Cortical Thickness
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2021 ◽  
yi li ◽  
Henry Rusinek ◽  
Tracy Butler ◽  
Lidia Glodzik ◽  
Elizabeth Pirraglia ◽  

Abstract In sporadic Alzheimer’s disease (AD), brain amyloid-beta (Aβ) deposition is believed to be a consequence of impaired Aβ clearance, but this relationship is not well established in living human subjects. CSF clearance, a major feature of brain glymphatic clearance (BGC), has been shown to be abnormal in AD murine models. Prior MRI phase contrast studies have reported reduced aqueductal CSF flow in AD. Using PET and tau tracer 18F-THK5117, we previously reported that the ventricular CSF clearance of the PET tracer was reduced in AD and associated with elevated brain Aβ levels. In the present study, using two PET tracers, 18F-THK5351 and 11C-PiB to estimate CSF clearance, we observe that the ventricular CSF clearance measures were correlated (r = .66, p < .01), with reductions in AD of 18 and 27%, respectively. We also replicated a significant relationship between ventricular CSF clearance (18F-THK5331) and brain Aβ load (r = −.64, p < .01). With a larger sample size, we extended our observations to show that reduced CSF clearance is associated with reductions in cortical thickness and cognitive performance. Overall, the findings support the hypothesis that failed CSF clearance is a feature of AD that is related to Aβ deposition and to the pathology of AD. Longitudinal studies are needed to determine whether failed CSF clearance is a predictor of progressive amyloidosis or its consequence.

2021 ◽  
Vol 12 ◽  
Yifan Yang ◽  
Yuqi Cheng ◽  
Xiangyu Wang ◽  
Bibhuti Upreti ◽  
Ruomei Cui ◽  

Background: Hyperuricemia is the cause of gout. The antioxidant and neuroprotective effects of uric acid seem to benefit some patients with central nervous system injury. However, changes in the brain structure have not been discovered in patients with gout.Object: Clarify the changes in cortical thickness in patients with gout and the alteration of the structural covariance networks (SCNs) based on cortical thickness.Methods: We collected structural MRIs of 23 male gout patients and 23 age-matched healthy controls. After calculating and comparing the difference in cortical thickness between the two groups, we constructed and analyzed the cortical thickness covariance networks of the two groups, and we investigated for any changes in SCNs of gout patients.Results: Gout patients have thicker cortices in the left postcentral, left supramarginal, right medial temporal, and right medial orbitofrontal regions; and thinner cortices were found in the left insula, left superior frontal, right pericalcarine, and right precentral regions. In SCN analysis, between-group differences in global network measures showed that gout patients have a higher global efficiency. In regional network measures, more nodes in gout patients have increased centrality. In network hub analysis, we found that the transfer of the core hub area, rather than the change in number, may be the characteristic of the gout's cortical thickness covariance network.Conclusion: This is the first study on changes in brain cortical thickness and SCN based on graph theory in patients with gout. The present study found that, compared with healthy controls, gout patients show regional cortical thinning or thickening, and variation in the properties of the cortical thickness covariance network also changed. These alterations may be the combined effect of disease damage and physiological compensation. More research is needed to fully understand the complex underlying mechanisms of gout brain variation.

2021 ◽  
Dylan James Kiltschewskij ◽  
William R Reay ◽  
Murray J Cairns

Psychiatric disorders such as schizophrenia are commonly associated with structural brain alterations affecting the cortex, which frequently vary with clinically relevant factors including antipsychotic treatment, duration of illness and age of onset. While the underlying variables mediating these structural changes are poorly understood, recent genetic evidence suggests circulating metabolites and other biochemical traits play a causal role in a number of psychiatric disorders which could be mediated by changes in the cerebral cortex. In the current study, we leveraged publicly available genome-wide association study (GWAS) data to explore shared genetic architecture and evidence for causal relationships between a panel of 50 biochemical traits and measures of cortical thickness and surface area at both the global and regional levels. Linkage disequilibrium score regression identified a total of 20 significant and 156 suggestive genetically correlated biochemical-cortical trait pairings, of which six exhibited strong evidence for causality in a latent causal variable model. Interestingly, a negative causal relationship was identified between a unit increase in serum C-reactive protein levels and thickness of the lingual and lateral occipital regions that was also supported by Mendelian randomisation, while circulating vitamin D (25-hydroxyvitamin D) levels exhibited a positive causal effect on temporal pole thickness. Taken together, our findings suggest a subset of biochemical traits exhibit shared genetic architecture and potentially causal relationships with cortical thickness in functionally distinct regions, which may contribute to alteration of cortical structure in psychiatric disorders.

