Longitudinal Changes In Cortical Thickness Research Articles

The Relationship between History of Traumatic Brain Injury and Longitudinal Changes in Cortical Thickness among Patients with Alzheimer's Disease.

There has been little direct examination of how traumatic brain injury (TBI) affects the rate of neurodegeneration for individuals with Alzheimer's disease (AD). The study examined 89 cognitively normal adults (65 with and 24 without prior TBI) and 65 with AD (16 with and 49 without prior TBI). Cortical thickness was quantified from T1-weighted MRI scans at baseline and follow-up (mean interval 33.4 months). Partial least squares analysis was used to evaluate the effects of AD and TBI history on the longitudinal change in cortical thickness. Significant group effects were identified throughout the frontal and temporal cortices. Comparison of the AD groups to their control cohorts showed greater relative atrophy for the AD cohort with prior TBI. These results indicate that a history of TBI exacerbates longitudinal declines in cortical thickness among AD patients, providing new insights into the shared pathomechanisms between these neurological conditions.

Age-related change in cortical thickness in adolescents at clinical high risk for psychosis: a longitudinal study.

Progression to psychosis has been associated with increased cortical thinning in the frontal, temporal and parietal lobes in individuals at clinical high risk for the disorder (CHR-P). The timing and spatial extent of these changes are thought to be influenced by age. However, most evidence so far stems from adult samples. Longitudinal studies are essential to understanding the neuroanatomical changes associated to transition to psychosis during adolescence, and their relationship with age. We conducted a longitudinal, multisite study including adolescents at CHR-P and healthy controls (HC), aged 10-17years. Structural images were acquired at baseline and at 18-month follow-up. Images were processed with the longitudinal pipeline in FreeSurfer. We used a longitudinal two-stage model to compute the regional cortical thickness (CT) change, and analyze between-group differences controlling for age, sex and scan, and corrected for multiple comparisons. Linear regression was used to study the effect of age at baseline. A total of 103 individuals (49 CHR-P and 54 HC) were included in the analysis. During follow-up, the 13 CHR-P participants who transitioned to psychosis exhibited greater CT decrease over time in the right parietal cortex compared to those who did not transition to psychosis and to HC. Age at baseline correlated with longitudinal changes in CT, with younger individuals showing greater cortical thinning in this region. The emergence of psychosis during early adolescence may have an impact on typical neuromaturational processes. This study provides new insights on the cortical changes taking place prior to illness onset.

Poorer aging trajectories are associated with elevated serotonin synthesis capacity.

The dorsal raphe nucleus (DRN) is one of the earliest targets of Alzheimer's disease-related tau pathology and is a major source of brain serotonin. We used [18F]Fluoro-m-tyrosine ([18F]FMT) PET imaging to measure serotonin synthesis capacity in the DRN in 111 healthy adults (18-85 years-old). Similar to reports in catecholamine systems, we found elevated serotonin synthesis capacity in older adults relative to young. To establish the structural and functional context within which serotonin synthesis capacity is elevated in aging, we examined relationships among DRN [18F]FMT net tracer influx (Ki) and longitudinal changes in cortical thickness using magnetic resonance imaging, longitudinal changes in self-reported depression symptoms, and AD-related tau and β-amyloid (Aβ) pathology using cross-sectional [18F]Flortaucipir and [11C]Pittsburgh compound-B PET respectively. Together, our findings point to elevated DRN [18F]FMT Ki as a marker of poorer aging trajectories. Older adults with highest serotonin synthesis capacity showed greatest temporal lobe cortical atrophy. Cortical atrophy was associated with increasing depression symptoms over time, and these effects appeared to be strongest in individuals with highest serotonin synthesis capacity. We did not find direct relationships between serotonin synthesis capacity and AD-related pathology. Exploratory analyses revealed nuanced effects of sex within the older adult group. Older adult females showed the highest DRN synthesis capacity and exhibited the strongest relationships between entorhinal cortex tau pathology and increasing depression symptoms. Together these findings reveal PET measurement of the serotonin system to be a promising marker of aging trajectories relevant to both AD and affective changes in older age.

Baseline long-term potentiation-like cortical plasticity is associated with longitudinal cortical thinning in healthy adults and in adults with bipolar disorder type II.

