Local Gray Matter Volume Research Articles

Gray matter volume reductions in patients with schizophrenia: A replication study across two cultural backgrounds

Structural gray matter (GM) volume reductions in patients with schizophrenia have rarely been replicated across two different sites, the impact of culture and clinical characteristics remains unresolved. Hence, we assessed GM volume reductions in patients with schizophrenia using 3 T magnetic resonace imaging to replicate results across two independent and culturally different backgrounds (Germany, Japan), and to investigate the impact of brain volume reductions on clinical characteristics. In total, 163 German (80 patients) and 203 Japanese (83 patients) participants were included in the analysis. Voxel-based morphometry (VBM) was used to investigate structural differences between the groups and across the two sites, comparing local GM volumes. Clinical variables were used to analyze effects unrelated to the socio-cultural background. Across both data sets, widespread GM reductions in frontal and temporal cortical parts were found between patients and controls, indicating strong effects of diagnosis and only small effects of site. The investigation of clinical characteristics revealed the strongest effects for chlorpromazine equivalents on GM volume reductions primarily in the Japanese sample. Although the effects of site are small, several brain regions do not overlap between the two groups. Thus, GM may be affected differently at the two sites in patients with schizophrenia.

Novel findings from 2,838 Adult Brains on Sex Differences in Gray Matter Brain Volume

There is still disagreement among studies with respect to the magnitude, location, and direction of sex differences of local gray matter volume (GMV) in the human brain. Here, we applied a state-of-the-art technique examining GMV in a well-powered sample (n = 2,838) validating effects in two independent general-population cohorts, age range 21–90 years, measured using the same MRI scanner. More GMV in women than in men was prominent in medial and lateral prefrontal areas, the superior temporal sulcus, the posterior insula, and orbitofrontal cortex. In contrast, more GMV in men than in women was detected in subcortical temporal structures, such as the amygdala, hippocampus, temporal pole, fusiform gyrus, visual primary cortex, and motor areas (premotor cortex, putamen, anterior cerebellum). The findings in this large-scale study may clarify previous inconsistencies and contribute to the understanding of sex-specific differences in cognition and behavior.

Atypical intrinsic neural timescale in autism.

How long neural information is stored in a local brain area reflects functions of that region and is often estimated by the magnitude of the autocorrelation of intrinsic neural signals in the area. Here, we investigated such intrinsic neural timescales in high-functioning adults with autism and examined whether local brain dynamics reflected their atypical behaviours. By analysing resting-state fMRI data, we identified shorter neural timescales in the sensory/visual cortices and a longer timescale in the right caudate in autism. The shorter intrinsic timescales in the sensory/visual areas were correlated with the severity of autism, whereas the longer timescale in the caudate was associated with cognitive rigidity. These observations were confirmed from neurodevelopmental perspectives and replicated in two independent cross-sectional datasets. Moreover, the intrinsic timescale was correlated with local grey matter volume. This study shows that functional and structural atypicality in local brain areas is linked to higher-order cognitive symptoms in autism.

Cerebral grey matter changes of pre- and post-treatment in first-episode drug-naive adolescents schizophrenia

Objective: To investigate the gray matter(GM) volume and the change of GM volume after antipsychotic treatment for 8 weeks in first-episode drug-naive adolescents with schizophrenia. Methods: T1-weighted brain MRIs were obtained on a 3T scanner in 35 controls and 35 subjects with adolescents schizophrenia who were admitted to the Second Affiliated Hospital of Xinxiang Medical College from April 2015 to June 2016 and not given antipsychotic medication, the schizophrenia patients received second scan after 8 weeks of antipsychotic treatment. Positive and negative syndrome scale (PANSS) assessments were performed in patients pre- and post-treatment; voxel-based morphometry (VBM) was used to analyze changes of GM volume and the correlation between the baseline GM volume and the PANSS scores was further analyzed. Results: GM volumes in the left frontal gyrus (MIN(x, y, z): -13.5, 36, 46.5), left superior parietal lobule (MIN(x, y, z): -52.5, -42, 52.5), left inferior parietal lobule (MIN(x, y, z): -31.5, -45, 69) and left central anterior (MIN(x, y, z): 9, 21, 61.5) were significantly smaller than those in the normal control group (t=-4.384 0, -4.556 2, -6.430 9, -4.313 9 respectively, P<0.001); after treatment for 8 weeks PANSS scores were significantly lower than those of baseline (P<0.001), however, there was no significant difference in regional GM volume between the pre-and post-treatment (P>0.05) and no significant correlation was found between GM volume and PANSS scores. Conclusion: There are local GM volume reductions in subjects with adolescents schizophrenia and these regions may be independent to mental symptoms of patients.