2021 ◽  
Vol 13 (1) ◽  
Jason Hassenstab ◽  
Jessica Nicosia ◽  
Megan LaRose ◽  
Andrew J. Aschenbrenner ◽  
Brian A. Gordon ◽  

Abstract Background Comprehensive testing of cognitive functioning is standard practice in studies of Alzheimer disease (AD). Short-form tests like the Montreal Cognitive Assessment (MoCA) use a “sampling” of measures, administering key items in a shortened format to efficiently assess cognition while reducing time requirements, participant burden, and administrative costs. We compared the MoCA to a commonly used long-form cognitive battery in predicting AD symptom onset and sensitivity to AD neuroimaging biomarkers. Methods Survival, area under the receiver operating characteristic (ROC) curve (AUC), and multiple regression analyses compared the MoCA and long-form measures in predicting time to symptom onset in cognitively normal older adults (n = 6230) from the National Alzheimer’s Coordinating Center (NACC) cohort who had, on average, 2.3 ± 1.2 annual assessments. Multiple regression models in a separate sample (n = 416) from the Charles F. and Joanne Knight Alzheimer Disease Research Center (Knight ADRC) compared the sensitivity of the MoCA and long-form measures to neuroimaging biomarkers including amyloid PET, tau PET, and cortical thickness. Results Hazard ratios suggested that both the MoCA and the long-form measures are similarly and modestly efficacious in predicting symptomatic conversion, although model comparison analyses indicated that the long-form measures slightly outperformed the MoCA (HRs > 1.57). AUC analyses indicated no difference between the measures in predicting conversion (DeLong’s test, Z = 1.48, p = 0.13). Sensitivity to AD neuroimaging biomarkers was similar for the two measures though there were only modest associations with tau PET (rs = − 0.13, ps < 0.02) and cortical thickness in cognitively normal participants (rs = 0.15–0.16, ps < 0.007). Conclusions Both test formats showed weak associations with symptom onset, AUC analyses indicated low diagnostic accuracy, and biomarker correlations were modest in cognitively normal participants. Alternative assessment approaches are needed to improve how clinicians and researchers monitor cognitive changes and disease progression prior to symptom onset.

Goretti España‐Irla ◽  
Joyce Gomes‐Osman ◽  
Gabriele Cattaneo ◽  
Sergiu Albu ◽  
María Cabello‐Toscano ◽  

Background Evidence in older adults suggests that higher cardiorespiratory fitness and lower cardiovascular risk are associated with greater cognition. However, given that changes in the brain that lead to cognitive decline begin decades before the onset of symptoms, understanding the mechanisms by which modifiable cardiovascular factors are associated with brain health in midlife is critical and can lead to the development of strategies to promote and maintain brain health as we age. Methods and Results In 501 middle‐aged (aged 40–65 years) adult participants of the BBHI (Barcelona Brain Health Initiative), we found differential associations among cardiorespiratory fitness, cardiovascular risk, and cognition and cortical thickness. Higher cardiorespiratory fitness was significantly associated with better visuospatial abilities and frontal loading abstract problem solving (β=3.16, P =0.049) in the older middle‐aged group (aged 55–65 years). In contrast, cardiovascular risk was negatively associated with better visuospatial reasoning and problem‐solving abilities (β=−0.046, P =0.002), flexibility (β=−0.054, P <0.001), processing speed (β=−0.115, P <0.001), and memory (β=−0.120, P <0.001). Cortical thickness in frontal regions mediated the relationship between cardiorespiratory fitness and cognition, whereas cortical thickness in a disperse network spanning multiple cortical regions across both hemispheres mediated the relationship between cardiovascular risk and cognition. Conclusions The relationships between modifiable cardiovascular factors, cardiorespiratory fitness, and cardiovascular risk, and cognition are present in healthy middle‐aged adults. These relationships are also mediated by brain structure highlighting a potential mechanistic pathway through which higher cardiorespiratory fitness and lower cardiovascular risk can positively impact cognitive function in midlife.

Biomedicines ◽  
2021 ◽  
Vol 9 (9) ◽  
pp. 1195
Stefano Ferrea ◽  
Frederick Junker ◽  
Mira Korth ◽  
Kai Gruhn ◽  
Torsten Grehl ◽  