The precise neurobiological processes underlying cerebral cortical thinning in aging and psychiatric illnesses remain undetermined, yet aging- and synaptic dysfunction-related loss of synapses are potentially important mechanisms. We used long-term potentiation-like plasticity of the visual evoked potential as an index of synaptic function in the cortex and hypothesized that plasticity at baseline would be negatively associated with future cortical thinning in healthy adults and in adults with bipolar disorder type II. Thirty-two healthy adults and 15 adults with bipolar disorder type II underwent electroencephalography-based measurement of visual evoked potential plasticity and 3T magnetic resonance imaging of the brain at baseline and a follow-up brain scan on average 2.3 years later. The relationships between visual evoked potential plasticity at baseline and longitudinal cortical thickness changes were examined using Freesurfer and the Permutation Analysis of Linear Models tool. The analyses showed a negative association between the plasticity of the N1 visual evoked potential amplitude at baseline and thinning rate in the medial and lateral parietal and medial occipital cortices in healthy adults and in the right medial occipital cortex in the total sample of healthy adults and adults with bipolar disorder type II, indicating greater thinning over time in subjects with less N1 plasticity (pFWER < .05). Although preliminary, the results indicate an association between visual evoked potential plasticity and the future rate of cortical thinning in healthy adults and in bipolar disorder type II, supporting the hypothesis that cortical thinning might be related to synaptic dysfunction.

Longitudinal changes in brain structure and their relationship with subclinical psychiatric symptoms in parents who lost their only child in China

ABSTRACT Background: Losing an only child (Shidu) is a grievous traumatic event that may affect brain structure, even if it does not lead to psychiatric disorders. However, longitudinal changes in brain structure and their relationship to subclinical psychiatric symptoms (SPS) have not been well investigated in Shidu parents without any psychiatric disorders (SDNP). Objectives: This study aimed to investigate cross-sectional and longitudinal changes in cortical thickness and surface area in SDNP, and to explore their relationship with SPS. Methods: A total of 50 SDNP and 40 matched healthy controls (HC) were enrolled. All participants underwent structural MRI scans and clinical assessment at baseline and at the 5-year follow-up. Differences in brain structural phenotypes (cortical thickness, surface area, and their annual rate of change) between the SDNP and HC groups were compared using FreeSurfer. Correlations between significant brain structural phenotypes and SPS in the SDNP group were evaluated using multiple linear regressions. Results: The SDNP group showed a smaller surface area in the left inferior parietal cortex than the HC group at baseline and follow-up. The SDNP group showed slower rates of cortical thinning and surface area loss in several brain regions than the HC group from baseline to follow-up. Moreover, slower rates of cortical thinning in the left insula, superior frontal cortex, and superior temporal cortex were associated with greater reductions in avoidance, depression, and trauma re-experiencing symptoms scores over time in the SDNP group, respectively. Conclusions: Shidu trauma-induced structural abnormalities in the inferior parietal cortex may persist over time and be independent of the severity of psychiatric symptoms. The expansion of prefrontal, temporal, and insular cortex implicated in emotional regulation may contribute to improvements in psychiatric symptoms in Shidu parents.

Development of Human Lateral Prefrontal Sulcal Morphology and Its Relation to Reasoning Performance.

Previous findings show that the morphology of folds (sulci) of the human cerebral cortex flatten during postnatal development. However, previous studies did not consider the relationship between sulcal morphology and cognitive development in individual participants. Here, we fill this gap in knowledge by leveraging cross-sectional morphologic neuroimaging data in the lateral PFC (LPFC) from individual human participants (6-36 years old, males and females; N = 108; 3672 sulci), as well as longitudinal morphologic and behavioral data from a subset of child and adolescent participants scanned at two time points (6-18 years old; N = 44; 2992 sulci). Manually defining thousands of sulci revealed that LPFC sulcal morphology (depth, surface area, and gray matter thickness) differed between children (6-11 years old)/adolescents (11-18 years old) and young adults (22-36 years old) cross-sectionally, but only cortical thickness showed differences across childhood and adolescence and presented longitudinal changes during childhood and adolescence. Furthermore, a data-driven approach relating morphology and cognition identified that longitudinal changes in cortical thickness of four left-hemisphere LPFC sulci predicted longitudinal changes in reasoning performance, a higher-level cognitive ability that relies on LPFC. Contrary to previous findings, these results suggest that sulci may flatten either after this time frame or over a longer longitudinal period of time than previously presented. Crucially, these results also suggest that longitudinal changes in the cortex within specific LPFC sulci are behaviorally meaningful, providing targeted structures, and areas of the cortex, for future neuroimaging studies examining the development of cognitive abilities.SIGNIFICANCE STATEMENT Recent work has shown that individual differences in neuroanatomical structures (indentations, or sulci) within the lateral PFC are behaviorally meaningful during childhood and adolescence. Here, we describe how specific lateral PFC sulci develop at the level of individual participants for the first time: from both cross-sectional and longitudinal perspectives. Further, we show, also for the first time, that the longitudinal morphologic changes in these structures are behaviorally relevant. These findings lay the foundation for a future avenue to precisely study the development of the cortex and highlight the importance of studying the development of sulci in other cortical expanses and charting how these changes relate to the cognitive abilities those areas support at the level of individual participants.

