Browse
Submit Data
Databases
API
Help

Dataset Information

18 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of radiation therapy on cerebral cortical thickness in glioma patients: Treatment-induced thinning of the healthy cortex.

ABSTRACT: AbstractBackgroundWith overall survival of brain tumors improving, radiation induced brain injury is becoming an increasing issue. One of the effects of radiation therapy (RT) is thinning of the cerebral cortex, which could be one of the factors contributing to cognitive impairments after treatment. In healthy brain, cortex thickness varies between 1 and 4.5 mm. In this study, we assess the effect of RT on the thickness of the cerebral cortex and relate the changes to the local dose.MethodsWe identified 28 glioma patients with optimal scan quality. Clinical CTs and MRIs at baseline and 1 year post-RT were collected and coregistered. The scans were processed via an automated image processing pipeline, which enabled measuring changes of the cortical thickness, which were related to local dose.ResultsThree areas were identified where significant dose-dependent thinning occurred, with thinning rates of 5, 6, and 26 ?m/Gy after 1 year, which corresponds to losses of 5.4%, 7.2%, and 21.6% per 30 Gy per year. The first area was largely located in the right inferior parietal, supramarginal, and superior parietal regions, the second in the right posterior cingulate and paracentral regions, and the third almost completely in the right lateral orbital frontal region.ConclusionsWe have identified three areas susceptible to dose-dependent cortical thinning after radiation therapy. Should future prospective studies conclude that irradiation of these areas lead to cognitive decline, they need to be spared in order to prevent this debilitating consequence of treatment.

SUBMITTER: Nagtegaal SHJ

PROVIDER: S-EPMC7284116 | biostudies-literature | 2020 Jan-Dec

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Similar Datasets

Decreased regional cortical thickness and thinning rate are associated with inattention symptoms in healthy children.

Project description:OBJECTIVE:Children with attention-deficit/hyperactivity disorder (ADHD) have delayed cortical maturation, evidenced by regionally specific slower cortical thinning. However, the relationship between cortical maturation and attention capacities in typically developing children is unknown. This study examines cortical thickness correlates of inattention symptoms in a large sample of healthy children. METHOD:Data from 357 healthy subjects (6.0-18.4 years of age) were obtained from the NIH MRI Study of Normal Brain Development. In cross-sectional analysis (first visit, n = 257), Child Behavior Checklist Attention Problems (AP) scores were linearly regressed against cortical thickness, controlling for age, gender, total brain volume, and site. For longitudinal data (up to three visits, n = 357/672 scans), similar analyses were performed using mixed-effects linear regressions. Interactions of AP with age and gender were tested. RESULTS:A cross-sectional "AP by age" interaction was found in bilateral orbito-frontal cortex, right inferior frontal cortex, bilateral ventromedial prefrontal cortex, bilateral dorsolateral prefrontal cortex, and several additional attention network regions. The interaction was due to negative associations between AP and thickness in younger subjects (6-10 years of age) that gradually disappeared over time secondary to slower cortical thinning. Similar trends were present in longitudinal analyses. CONCLUSIONS:Higher AP scores were associated with thinner cortex at baseline and slower cortical thinning with aging in multiple areas involved in attention processes. Similar patterns have been identified in ADHD, suggesting a dimensional component to the link between attention and cortical maturation. The identified association between cortical maturation and attention in healthy development will help to inform studies of neuroimaging biomarkers of ADHD.

| S-EPMC3297982 | biostudies-literature

Chromatin regulation by BAF170 controls cerebral cortical size and thickness.

Project description:Increased cortical size is essential to the enhanced intellectual capacity of primates during mammalian evolution. The mechanisms that control cortical size are largely unknown. Here, we show that mammalian BAF170, a subunit of the chromatin remodeling complex mSWI/SNF, is an intrinsic factor that controls cortical size. We find that the conditional deletion of BAF170 promotes indirect neurogenesis by increasing the pool of intermediate progenitors (IPs) and results in an enlarged cortex, whereas cortex-specific BAF170 over-expression results an opposing phenotype. Mechanistically, BAF170 competes with BAF155 subunit in the BAF complex, affecting the euchromatin structure and thereby modulating the binding efficiency of Pax6/REST-corepressor complex to Pax6 target genes that regulate the generation of IPs and late cortical progenitors. Our findings reveal a molecular mechanism mediated by the mSWI/SNF chromatin-remodeling complex that controls cortical architecture. Cortical gene expression is compared between three E12.5 mouse embryos with cortex-specific loss of BAF170 function and three littermate control embryos.

2013-05-02 | E-GEOD-45629 | biostudies-arrayexpress

Altered cerebral hemodyamics and cortical thinning in asymptomatic carotid artery stenosis.

