with the GMV in bilateral insula (involved in pain processing) and pre- and post-central gyrus. FCP was negatively correlated with the right insula. Further cytokine assays of TNFα and IL-1β are presently underway in this study. Conclusions A significant reduction in CT and GMV in cortical areas has been shown in patients with active CD compared with HCs. This observation may be associated with a chronic inflammatory response, attributed to high levels of circulating neurotoxic cytokines. Serum TNFα and IL-1β levels will also be correlated to CT and GMV in this study to validate the aforementioned observation. Investigating structural brain changes in active CD will aid our understanding of the cross-linking between chronic inflammation, brain morphology and changes in behaviour, cognitive function and unexplained symptoms such as fatigue in CD. This will inform new medical and psychological therapies.

The FKBP5 gene codes for a co-chaperone that regulates glucocorticoid receptor sensitivity and thereby impacts the reactivity of the hypothalamic-pituitary-adrenal (HPA)-axis. Evidence suggested that subjects exposed to childhood abuse and carrying the TT genotype of the FKBP5 gene single nucleotide polymorphism (SNP) rs1360780 have an increased susceptibility to stress-related disorders. The hypothesis that abused TT genotype carriers show changes in gray matter (GM) volumes in affect-processing brain areas was investigated. About 1,826 Caucasian subjects (age ≤ 65 years) from the general population [Study of Health in Pomerania (SHIP)] in Germany were investigated. The interaction between rs1360780 and child abuse (Childhood Trauma Questionnaire) and its effect on GM were analyzed. Voxel-based whole-brain interaction analysis revealed three large clusters (FWE-corrected) of reduced GM volumes comprising the bilateral insula, the superior and middle temporal gyrus, the bilateral hippocampus, the right amygdala, and the bilateral anterior cingulate cortex in abused TT carriers. These results were not confounded by major depressive disorders. In region of interest analyses, highly significant volume reductions in the right hippocampus/parahippocampus, the bilateral anterior and middle cingulate cortex, the insula, and the amygdala were confirmed in abused TT carriers compared with abused CT/CC carriers. The results supported the hypothesis that the FKBP5 rs1360780 TT genotype predisposes subjects who have experienced childhood abuse to widespread structural brain changes in the subcortical and cortical emotion-processing brain areas. Those brain changes might contribute to an increased vulnerability of stress-related disorders in TT genotype carriers.

Cannabis use and progressive cortical thickness loss in areas rich in CB1 receptors during the first five years of schizophrenia

To describe the structural brain changes, neurocognitive and mental health associations in adolescents perinatally infected with HIV-1 infection. Cross-sectional. Two hundred and four adolescents with perinatally acquired HIV and 44 uninfected frequency-matched controls aged 9-11 years were enrolled within the Cape Town Adolescent Antiretroviral Cohort. Diffusion tensor imaging and structural brain MRI was done to determine fractional anisotropy, mean diffusivity, grey and white matter volumes, cortical thickness and cortical surfractional anisotropy area. Correlation coefficients were calculated between total grey and white matter volume, cortical surface area, cortical thickness, whole brain fractional anisotropy and whole brain mean diffusivity and clinical and laboratory parameters including general intellectual functioning, Becks Youth Inventory, Child Motivation Scale and Child Behaviour Checklist. HIV-infected adolescents performed worse than controls on the Wechsler Abbreviated Scale of Intelligence (WASI; P < 0.01). HIV-infected adolescents had significant fractional anisotropy decreases, mean diffusivity increases and decreases in cerebral grey matter volumes, cortical surface area and decreased gyrification. Whole-brain mean fractional anisotropy was significantly reduced in the HIV-infected group (P = 0.031). There were significant correlation coefficients between greater total grey (P = 0.008) and white matter volume (P = 0.004) with the WASI and the Becks self-concept subscale (P = 0.038). Lower whole brain fractional anisotropy was associated with higher scores on the Becks anger (P = 0.018) and disruptive behaviour subscales (P = 0.031). Higher whole brain mean diffusivity was associated with apathy (P = 0.046). The pattern of increased risk of white matter microstructure alterations, smaller grey matter volumes, reduced cortical surface area and decreased gyrification, suggests abnormal neurodevelopment in perinatally infected younger adolescents.