Longitudinal changes in surface based brain morphometry measures in amnestic mild cognitive impairment and Alzheimer’s Disease

BackgroundAlzheimer’s disease (AD) is associated with marked brain atrophy. While commonly used structural MRI imaging methods do not account for the complexity of human brain morphology, little is known about the longitudinal changes of cortical geometry and their relationship with cognitive decline in subjects with AD. MethodsData from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) were used to perform two-sample t-tests to investigate longitudinal changes of cortical thickness (CTh) and three surface-based morphometry measures: fractal dimension (i.e. cortical complexity; FD), gyrification index (GI), and sulcal depth (SD) in subjects with AD, amnestic mild cognitive impairment (aMCI) in comparison to cognitively unimpaired controls (CU) in baseline and 2-year follow-up sMRI scans. In addition, correlations of the morphological measures with two-year cognitive decline as assessed by the modified AD Assessment Scale-Cognitive Subscale (ADAS-Cog 11) were calculated via regression analyses. ResultsCompared to CU, both AD and aMCI showed marked decreases in CTh. In contrast, analyses of FD and GI yielded a more nuanced decline of the respective measures with some areas showing increases in FD and GI. Overall changes in FD and GI were more pronounced in AD as compared to aMCI. Analyses of SD yielded widespread decreases. Interestingly, cognitive decline corresponded well with CTh declines in aMCI but not AD, whereas changes in FD corresponded with AD only but not aMCI, whereas GI and SD were associated with cognitive decline in aMCI and AD. ConclusionPatterns of longitudinal changes in FD, GI and SD were only partially overlapping with CTh reductions. In AD, surface-based morphometry measures for brain-surface complexity showed better correspondence than CTh with cognitive decline over a two-year period of time. Being drawn from measures reflecting changes in more intricate aspects of human brain morphology, these data provide new insight into the complexity of AD-related brain atrophy and its relationship with cognitive decline.

Longitudinal evolution of neuropathological substrates of Alzheimer’s disease in obese patients

AbstractBackgroundObesity is a metabolic condition with increasing prevalence all over the world. Patients with a body mass index (BMI) higher than 30 are considered obese. Obesity is also a risk factor for chronic morbidities such as type 2 diabetes and may increase the risk of developing Alzheimer's disease (AD). Not much is known about longitudinal changes in Alzheimer’s pathology in these patients. We hypothesised that BMI would predict longitudinal pathological alterations derived from imaging parameters.Method252 participants (n=107 obese non‐diabetic patients with BMI&gt;30) cognitively normal (n=80) and with mild cognitive impairment (n=172) were evaluated from the Alzheimer’s Disease Neuroimaging Initiative (Mean age = 73.6 years, SD = 8.0). All participants had two T1‐weighted MPRAGE MRI scans within two‐years (Mean gap=718 days, SD=107). Regional cortical thickness was measured on T1‐MPRAGE using FreeSurfer v.6.0. Individual gray matter density maps were computed using voxel‐based morphometry (VBM) and regional values were sampled in various cortical regions. Regional cortical thickness and gray matter density are expressed as delta values between baseline and followup (Value followup ‐ Value Baseline). Spearman’s correlation coefficients were calculated to assess the relationship between BMI and imaging biomarkers.ResultIn the whole cohort, we found that BMI is significantly negatively correlated with longitudinal changes in cortical thickness in anterior cingulate (ACC, p=0.0073, r=‐0.17) and posterior cingulate (PCC, p=0.0147, r=‐0.15) cortical thickness. We also found that BMI is significantly negatively correlated with longitudinal changes in frontal (p=0.0184, r=‐0.15), parietal (p=0.0057, r=‐0.18) and temporal (p=0.0141, r=‐0.16) gray matter density. When looking only at MCI participants, we found similar results with even stronger correlations. BMI is significantly negatively correlated with delta anterior cingulate (ACC, p=0.0008, r=‐0.25) and posterior cingulate (PCC, p=0.004, r=‐0.22) cortical thickness.ConclusionIn this cohort of obese and non‐obese participants cognitively normal and with MCI, we found that obesity was associated with a longitudinal 2‐years worsening of macrostructural changes. Higher BMI was associated with a higher reduction of cortical thickness and with a decreased gray matter density in several brain regions.