Project description:Cortical thinning is a potentially important biomarker, but the pathophysiology in cerebrovascular disease is unknown. We investigated the association between regional cortical blood flow and regional cortical thickness in patients with asymptomatic unilateral high-grade internal carotid artery disease without stroke. Twenty-nine patients underwent high resolution anatomical and single-delay, pseudocontinuous arterial spin labeling magnetic resonance imaging with partial volume correction to assess gray matter baseline flow. Cortical thickness was estimated using Freesurfer software, followed by co-registration onto each patient's cerebral blood flow image space. Paired t-tests assessed regional cerebral blood flow in motor cortex (supplied by the carotid artery) and visual cortex (indirectly supplied by the carotid) on the occluded and unoccluded side. Pearson correlations were calculated between cortical thickness and regional cerebral blood flow, along with age, hypertension, diabetes and white matter hyperintensity volume. Multiple regression and generalized estimating equation were used to predict cortical thickness bilaterally and in each hemisphere separately. Cortical blood flow correlated with thickness in motor cortex bilaterally (p = 0.0002), and in the occluded and unoccluded sides individually; age (p = 0.002) was also a predictor of cortical thickness in the motor cortex. None of the variables predicted cortical thickness in visual cortex. Blood flow was significantly lower on the occluded versus unoccluded side in the motor cortex (p<0.0001) and in the visual cortex (p = 0.018). On average, cortex was thinner on the side of occlusion in motor but not in visual cortex. The association between cortical blood flow and cortical thickness in carotid arterial territory with greater thinning on the side of the carotid occlusion suggests that altered cerebral hemodynamics is a factor in cortical thinning.

| S-EPMC5730122 | biostudies-literature

Thinning Faster? Age-Related Cortical Thickness Differences in Adults with Autism Spectrum Disorder.

Project description:Background:Over the course of the last 30 years, autism spectrum disorder (ASD) diagnoses have increased, thus identifying a large group of aging individuals with ASD. Currently, little is known regarding how aging will affect these individual's neuroanatomy, compared to the neurotypical (NT) population. Because of the anatomical overlap of ASD-related cortical pathology and age-related cortical thinning, both following an anterior-to-posterior severity gradient, we hypothesize adults with ASD will show larger age-related cortical thinning than NT adults. Methods:We analyzed cortical measurements using available data from the multi-site Autism Brain Imaging Data Exchange I (ABIDE I; n=282) and our own cohort of middle-age to older adults with and without ASD (n=47) mostly available in ABIDE II (n=35). We compared correlations between cortical measures and age in right-handed adults with ASD (n=157) and similar NT adults (n = 172), controlling for IQ and site. Participants were 18 to 64 years of age (mean=29.8 years; median=26 years). Results:We found significant differences between diagnosis groups in the relationship between age and cortical thickness for areas of left frontal lobe (pars opercularis), temporal lobe (inferior gyrus, middle gyrus, banks of the superior temporal sulcus, and entorhinal cortex), parietal lobe (inferior gyrus), and lateral occipital lobe. For all areas, adults with ASD showed a greater negative correlation between age and cortical thickness than NT adults. Conclusion:As hypothesized, adults with ASD demonstrated exacerbated age-related cortical thinning, compared to NT adults. These differences were the largest and most extensive in the left temporal lobe. Future longitudinal work is warranted to investigate whether differences in brain age trajectories will translate to unique behavioral needs in older adults with ASD.

| S-EPMC7304569 | biostudies-literature

Chromatin regulation by BAF170 controls cerebral cortical size and thickness.

2013-05-02 | GSE45629 | GEO

Normative cerebral cortical thickness for human visual areas.

Project description:Studies of changes in cerebral neocortical thickness often rely on small control samples for comparison with specific populations with abnormal visual systems. We present a normative dataset for FreeSurfer-derived cortical thickness across 25 human visual areas derived from 960 participants in the Human Connectome Project. Cortical thickness varies systematically across visual areas, in broad agreement with canonical visual system hierarchies in the dorsal and ventral pathways. In addition, cortical thickness estimates show consistent within-subject variability and reliability. Importantly, cortical thickness estimates in visual areas are well described by a normal distribution, making them amenable to direct statistical comparison.

| S-EPMC6892250 | biostudies-literature

Mapping cortical thickness of the patients with unilateral end-stage open angle glaucoma on planar cerebral cortex maps.