BackgroundNew daily persistent headache (NDPH) is a rare but debilitating primary headache disorder that poses a significant burden on individuals and society. Despite its clinical importance, the underlying pathophysiological mechanisms of NDPH remain unclear. In this study, we aimed to investigate the brain structural changes and neural activity patterns in patients with NDPH using multimodal brain imaging analysis of structural magnetic resonance imaging (sMRI) combined with magnetoencephalography (MEG).MethodsTwenty-eight patients with NDPH and 37 healthy controls (HCs) were recruited for this study, and their structural and resting-state data were collected by 3.0 Tesla MRI and MEG. We analyzed the brain morphology using voxel-based morphometry and source-based morphometry. In each brain region, MEG sensor signals from 1 to 200 Hz were analyzed using an adapted version of Welch's method. MEG source localization was conducted using the dynamic statistical parametric mapping, and the difference of source distribution between patients with NDPH and HCs was examined.ResultsOur results revealed significant differences in the regional grey matter volume, cortical thickness, and cortical surface area between the two groups. Specifically, compared with HCs, patients with NDPH showed a significant decrease in cortical thickness of the left rostral cortex in the middle frontal gyrus, decreased cortical surface area of the left fusiform gyrus, decreased grey matter volume of the left superior frontal gyrus and the left middle frontal gyrus, and increased grey matter volume of the left calcarine. Furthermore, the power of the whole brain, bilateral frontal lobes, and right temporal lobe in the NDPH group were higher than that in HCs in the ripple frequency band (80-200 Hz). Functional and structural analysis suggested that there were structural changes and abnormal high frequency cortical activity in both frontal and temporal lobes in patients with NDPH.ConclusionOur findings indicated that patients with NDPH have abnormalities in brain morphology, such as cortical area, cortical thickness, and grey matter volume, accompanied by abnormal cortical neural activity. Brain structural changes in the frontotemporal cortex and abnormalities in cortical ripple activity may be involved in the pathogenesis of NDPH.

Previous studies have suggested that discrete cross-sensory events could be incorrectly combined in the brain of older adults with a history of falls, possibly undermining motor and balance control. Based on previous findings that multisensory integration is modifiable with practice, even in an ageing population, we designed a serious game, named CityQuest, to train typical, everyday multisensory processes including sensori-motor control, spatial navigation, obstacle avoidance and balance control. Played over several sessions, this game was shown to improve these functions in older adults with and without a history of falls, depending on the specific condition of the game on which they were trained. Here, using voxel-based morphometry analysis of anatomical magnetic resonance imaging (MRI) data, we investigated structural changes in the brain of a smaller group of older adults from those who successfully completed this five-week intervention. A grey-matter (GM) volume increase in the precentral gyrus, and GM volume reduction in the inferior temporal and orbitofrontal gyri, was found for all participants. Changes in GM volume within regions of the cerebellum were differentially associated with fall-prone and healthy older adults. Furthermore, a greater GM volume increase in the precentral gyrus was observed in participants who performed the full CityQuest intervention relative to those required to avoid obstacles only. Our results support previous evidence that multisensory training can affect structural changes in the older brain and have implications for programmes designed for the successful rehabilitation of perceptual and cognitive functions.

Background: Neuroanatomical variations are increasingly recognized for their role in influencing cognitive functions, particularly in individuals with subjective cognitive decline (SCD). Structural differences in gray matter (GM) and white matter (WM) volumes, as well as cortical thickness, may underlie the cognitive impairments observed in SCD. Understanding these neuroanatomical changes is crucial for early detection and intervention strategies in cognitive decline. Objective: This study aimed to investigate the neuroanatomical variations between individuals with SCD and healthy controls and to examine the impact of these variations on cognitive functions. Methods: The study was conducted at the Faculty of Rehabilitation Sciences, Lahore University of Biological and Applied Sciences, Pakistan. A total of 42 participants were included, with 21 individuals in the SCD group and 21 in the control group. Participants were recruited through advertisements and referrals, and inclusion criteria for the SCD group included individuals aged 60 and above with self-reported cognitive concerns but no objective impairment on neuropsychological tests. Neuroimaging data were acquired using a 3.0 Tesla MRI scanner, and high-resolution T1-weighted images were analyzed using Statistical Parametric Mapping (SPM) software version 12 and FreeSurfer software. Cognitive function was assessed using the Mini-Mental State Examination (MMSE), Trail Making Test (TMT) Parts A and B, California Verbal Learning Test (CVLT), and Boston Naming Test (BNT). Data analysis was performed using SPSS version 25, with independent t-tests and chi-square tests to compare groups and ANCOVA to adjust for confounders. Effect sizes were calculated using Cohen’s d. Results: Significant differences were observed between the SCD and control groups in several neuroanatomical measures. Individuals with SCD had reduced GM volume in the anterior cingulate cortex (R, p=0.018; L, p=0.025), midcingulate cortex (R, p=0.037), and middle frontal gyrus (L, p=0.030). Significant reductions in WM volume were also found in the inferior frontal gyrus (L, p=0.028) and postcentral gyrus (L, p=0.047). Cortical thickness was significantly reduced in the inferior temporal gyrus (L, p=0.0002; Cohen’s d=1.06), entorhinal cortex (L, p=0.008; Cohen’s d=1.03), and middle temporal gyrus (R, p=0.0004; Cohen’s d=1.02). Cognitive assessments revealed that the SCD group had significantly lower scores on the MMSE (p=0.294, d=0.33), GDS-15 (p=0.001, d=-1.08), and subjective cognitive complaints from patients (p&lt;0.001, d=-2.89). Conclusion: The study found significant neuroanatomical differences between individuals with SCD and healthy controls, particularly in GM and WM volumes and cortical thickness. These structural variations were associated with cognitive impairments observed in the SCD group, underscoring the importance of early detection and targeted interventions. Future research should focus on longitudinal studies and the integration of biomarkers to enhance the understanding of neuroanatomical changes in cognitive decline. Keywords: Neuroanatomical Variations, Subjective Cognitive Decline, Gray Matter Volume, White Matter Volume, Cortical Thickness, Cognitive Functions, MRI, Neuroimaging, Early Detection, Cognitive Decline.