Helmet Technology, Head Impact Exposure, and Cortical Thinning Following a Season of High School Football.

The purpose of this study was to compare the effects of wearing older, lower-ranked football helmets (LRank) to wearing newer, higher-ranked football helmets (HRank) on pre- to post-season changes in cortical thickness in response to repetitive head impacts and assess whether changes in cortical thickness are associated with head impact exposure for either helmet type. 105 male high-school athletes (NHRank = 52, NLRank = 53) wore accelerometers affixed behind the left mastoid during all practices and games for one regular season of American football to monitor head impact exposure. Pre- and post-season magnetic resonance imaging (MRI) were completed to assess longitudinal changes in cortical thickness. Significant reductions in cortical thickness (i.e., cortical thinning) were observed pre- to post-season for each group, but these longitudinal alterations were not significantly different between the LRank and HRank groups. Further, significant group-by-head impact exposure interactions were observed when predicting changes in cortical thickness. Specifically, a greater frequency of high magnitude head impacts during the football season resulted in greater cortical thinning for the LRank group, but not for the HRank group. These data provide preliminary in vivo evidence that HRank helmets may provide a buffer between the specific effect of high magnitude head impacts on regional thinning by dissipating forces more evenly throughout the cortex. However, future research with larger sample sizes, increased longitudinal measures and additional helmet technologies is warranted to both expand upon and further validate the present study findings.

Accelerated longitudinal cortical atrophy in OEF/OIF/OND veterans with severe PTSD and the impact of comorbid TBI.

Veterans who deployed in support of Operation Enduring Freedom (OEF), Iraqi Freedom (OIF), and New Dawn (OND) commonly experience severe psychological trauma, often accompanied by physical brain trauma resulting in mild traumatic brain injury (mTBI). Prior studies of individuals with posttraumatic stress disorder (PTSD) have revealed alterations in brain structure, accelerated cellular aging, and impacts on cognition following exposure to severe psychological trauma and potential interactive effects of military‐related mTBI. To date, however, little is known how such deployment‐related trauma changes with time and age of injury of the affected veteran. In this study, we explored changes in cortical thickness, volume, and surface area after an average interval of approximately 2 years in a cohort of 254 OEF/OIF/OND Veterans ranging in age from 19 to 67 years. Whole‐brain vertex‐wise analyses revealed that veterans who met criteria for severe PTSD (Clinician‐Administered PTSD Scale ≥60) at baseline showed greater negative longitudinal changes in cortical thickness, volume, and area over time. Analyses also revealed a significant severe‐PTSD by age interaction on cortical measures with severe‐PTSD individuals exhibiting accelerated cortical degeneration with increasing age. Interaction effects of comorbid military‐related mTBI within the severe‐PTSD group were also observed in several cortical regions. These results suggest that those exhibiting severe PTSD symptomatology have accelerated atrophy that is exacerbated with increasing age and history of mTBI.

Clinicopathologic Factors Associated With Reversion to Normal Cognition in Patients With Mild Cognitive Impairment.