Project description:PURPOSE: To estimate and compare cerebral cortex thickness in patients with unilateral end-stage glaucoma with that of age-matched individuals with unaffected vision. METHODS: 14 patients with unilateral end-stage primary open angle glaucoma (POAG) and 12 age-matched control individuals with no problems with vision were selected for the study based on detailed ophthalmic examination. For each participant 3D high-resolution structural brain T1-weighted magnetization prepared MR images were acquired on a 3.0 T scanner. Brain cortex thickness was estimated using the FreeSurfer image analysis environment. After warping of subjects' cortical surfaces to FreeSurfer common space, differences between POAG and control groups were inferred at the group analysis level with the General Linear Model. RESULTS: The analysis performed revealed local thinning in the visual cortex areas in the POAG group. Statistically significant differences form 600 mm2 clusters located in the Brodmann area BA19 in the left and right hemisphere. CONCLUSION: Unilateral vision loss due to end-stage neuropathy from POAG is associated with significant thinning of cortical areas employed in vision.

| S-EPMC3977872 | biostudies-literature

Quantifying the Polygenic Architecture of the Human Cerebral Cortex: Extensive Genetic Overlap between Cortical Thickness and Surface Area.

Project description:The thickness of the cerebral cortical sheet and its surface area are highly heritable traits thought to have largely distinct polygenic architectures. Despite large-scale efforts, the majority of their genetic determinants remain unknown. Our ability to identify causal genetic variants can be improved by employing brain measures that better map onto the biology we seek to understand. Such measures may have fewer variants but with larger effects, that is, lower polygenicity and higher discoverability. Using Gaussian mixture modeling, we estimated the number of causal variants shared between mean cortical thickness and total surface area, as well as the polygenicity and discoverability of regional measures. We made use of UK Biobank data from 30 880 healthy White European individuals (mean age 64.3, standard deviation 7.5, 52.1% female). We found large genetic overlap between total surface area and mean thickness, sharing 4016 out of 7941 causal variants. Regional surface area was more discoverable (P = 2.6 × 10-6) and less polygenic (P = 0.004) than regional thickness measures. These findings may serve as a roadmap for improved future GWAS studies; knowledge of which measures are most discoverable may be used to boost identification of genetic predictors and thereby gain a better understanding of brain morphology.

| S-EPMC7472200 | biostudies-literature

Association of Prefrontal Cortex Thinning with High Impulsivity in Healthy Adults.

Project description:ObjectiveStudies have been conducted to identify brain structural alterations related to high impulsivity in psychiatric populations. However, research on healthy subjects is relatively less extensive. Therefore, we aimed to investigate the correlation between the cortical thickness of whole brain regions and the impulsivity level in a healthy population.MethodsWe included 100 healthy participants aged 19-65 years. Their T1-weighted magnetic resonance images and the 23-item Barratt Impulsiveness Scale (BIS) score were obtained. The patients were divided into high and low impulsivity groups according to the 75th percentile score of the BIS in the sample. The thickness of each cortical region was calculated using the FreeSurfer, and the difference in cortical thickness of the whole brain between the high and low impulsivity groups was analyzed using one-way analysis of covariance including age, sex, education level, and total intracranial cavity volume as covariates.ResultsThe high impulsivity group showed significant cortical thinning in the left pars opercularis. The cortical thickness of the left pars opercularis significantly correlated negatively with the total, attention, and motor scores of the BIS scale.ConclusionOur findings suggest that prefrontal cortex thinning may play an important role in the development of high impulsivity in healthy adults.

| S-EPMC8256145 | biostudies-literature

Cerebral perfusion and cortical thickness indicate cortical involvement in mild Parkinson's disease.

Project description:Cortical dysfunction in Parkinson's disease (PD) may be caused by disruption to ascending systems or by intrinsic cortical neuropathology. We introduce and conduct a joint analysis of metabolism and atrophy capable of identifying whether metabolic disruption occurs in mild PD without cortical atrophy, to determine the extent and spatial pattern of cortical involvement in mild PD. The design was observational, studying 23 cognitively normal participants with mild PD (mean Hoehn & Yahr stage 2) and 21 healthy controls. Cortical thickness (obtained from analysis of structural magnetic resonance imaging [MRI] with FreeSurfer) and cerebral perfusion measures (obtained from arterial spin labeling [ASL]) analyzed independently and then together in a joint multiple factorial analysis to identify spatial patterns of perfusion and cortical thickness. We identify a pattern of changes in perfusion and cortical thickness characterized by symmetric parietal cortical thinning and reduced precuneus perfusion, with relative preservation of thickness and perfusion in the anterior cingulate cortex (ACC), right prefrontal gyrus, and medial frontal gyrus. The expression of this pattern is correlated with motor system symptoms and speed of processing. A spatial pattern of joint parietal cortical thinning and disproportionate reduction in perfusion occurs in our nondemented PD sample. We found no PD-related components of reduced perfusion without cortical thinning. This suggests that PD affects the cortex itself, even when symptoms are relatively mild.

| S-EPMC4567553 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data