White matter network alterations in patients with depersonalization/derealization disorder.

Depersonalization/derealization disorder (DPD) is a chronic and distressing condition characterized by detachment from oneself and/or the external world. Neuroimaging studies have associated DPD with structural and functional alterations in a variety of distinct brain regions. Such local neuronal changes might be mediated by altered interregional white matter connections. However, to our knowledge, no research on network characteristics in this patient population exists to date. We explored the structural connectome in 23 individuals with DPD and 23 matched, healthy controls by applying graph theory to diffusion tensor imaging data. Mean interregional fractional anisotropy (FA) was used to define the network weights. Group differences were assessed using network-based statistics and a link-based controlling procedure. Our main finding refers to lower FA values within left temporal and right temporoparietal regions in individuals with DPD than in healthy controls when using a link-based controlling procedure. These links were also associated with dissociative symptom severity and could not be explained by anxiety or depression scores. Using network-based statistics, no significant results emerged. However, we found a trend for 1 subnetwork that may support the model of frontolimbic dysbalance suggested to underlie DPD symptomatology. To ensure ecological validity, patients with certain comorbidities or psychotropic medication were included in the study. Confirmatory replications are necessary to corroborate the results of this explorative investigation. In patients with DPD, the structural connectivity between brain regions crucial for multimodal integration and emotion regulation may be altered. Aberrations in fibre tract communication seem to be not solely a secondary effect of local grey matter volume loss, but may present a primary pathophysiology in patients with DPD.

No evidence for cerebellar abnormality in adults with developmental dyslexia

Developmental dyslexia is commonly believed to result from a deficiency in the recognition and processing of speech sounds. According to the cerebellar deficit hypothesis, this phonological deficit is caused by deficient cerebellar function. In the current study, 26 adults with developmental dyslexia and 25 non-dyslexic participants underwent testing of reading-related skills, cerebellar functions, and MRI scanning of the brain. Anatomical assessment of the cerebellum was conducted with voxel-based morphometry. Behavioural evidence, that was indicative of impaired cerebellar function, was found to co-occur with reading impairments in the dyslexic subjects, but a causal relation between the two was not observed. No differences in local grey matter volume, nor in structure–function relationships within the cerebellum were found between the two groups. Possibly, the observed behavioural pattern is due to aberrant white matter connectivity. In conclusion, no support for the cerebellar deficit hypothesis or the presence of anatomical differences of the cerebellum in adults with developmental dyslexia was found.

P1-1-7. Relationship between gray matter volume of posterior cingulate cortex and frontal activation

Posterior cingulate cortex (PCC) is one of key nodes of default mode network. Recent studies have suggested that the connectivities between PCC and the other brain regions have important role in working memory performance. Therefore, we hypothesized that the local gray matter volume of PCC can affect the functions of frontal cortex. To address this issue, we acquired T1 weighted images for voxel-based morphometry, and measured time course of frontal oxygenated hemoglobin (Oxy-Hb) during letter verbal fluency task (VFT). Seventeen healthy volunteers were enrolled in the present study. We carried out the regression analysis between the gray matter concentration in PCC and the frontal oxy-Hb level during 0–60 s of VFT. This analysis found a significant cluster where the gray matter concentration is associated with frontal oxy-Hb level, even after adjustment of confounding factors including age and sex. Interestingly, there is no correlation between the gray matter concentration in frontal cortex and the frontal Oxy-Hb. These results suggest that gray matter volume of PCC rather than that of frontal cortex affects the extent of frontal activation during VFT. Our preliminary study may contribute to clarifying a role of PCC in the cognitive process.