To identify clinicopathologic factors contributing to mild cognitive impairment (MCI) reversion to normal cognition. We analyzed 3 longitudinal cohorts in this study: the Mayo Clinic Study of Aging (MCSA), the Religious Orders Study and Memory and Aging Project (ROSMAP), and the National Alzheimer's Coordinating Center (NACC). Demographic characteristics and clinical outcomes were compared between patients with MCI with or without an experience of reversion to normal cognition (referred to as reverters and nonreverters, respectively). We also compared longitudinal changes in cortical thickness, glucose metabolism, and amyloid and tau load in a subcohort of reverters and nonreverters in MCSA with MRI or PET imaging information from multiple visits. We identified 164 (56.4%) individuals in MCSA, 508 (66.8%) individuals in ROSMAP, and 280 (34.1%) individuals in NACC who experienced MCI reversion to normal cognition. Cox proportional hazards regression models showed that MCI reverters had an increased chance of being cognitively normal at the last visit in MCSA (HR 3.31, 95% CI 2.14-5.12), ROSMAP (HR 3.72, 95% CI 2.50-5.56), and NACC (HR 9.29, 95% CI 6.45-13.40) and a reduced risk of progression to dementia (HR 0.12, 95% CI 0.05-0.29 in MCSA; HR 0.41, 95% CI 0.32-0.53 in ROSMAP; and HR 0.29, 95% CI 0.21-0.40 in NACC). Compared with MCI nonreverters, reverters had better-preserved cortical thickness (β = 0.082, p <0.001) and glucose metabolism (β = 0.119, p = 0.001) and lower levels of amyloid, albeit statistically nonsignificant (β = -0.172, p = 0.090). However, no difference in tau load was found between reverters and nonreverters (β = 0.073, p = 0.24). MCI reversion to normal cognition is likely attributed to better-preserved cortical structure and glucose metabolism.

Longitudinal Changes in Cortical Thickness in Adolescents with Autism Spectrum Disorder and Their Association with Restricted and Repetitive Behaviors.

The neuroanatomy of autism spectrum disorder (ASD) shows highly heterogeneous developmental trajectories across individuals. Mapping atypical brain development onto clinical phenotypes, and establishing their molecular underpinnings, is therefore crucial for patient stratification and subtyping. In this longitudinal study we examined intra- and inter-individual differences in the developmental trajectory of cortical thickness (CT) in childhood and adolescence, and their genomic underpinnings, in 33 individuals with ASD and 37 typically developing controls (aged 11–18 years). Moreover, we aimed to link regional atypical CT development to intra-individual variations in restricted and repetitive behavior (RRB) over a two-year time period. Individuals with ASD showed significantly reduced cortical thinning in several of the brain regions functionally related to wider autism symptoms and traits (e.g., fronto-temporal and cingulate cortices). The spatial patterns of the neuroanatomical differences in CT were enriched for genes known to be associated with ASD at a genetic and transcriptomic level. Further, intra-individual differences in CT correlated with within-subject variability in the severity of RRBs. Our findings represent an important step towards characterizing the neuroanatomical underpinnings of ASD across development based upon measures of CT. Moreover, our findings provide important novel insights into the link between microscopic and macroscopic pathology in ASD, as well as their relationship with different clinical ASD phenotypes.

Reproducibility of Longitudinal Changes in Cortical Thickness Determined by Surface-Based Morphometry Between Non-Accelerated and Accelerated MR Imaging.

Scan acceleration such as parallel imaging reduces scan time, but shorter scan time may reduce the signal-to-noise ratio and affect image quality. The reproducibility of longitudinal changes in the brain structure between non-accelerated and accelerated imaging by surface-based analysis is unclear. To determine the reproducibility of longitudinal changes in cortical thickness, measured by surface-based morphometry, between non-accelerated and accelerated structural T1 -weighted imaging in the healthy elderly and those with mild cognitive impairment (MCI) and Alzheimer's disease (AD). Retrospective. Fifty healthy elderly subjects (age=73 ± 5 years, 29 females, 21 males), 54 MCI patients (age=71 ± 7 years, 23 females, 31 males), and 8 AD patients (age=78 ± 6 years, 6 females, 2 males). 3 T, magnetization-prepared rapid gradient-echo. Longitudinal changes in cortical thickness estimated by the longitudinal stream in FreeSurfer from 2-year interval data, and visual assessment of image quality by three radiologists. Intraclass correlation coefficient (ICC) and Kruskal-Wallis test. A P value <0.05 was considered significant. Healthy elderly subjects, MCI patients, and AD patients showed different patterns in the ICC maps. For the smoothing of 20 mm full width at half maximum, the mean ICC was 0.45 overall (healthy elderly, 0.33; MCI patients, 0.49; AD patients, 0.31). The within-subject SDs of the symmetrized percent changes were similar between healthy elderly subjects (mean, 1.3%/year) and MCI patients (mean, 1.3%/year) but larger in AD patients (mean, 1.7%/year). Image quality did not significantly differ per group (P=0.18). The results of this study indicate the reproducibility of longitudinal changes in cortical thickness measured by surface-based morphometry between non-accelerated and accelerated imaging, and that the reproducibility varies by disease and region. 3 TECHNICAL EFFICACY: Stage 1.