Background: Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder clinically characterized by muscle atrophy and progressive paralysis. In addition to the classical ALS affecting both the upper and lower motoneurons (UMN and LMN), other subtypes with the predominant (or even exclusive) affection of the UMN or LMN have been identified. This work sought to detect specific patterns of cortical brain atrophy in the UMN and LMN phenotypes to distinguish these two forms from the healthy state. Methods: Using high-resolution structural MRI and cortical thickness analysis, 38 patients with a diagnosis of ALS and predominance of either the UMN (n = 20) or the LMN (n = 18) phenotype were investigated. Results: Significant cortical thinning in the temporal lobe was found in both the ALS groups. Additionally, UMN patients displayed a significant thinning of the cortical thickness in the pre- and postcentral gyrus, as well as the paracentral lobule. By applying multivariate analyses based on the cortical thicknesses of 34 brain regions, ALS patients with either a predominant UMN or LMN phenotype were distinguished from healthy controls with an accuracy of 94% and UMN from LMN patients with an accuracy of 75%. Conclusions: These findings support previous hypothesis that neural degeneration in ALS is not confined to the sole motor regions. In addition, the amount of cortical thinning in the temporal lobe helps to distinguish ALS patients from healthy controls, that is, to support or discourage the diagnosis of ALS, while the cortical thickness of the precentral gyrus specifically helps to distinguish the UMN from the LMN phenotype.

Yoonmi Woo ◽  
Wooyoung Kang ◽  
Youbin Kang ◽  
Aram Kim ◽  
Kyu-Man Han ◽  

2021 ◽  
pp. appi.ajp.2021.2
Christine Ecker ◽  
Charlotte M. Pretzsch ◽  
Anke Bletsch ◽  
Caroline Mann ◽  
Tim Schaefer ◽  

2021 ◽  
Vol 11 (9) ◽  
pp. 1180
Chendi Cui ◽  
Aya Higashiyama ◽  
Brian J. Lopresti ◽  
Masafumi Ihara ◽  
Howard J. Aizenstein ◽  

The Alzheimer’s Disease Neuroimaging Initiative showed that Japanese had significantly lower brain Aβ burden than Americans among a cognitively normal population. This cross-sectional study aimed to compare vascular disease burden, Aβ burden, and neurodegeneration between cognitively normal elderly Japanese and Americans. Japanese and American participants were matched for age (± 4-year-old), sex, and Apolipoprotein E (APOE) genotype. Brain vascular disease burden and brain Aβ burden were measured using white matter lesions (WMLs) and 11C-labeled Pittsburgh Compound B (PiB) retention, respectively. Neurodegeneration was measured using hippocampal volumes and cortical thickness. A total of 95 Japanese and 95 Americans were recruited (50.5% men, mean age = 82). Compared to Americans, Japanese participants had larger WMLs, and a similar global Aβ standardized uptake value ratio (SUVR), cortical thickness and hippocampal volumes. Japanese had significantly lower regional Aβ SUVR in the anterior ventral striatum, posterior cingulate cortex, and precuneus. Cognitively normal elderly Japanese and Americans had different profiles regarding vascular disease and Aβ burden. This suggests that multiple risk factors are likely to be involved in the development of dementia. Additionally, Japanese might have a lower risk of dementia due to lower Aβ burden than Americans. Longitudinal follow-up of these cohorts is warranted to ascertain the predictive accuracy of these findings.

2021 ◽  
Allison L. Moreau ◽  
Michaela Voss ◽  
Isabella Hansen ◽  
Sarah E. Paul ◽  
Cynthia E. Rogers ◽  

Objective: Prenatal selective serotonin reuptake inhibitor (SSRI) exposure has been inconsistently linked to depression. Potential neural intermediaries remain understudied. We examined whether prenatal SSRI exposure is associated with depressive symptoms and brain structure during middle childhood. Methods: Prenatal SSRI exposure (retrospective caregiver-report), depressive symptoms (caregiver-reported Child Behavior Checklist) and brain structure (MRI-derived subcortical volume; cortical thickness and surface area) were assessed in children (analytic ns=5,420-7,528; 235 with prenatal SSRI exposure; 9-10 years old) who completed the baseline session of the Adolescent Brain and Cognitive DevelopmentSM Study. Covariates included familial (e.g., 1st degree relative depression density), pregnancy (e.g., planned pregnancy), and child (e.g., birthweight) variables. Matrix spectral decomposition was used to address multiple testing. Results: There was no evidence that prenatal SSRI exposure was associated with child depression after accounting for recent maternal depressive symptoms. Prenatal SSRI exposure was associated with greater left superior parietal surface area (b=145.3 mm2, p=0.00038) and lateral occipital cortical thickness (b=0.0272 mm, p=0.0000079), neither of which was associated with depressive symptoms. Conclusions: Our findings, combined with adverse associations of prenatal exposure to maternal depression and the utility of SSRIs for treating depression, suggest that risk for child depression during middle childhood should not discourage SSRI use during pregnancy. It will be important for future work to examine associations between prenatal SSRI exposure and depression through young adulthood, when risk for depression increases.

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