Gray matter correlates of pressure pain thresholds and self-rated pain sensitivity: a voxel-based morphometry study.

Individual differences in sensitivity to pain are large and have clinical and scientific importance. Although heavily influenced by situational factors, they also relate to genetic factors and psychological traits, and are reflected by differences in functional activation in pain-related brain regions. Here, we used voxel-based morphometry to investigate if individual pain sensitivity is related to local gray matter volumes. Pain sensitivity was determined using (1) index finger pressure pain thresholds (PPTs) and (2) pain intensity ratings of imagined painful situations as assessed by the Pain Sensitivity Questionnaire (PSQ) in 501 population-based subjects participating in the BiDirect Study. Pain Sensitivity Questionnaire scores were positively associated with gray matter in 2 symmetrical clusters, with a focus on the parahippocampal gyrus, extending to the hippocampus, fusiform gyrus, BA19, putamen, and insula (P < 0.05 corrected), but the effect was small (R = 0.045-0.039). No negative associations with the PSQ and no associations with the PPT reached significance. Parahippocampal activation during pain and altered parahippocampal gray matter in chronic pain have been reported, which would be consistent with positive associations with PSQ scores. Alternatively, associations of PSQ scores with the parahippocampal and fusiform gray matter could relate to the visual imagination of painful situations required by the PSQ, not to pain sensitivity itself. Regarding PPTs, the present data obtained in a large sample strongly suggest an absence of associations of this parameter with gray matter volume. In conclusion, the present results argue against a strong association between pain sensitivity and local gray matter volumes.

Network Neuroscience and Personality.

Personality and individual differences originate from the brain. Despite major advances in the affective and cognitive neurosciences, however, it is still not well understood how personality and single personality traits are represented within the brain. Most research on brain-personality correlates has focused either on morphological aspects of the brain such as increases or decreases in local gray matter volume, or has investigated how personality traits can account for individual differences in activation differences in various tasks. Here, we propose that personality neuroscience can be advanced by adding a network perspective on brain structure and function, an endeavor that we label personality network neuroscience. With the rise of resting-state functional magnetic resonance imaging (MRI), the establishment of connectomics as a theoretical framework for structural and functional connectivity modeling, and recent advancements in the application of mathematical graph theory to brain connectivity data, several new tools and techniques are readily available to be applied in personality neuroscience. The present contribution introduces these concepts, reviews recent progress in their application to the study of individual differences, and explores their potential to advance our understanding of the neural implementation of personality. Trait theorists have long argued that personality traits are biophysical entities that are not mere abstractions of and metaphors for human behavior. Traits are thought to actually exist in the brain, presumably in the form of conceptual nervous systems. A conceptual nervous system refers to the attempt to describe parts of the central nervous system in functional terms with relevance to psychology and behavior. We contend that personality network neuroscience can characterize these conceptual nervous systems on a functional and anatomical level and has the potential do link dispositional neural correlates to actual behavior.

Regional patterns of gray matter volume, hypometabolism, and beta-amyloid in groups at risk of Alzheimer's disease

Alzheimer's disease (AD) is characterized by the presence of β-amyloid (Aβ) deposition and neurodegeneration. To seek for signs of such pathologies, we compared regional biomarker degrees and patterns of Aβ deposition, glucose hypometabolism, and gray matter volume (GMV) reduction in 3 groups at risk of AD. In elderly carriers of the apolipoprotein E ε4 (APOE4, n = 17), patients with subjective cognitive decline (n = 16), and patients with mild cognitive impairment (n = 30), head-to-head intermodality comparisons were performed on cross-sectional structural magnetic resonance images as well as 18F-fluorodeoxyglucose and 18F-florbetapir positron emission tomography scans. In mild cognitive impairment patients, 3 distinct biomarker patterns were recovered, similarly seen in AD patients: (1) in medial temporal regions, local GMV reduction exceeded hypometabolism, (2) in temporoparietal regions, hypometabolism predominated over GMV reduction, and (3) in frontal regions, Aβ deposition exceeded GMV reduction and hypometabolism. In subjective cognitive decline patients, only pattern 1 was detected, while APOE4 carriers demonstrated only pattern 3. Our findings highlight that regional AD-like biomarker patterns may vary across different at-risk populations, potentially reflecting differential mediators of these risks.