Cortical Thickness in the Right Anterior Cingulate Cortex Relates to Clinical Response to Left Prefrontal Accelerated Intermittent Theta Burst Stimulation: An Exploratory Study

ObjectivesAccelerated intermittent theta burst stimulation (aiTBS) is a promising treatment option for depressed patients. However, there is a large interindividual variability in clinical effectiveness and individual biomarkers to guide treatment outcome are needed.Materials and MethodsHere, the relation between cortical thickness and clinical response (17‐item Hamilton Depression Rating Scale) was studied using anatomical MRI data of 50 depressed patients who were included in a randomized, sham‐controlled, double‐blinded, cross‐over aiTBS design (NCT01832805).ResultsBaseline cortical thickness in the right caudal part of the anterior cingulate cortex (cACC) was significantly correlated with direct clinical responses in the subgroup who received active aiTBS during the first stimulation week. No correlations were found between baseline cortical thickness and delayed clinical effectiveness. In this particular region, longitudinal changes in cortical thickness were significantly correlated with clinical effectiveness. Furthermore, direct changes in cortical thickness in the right cACC showed predictive potential of delayed clinical responses.ConclusionCortical thickness within the right cACC might be an important biomarker to predict clinical responses to aiTBS. Additional studies are warranted to substantiate the specific biomarker potential of these parts of the ACC.

Longitudinal cortical thinning progression differs across multiple sclerosis phenotypes and is clinically relevant: A multicentre study

Background: Longitudinal evolution of cortical thickness (CTh) in different MS phenotypes has been rarely studied. Aim: To investigate the regional pattern and 1-year progression of cortical thinning in relapsing-remitting (RR) and progressive (P) MS. Methods: 3T high-resolution T1-weighted magnetic resonance imaging (MRI) was obtained from 86 patients (75 RRMS, 11 PMS) and 34 healthy controls (HC) at three European sites at baseline and 1-year follow-up. Using FreeSurfer, baseline CTh between-group differences, longitudinal CTh changes and their correlations with clinical and MRI variables were assessed. Results: Baseline frontal, parietal and sensorimotor atrophy was found in MS versus HC. Such pattern was driven by RRMS, while PMS showed additional parietal, insular and sensorimotor cortical atrophy versus RRMS. At 1-year versus baseline, additional frontal and temporal cortical thinning was detected in RRMS patients, while a widespread CTh reduction was found in PMS patients (significant at time-by-group interaction vs RRMS). In MS, baseline fronto-parietal atrophy correlated with more severe disability and higher lesion volume. Baseline inferior parietal CTh decrease and 1-year temporal cortical thinning correlated with more severe disability. Conclusion: Parieto-temporal baseline CTh abnormalities and thinning pattern over time characterized the main MS clinical phenotypes and were associated with 1-year disability worsening.

Effect of aerobic exercise combined with cognitive remediation on cortical thickness and prediction of social adaptation in patients with schizophrenia

Aerobic exercise is a promising intervention for patients with schizophrenia, but structural neuroplastic effects on brain regions relevant to the pathophysiology of the disease remain unclear. This study aimed to elucidate longitudinal changes in cortical thickness after aerobic exercise intervention in schizophrenia patients and the relationship of these changes to clinical correlates.We investigated 21 schizophrenia patients and 23 healthy controls who performed aerobic exercise and 21 schizophrenia patients who played table soccer. The 12-week exercise intervention was combined with computer-assisted cognitive remediation training from week 6 to week 12. Magnetic resonance imaging (MRI) scans were acquired at baseline and weeks 6, 12, and 24. The thickness of the entorhinal, parahippocampal, and lateral and medial prefrontal cortices was assessed with FreeSurfer 6.0.The schizophrenia aerobic exercise group showed a significant increase of cortical thickness in the right entorhinal cortex at week 6, and we found a significant correlation between the cortical thickness of the right lateral prefrontal cortex at baseline and improvement of social adaptation at week 12. In the schizophrenia table soccer and healthy control groups, we found no significant longitudinal change in cortical thickness through the intervention and follow-up period and no correlation of cortical thickness at baseline with clinical measures.Our results suggest that aerobic exercise in schizophrenia modulates the thickness of the entorhinal cortex, a structure adjacent to the hippocampus. Greater cortical thickness of the right lateral prefrontal cortex appears to predict better clinical response to an aerobic exercise intervention in patients with schizophrenia.