Reductions in body weight and insulin resistance are not associated with changes in grey matter volume or cortical thickness during the PREVIEW study

Biochemical changes in the cerebrospinal fluid (CSF) could reflect pathophysiological processes in Alzheimer's disease (AD). However, it is still not clear how these processes correlate with grey matter (GM) volume and microstructural changes in the brain. To assess the relationship between CSF biomarkers and structural brain changes in AD. Cross-sectional study in a memory clinic-based sample. A total of 78 subjects were included in the study: 22 with subjective cognitive impairment (SCI), 35 with mild cognitive impairment (MCI) and 21 with AD. Voxel-wise correlations between CSF biomarkers, including β-amyloid42 (Aβ42), tau phosphorylated at position threonine 181 and total tau protein, and GM volume, self-diffusion fractional anisotropy (FA) and mean diffusivity (MD) maps using voxel-based morphometry and tract-based spatial statistical analyses. FA and MD maps were obtained using diffusion tensor imaging. In the whole sample (patients with SCI, MCI and AD), there was positive correlation between GM volume and Aβ42 concentration, and negative correlation with total tau protein. Higher FA was only related to higher concentration of Aβ42. MD showed significant negative correlation with Aβ42 and positive correlation with T-tau levels. The majority of brain regions with significant correlation with CSF biomarkers overlapped with the default mode network and extended to the adjacent white matter. Early AD pathological changes can be detected with voxel-based morphometric analysis and diffusion tensor imaging measurements. Furthermore, there was an association between CSF AD biomarkers and structural brain changes in areas related to the default mode network.

Su1293 Neuroimaging Changes and Behavioral Correlates in Patients With Crohn's Disease

Cortical thickness analysis and optimized voxel-based morphometry in children and adolescents with prelingually profound sensorineural hearing loss

This review aims to summarise the current knowledge on structural brain changes among people diagnosed with gaming disorder and the resulting clinical implications. The review will show the theoretical psychological and neurobiological models of computer gaming disorder in conjunction with the results of structural neuroimaging studies. Previous epidemiological studies indicate that the prevalence of gaming disorder in the population may reach approx. 2%. Researchers indicate that the aetiopathogenesis of computer game use disorder is complex and includes psychological, social, as well as neurological and hormonal factors. From the perspective of psychological research exploring gaming disorder, it can be concluded that a person has certain specific psychopathological features and/or symptoms, which, through mediating factors, such as the inability to cope with stress or negative emotions, influence the formation of the symptoms of the disorder. In the context of the neurobiology of behavioural addictions, researchers point to disorders in the mesocorticolimbic reward system, which is influenced by dysfunctional neuronal mechanisms of emotion and stress regulation. When describing structural changes in the brain, researchers most often report differences in the volume of grey matter, which include areas of the dorsolateral prefrontal cortex, temporooccipital cortex, superior and posterior parietal cortex, anterior cingulate cortex, cerebellum, insular cortex, limbic system, and basal ganglia.

The time course of neuroanatomical structural and functional measures across the lifespan is commonly reported in association with aging. Blood oxygen-level dependent signal variability, estimated using the standard deviation of the signal, or “BOLDSD,” is an emerging metric of variability in neural processing, and has been shown to be positively correlated with cognitive flexibility. Generally, BOLDSD is reported to decrease with aging, and is thought to reflect age-related cognitive decline. Additionally, it is well established that normative aging is associated with structural changes in brain regions, and that these predict functional decline in various cognitive domains. Nevertheless, the interaction between alterations in cortical morphology and BOLDSD changes has not been modeled quantitatively. The objective of the current study was to investigate the influence of cortical morphology metrics [i.e., cortical thickness (CT), gray matter (GM) volume, and cortical area (CA)] on age-related BOLDSD changes by treating these cortical morphology metrics as possible physiological confounds using linear mixed models. We studied these metrics in 28 healthy older subjects scanned twice at approximately 2.5 years interval. Results show that BOLDSD is confounded by cortical morphology metrics. Respectively, changes in CT but not GM volume nor CA, show a significant interaction with BOLDSD alterations. Our study highlights that CT changes should be considered when evaluating BOLDSD alternations in the lifespan.

Structural alterations in patients with schizophrenia: An advanced neuroimaging VBM study