Tau pathology and neurodegeneration contribute to cognitive impairment in Alzheimer's disease.

Neuropathological and in vivo studies have revealed a tight relationship between tau pathology and cognitive impairment across the Alzheimer's disease spectrum. However, tau pathology is also intimately associated with neurodegeneration and amyloid pathology. The aim of the present study was therefore to assess whether grey matter atrophy and amyloid pathology contribute to the relationship between tau pathology, as measured with 18F-AV-1451-PET imaging, and cognitive deficits in Alzheimer's disease. We included 40 amyloid-positive patients meeting criteria for mild cognitive impairment due to Alzheimer's disease (n = 5) or probable Alzheimer's disease dementia (n = 35). Twelve patients additionally fulfilled the diagnostic criteria for posterior cortical atrophy and eight for logopenic variant primary progressive aphasia. All participants underwent 3 T magnetic resonance imaging, amyloid (11C-PiB) positron emission tomography and tau (18F-AV-1451) positron emission tomography, and episodic and semantic memory, language, executive and visuospatial functions assessment. Raw cognitive scores were converted to age-adjusted Z-scores (W-scores) and averaged to compute composite scores for each cognitive domain. Independent regressions were performed between 18F-AV-1451 binding and each cognitive domain, and we used the Biological Parametric Mapping toolbox to further control for local grey matter volumes, 11C-PiB uptake, or both. Partial correlations and causal mediation analyses (mediation R package) were then performed in brain regions showing an association between cognition and both 18F-AV-1451 uptake and grey matter volume. Our results showed that decreased cognitive performance in each domain was related to increased 18F-AV-1451 binding in specific brain regions conforming to established brain-behaviour relationships (i.e. episodic memory: medial temporal lobe and angular gyrus; semantic memory: left anterior temporal regions; language: left posterior superior temporal lobe and supramarginal gyrus; executive functions: bilateral frontoparietal regions; visuospatial functions: right more than left occipitotemporal regions). This pattern of regional associations remained essentially unchanged-although less spatially extended-when grey matter volume or 11C-PiB uptake maps were added as covariates. Mediation analyses revealed both direct and grey matter-mediated effects of 18F-AV-1451 uptake on cognitive performance. Together, these results show that tau pathology is related in a region-specific manner to cognitive impairment in Alzheimer's disease. These regional relationships are weakly related to amyloid burden, but are in part mediated by grey matter volumes. This suggests that tau pathology may lead to cognitive deficits through a variety of mechanisms, including, but not restricted to, grey matter loss. These results might have implications for future therapeutic trials targeting tau pathology.

Longitudinal Alterations of Local Spontaneous Brain Activity in Parkinson's Disease.

We used resting-state fMRI to evaluate longitudinal alterations in local spontaneous brain activity in Parkinson's disease (PD) over a 2-year period. Data were acquired from 23 PD patients at baseline and follow-up, and 27 age- and sex-matched normal controls. Regional homogeneity (ReHo) and voxel-based-morphometry (VBM) were used to identify differences in local spontaneous brain activity and grey matter volume. With disease progression, we observed a progressive decrease in ReHo in the sensorimotor cortex, default-mode network, and left cerebellum, but increased ReHo in the supplementary motor area, bilateral temporal gyrus, and hippocampus. Moreover, there was a significant positive correlation between the rates of ReHo change in the left cerebellum and the rates of change in the Unified Parkinson's Disease Rating Scale-III scores. VBM revealed no significant differences in the grey matter volume among the three sets of acquisitions. We conclude that ReHo may be a suitable non-invasive marker of progression in PD.