Longitudinal Cortical Thickness Changes in Bipolar Disorder and the Relationship to Genetic Risk, Mania, and Lithium Use

BackgroundBipolar disorder (BD) is a highly heritable psychiatric disorder characterized by episodes of manic and depressed mood states and associated with cortical brain abnormalities. Although the course of BD is often progressive, longitudinal brain imaging studies are scarce. It remains unknown whether brain abnormalities are static traits of BD or result from pathological changes over time. Moreover, the genetic effect on implicated brain regions remains unknown. MethodsPatients with BD and healthy control (HC) subjects underwent structural magnetic resonance imaging at baseline (123 patients, 83 HC subjects) and after 6 years (90 patients, 61 HC subjects). Cortical thickness maps were generated using FreeSurfer. Using linear mixed effects models, we compared longitudinal changes in cortical thickness between patients with BD and HC subjects across the whole brain. We related our findings to genetic risk for BD and tested for effects of demographic and clinical variables. ResultsPatients showed abnormal cortical thinning of temporal cortices and thickness increases in visual/somatosensory brain areas. Thickness increases were related to genetic risk and lithium use. Patients who experienced hypomanic or manic episodes between time points showed abnormal thinning in inferior frontal cortices. Cortical changes did not differ between diagnostic BD subtypes I and II. ConclusionsIn the largest longitudinal BD study to date, we detected abnormal cortical changes with high anatomical resolution. We delineated regional effects of clinical symptoms, genetic factors, and medication that may explain progressive brain changes in BD. Our study yields important insights into disease mechanisms and suggests that neuroprogression plays a role in BD.

Mood episodes are associated with increased cortical thinning: A longitudinal study of bipolar disorder type II.

Previous studies found evidence for thinner frontotemporal cortices in bipolar disorder (BD), yet whether this represents a stable disease trait or an effect of mood episodes remains unknown. Here, we assessed the reproducibility of thinner frontotemporal cortices in BD type II, compared longitudinal changes in cortical thickness between individuals with BD type II and healthy controls (HCs), and examined the effect of mood episodes on cortical thickness change. Thirty-three HCs and 29 individuals with BD type II underwent 3T magnetic resonance imaging at baseline, as published previously, and 2.4years later, at follow-up. Cross-sectional and longitudinal analyses of cortical thickness were performed using Freesurfer, and relationships with mood episodes from baseline to follow-up were assessed. Individuals with BD type II had thinner left and right prefrontal and left temporal cortex clusters at follow-up (all corrected P<0.001), consistent with baseline results. Both groups showed widespread longitudinal cortical thinning, and patients had increased thinning in a left temporal cortex cluster compared to HCs (corrected P<0.001). Patients with more (>2) depressive episodes between baseline and follow-up had greater left temporal cortical thinning than patients with fewer depressive episodes (corrected P<0.05). In addition, patients with more depressive episodes had greater thinning in bilateral ventromedial prefrontal clusters relative to HCs (uncorrected P<0.05), yet these results did not survive correction for multiple comparisons. Together, these findings support reduced frontotemporal cortical thickness in BD type II and provide the first preliminary evidence for an association between depressive episodes and increased cortical thinning.

Social Responsiveness Scale (SRS) in Relation to Longitudinal Cortical Thickness Changes in Autism Spectrum Disorder.

The relationship between brain development and clinical heterogeneity in autism (ASD) is unknown. This study examines the Social Responsiveness Scale (SRS) in relation to the longitudinal development of cortical thickness. Participants (N = 91 ASD, N = 56 TDC; 3-39years at first scan) were scanned up to three times over a 7-year period. Mixed-effects models examined cortical thickness in relation to SRS score. ASD participants with higher SRS scores showed regionally increased age-related cortical thinning. Regional thickness differences and reduced age-related cortical thinning were found in predominantly right lateralized regions in ASD with decreasing SRS scores over time. Our findings emphasize the importance of examining clinical phenotypes in brain-based studies of ASD.

Longitudinal Cortical Thickness Changes in Early Parkinson’s Disease Patients with Impulsive Compulsive Behaviors (P3.070)

Longitudinal Cortical Thickness Changes in Early Parkinson’s Disease Patients with Impulsive Compulsive Behaviors (P3.070)