FALSE-POSITIVE FDG-PET DIAGNOSIS OF AD IN GERIATRIC INPATIENTS WITH NEWLY MANIFESTED COGNITIVE IMPAIRMENT AND CEREBROVASCULAR DISEASE

In a study on the accuracy of the etiological diagnosis of newly manifested, clinically uncertain cognitive impairment in elderly geriatric inpatients (WHO Trials Registry DRKS00005041) the most probable etiological diagnosis made by an interdisciplinary academic expert team integrating all available data (clinical, laboratory, neuropsychological, structural MRI, and FDG PET) was Alzheimer's disease (AD) in 14 patients and mixed disease (MD), i.e., AD plus cerebrovascular disease (CVD), in 16 patients. The presence of an AD-typical reduction pattern in FDG PET was required for both AD and MD etiological diagnosis. Clinical follow-up including detailed neuropsychological testing after 15.7±3.1 months confirmed progressive neurodegeneration in all AD cases whereas the etiological diagnosis of MD was adjusted to CVD in 3 of the 16 cases. This suggests an increased risk of false positive FDG PET in cognitively impaired inpatients with CVD. Aim of this study was to provide some evidence for this hypothesis. The 3 patients in whom the etiological diagnosis of MD was adjusted by the follow-up to CVD only (MD-to-CVD converters) were compared to the 13 patients in whom the MD diagnosis was confirmed (MD-stables) with respect to various variables including total volume of white matter hyperintensities (WMH) estimated from FLAIR MRI using the lesion segmentation toolbox for SPM8, local and global grey matter volume estimated from MPRAGE MRI using a fully-automated atlas-based method, pons-scaled FDG-uptake in an AD meta-ROI, specific FDG dose, blood glucose concentration at the time of PET, duration of follow-up, and age. Unexpectedly, the total WMH volume was significantly smaller (not larger) in MD-to-CVD converters compared to MD-stable patients (20.6 vs. 40.1 ml, Mann-Whitney U-test p = 0.031). Grey matter volume in the right occipital lobe trended towards lower values in MD-to-CVD converters (14.8 vs. 19.2 ml, p = 0.070). None of the other variables showed an effect. These findings provide some evidence that false positive FDG PET with respect to the diagnosis of AD in cognitively impaired geriatric inpatients might be secondary to partial volume effects caused by occipital atrophy. They do not provide evidence for an association with white matter disease.

TAU PATHOLOGY AND GRAY MATTER ATROPHY CONTRIBUTE TO COGNITIVE IMPAIRMENT IN ALZHEIMER’S DISEASE

Neuropathological and in vivo studies have revealed a close relationship between tau pathology and cognitive impairment across the Alzheimer's disease (AD) spectrum. However, tau pathology is also intimately associated with neurodegeneration. We therefore assessed in a heterogeneous sample of AD patients whether the relationship between tau pathology, as measured with 18F-AV1451-PET imaging, and cognition remained significant after controlling for local gray matter atrophy and amyloid pathology. We also performed causal mediation analyses to further examine the potential intermediary role of gray matter atrophy. Forty Aβ-PET+ patients with heterogeneous AD phenotypes (Table 1) underwent 3T MRI, 11C-PiB-PET and 18F-AV1451-PET, and episodic and semantic memory, language, executive and visuo-spatial functions assessment. Raw cognitive scores were converted to age-adjusted Z-scores (W-scores) and averaged to compute composite scores for each cognitive domain. Independent regressions were performed between 18F-AV-1451 SUVR and each cognitive domain and Biological Parametric Mapping (BPM) was used to further control for local gray matter volumes, PIB-DVR, or both. Partial correlations and mediation analyses (mediation R package) were performed in brain regions showing an association between cognition and both 18F-AV-1451 SUVR and gray matter volume. The average direct effect (ADE) and average causal mediation effect (ACME), reflecting direct and indirect effects 18F-AV-1451 on cognition, were computed using the mediation R package (non-parametric bootstrapping, 5000 simulations). Decreased cognitive performance in each domain was related to increased 18F-AV-1451 SUVR in specific brain regions conforming to established brain-behavior relationships (Figure 1). This pattern of regional associations remained essentially unchanged – although less spatially extended – when gray matter volume or 11C-PiB uptake maps were added as covariates (Figure 2). Mediation analyses revealed both direct and gray matter-mediated effects of 18F-AV-1451 uptake on cognitive performance (Figure 3). Tau pathology is related in a region-specific manner to cognitive impairment in AD. These regional relationships are weakly related to amyloid burden, but are in part mediated by gray matter volumes. These results suggest that tau pathology may lead to cognitive deficits through a variety of mechanisms, including, but not restricted, to neuronal loss. Voxel-wise results and scatter plots of the independent regressions between 18F-AV-1451 SUVR and each cognitive domain score. (SPM, p<0.001 - k>500 mm3). Voxel-wise results of the multiple regressions between 18F-AV-1451 SUVR and each cognitive domain score controlling for local grey matter volume and/or local 11C-PiB DVR. (Biological Parametric Mapping, p<0.001 - k>500 mm3) Partial correlations and mediation analyses in the brain areas where both 18F-AV-1451 SUVR and gray matter volume were related to cognitive domain scores.

Resting-state brain networks in patients with Parkinson's disease and impulse control disorders

IntroductionTo investigate intrinsic neural networks connectivity changes in Parkinson's disease (PD) patients with and without impulse control disorders (ICD). MethodsFifteen patients with PD with ICD (ICD+), 15 patients with PD without ICD (ICD−) and 24 age and sex-matched healthy controls (HC) were enrolled in the study. To identify patients with and without ICD and/or punding, we used the Minnesota Impulsive Disorders Interview (MIDI) and a clinical interview based on diagnostic criteria for each symptom. All patients underwent a detailed neuropsychological evaluation. Whole brain structural and functional imaging was performed on a 3T GE MR scanner. Statistical analysis of functional data was completed using BrainVoyager QX software. Voxel-based morphometry (VBM) was used to test whether between-group differences in resting-state connectivity were related to structural abnormalities. ResultsThe presence of ICD symptoms was associated with an increased connectivity within the salience and default-mode networks, as well as with a decreased connectivity within the central executive network (p < .05 corrected). ICD severity was correlated with both salience and default mode networks connectivity changes only in the ICD+ group. VBM analysis did not reveal any statistically significant differences in local grey matter volume between ICD+ and ICD− patients and between all patients and HC (p < .05. FWE). ConclusionsThe presence of a disrupted connectivity within the three core neurocognitive networks may be considered as a potential neural correlate of ICD presence in patients with PD. Our findings provide additional insights into the mechanisms underlying ICD in PD, confirming the crucial role of an abnormal prefrontal-limbic-striatal homeostasis in their development.

Abnormal Gray Matter Shape, Thickness, and Volume in the Motor Cortico-Subcortical Loop in Idiopathic Rapid Eye Movement Sleep Behavior Disorder: Association with Clinical and Motor Features.

Idiopathic rapid eye movement sleep behavior disorder (iRBD) is a major risk factor for Parkinson's disease and dementia with Lewy bodies. Anatomical gray matter abnormalities in the motor cortico-subcortical loop areas remain under studied in iRBD patients. We acquired T1-weighted images and administrated quantitative motor tasks in 41 patients with polysomnography-confirmed iRBD and 41 healthy subjects. Cortical thickness and voxel-based morphometry (VBM) analyses were performed to investigate local cortical thickness and gray matter volume changes, vertex-based shape analysis to investigate shape of subcortical structures, and structure-based volumetric analyses to investigate volumes of subcortical and brainstem structures. Cortical thickness analysis revealed thinning in iRBD patients in bilateral medial superior frontal, orbitofrontal, anterior cingulate cortices, and the right dorsolateral primary motor cortex. VBM results showed lower gray matter volume in iRBD patients in the frontal lobes, anterior cingulate gyri, and caudate nucleus. Shape analysis revealed extensive surface contraction in the external and internal segments of the left pallidum. Clinical and motor impaired features in iRBD were associated with anomalies of the motor cortico-subcortical loop. In summary, iRBD patients showed numerous gray matter structural abnormalities in the motor cortico-subcortical loop, which are associated with lower motor performance and clinical manifestations of iRBD.

Neuroanatomical correlates of forgiving unintentional harms

Mature moral judgments rely on the consideration of a perpetrator’s mental state as well as harmfulness of the outcomes produced. Prior work has focused primarily on the functional correlates of how intent information is neurally represented for moral judgments, but few studies have investigated whether individual differences in neuroanatomy can also explain variation in moral judgments. In the current study, we conducted voxel-based morphometry analyses to address this question. We found that local grey matter volume in the left anterior superior temporal sulcus, a region in the functionally defined theory of mind or mentalizing network, was associated with the degree to which participants relied on information about innocent intentions to forgive accidental harms. Our findings provide further support for the key role of mentalizing in the forgiveness of accidental harms and contribute preliminary evidence for the neuroanatomical basis of individual differences in moral judgments.

Decision-making performance in Parkinson's disease correlates with lateral orbitofrontal volume

BackgroundPatients with Parkinson's disease (PD) exhibit poor decision-making, and the underlying neural correlates are unclear. We used voxel-based morphometry with Diffeomorphic Anatomical Registration through Exponentiated Lie algebra to examine this issue. MethodsThe decision-making abilities of 20 patients with PD and 37 healthy controls (HCs) were measured with a computerized Iowa Gambling Task (IGT). We assessed the local gray matter volumes of the patients and HCs and their correlations with decision-making performance, disease duration, disease severity, and anti-Parkinsonism medication dose. ResultsCompared with the HCs, the patients with PD exhibited poor IGT performances. The gray matter volumes in the medial orbitofrontal cortex, left inferior temporal cortex, and right middle frontal gyrus were decreased in the patients. Results in the regression analysis showed that lateral orbitofrontal volume correlated with performance in the IGT in PD. Regions that correlated with disease duration, severity, and medication dose did not overlap with orbitofrontal regions. ConclusionOur results indicate that the lateral and medial orbitofrontal cortex are related to decision-making in PD patients. Since the medial orbitofrontal cortex is shown to be involved in monitoring reward, reward monitoring seems to be impaired as a whole in PD patients. Meanwhile, the lateral region is related to evaluation of punishment, which is considered to have an influence on individual differences in decision-making performance in PD patients.

Gray matter network differences between behavioral variant frontotemporal dementia and Alzheimer's disease

We set out to study whether single-subject gray matter (GM) networks show disturbances that are specific for Alzheimer's disease (AD; n = 90) or behavioral variant frontotemporal dementia (bvFTD; n = 59), and whether such disturbances would be related to cognitive deficits measured with mini-mental state examination and a neuropsychological battery, using subjective cognitive decline subjects as reference. AD and bvFTD patients had a lower degree, connectivity density, clustering, path length, betweenness centrality, and small world values compared with subjective cognitive decline. AD patients had a lower connectivity density than bvFTD patients (F = 5.79, p = 0.02; mean ± standard deviation bvFTD 16.10 ± 1.19%; mean ± standard deviation AD 15.64 ± 1.02%). Lasso logistic regression showed that connectivity differences between bvFTD and AD were specific to 23 anatomical areas, in terms of local GM volume, degree, and clustering. Lower clustering values and lower degree values were specifically associated with worse mini-mental state examination scores and lower performance on the neuropsychological tests. GM showed disease-specific alterations, when comparing bvFTD with AD patients, and these alterations were associated with cognitive deficits.

Sex on the brain: Are gender-dependent structural and functional differences associated with behavior?

A substantial number of studies provide evidence documenting a variety of sex differences in the brain. It remains unclear whether sexual differentiation at the neural level is related to that observed in daily behavior, cognitive function, and the risk of developing certain psychiatric and neurological disorders. Some investigators have questioned whether the brain is truly sexually differentiated and support this view with several arguments including the following: (1) brain structural or functional differences are not necessarily reflected in appropriate differences at the behavioral level, which might suggest that these two phenomena are not linked to each other; and (2) sex-related differences in the brain are rather small and concern features that significantly overlap between males and females. This review polemicizes with those opinions and presents examples of sex-related local neural differences underpinning a variety of sex differences in behaviors, skills, and cognitive/emotional abilities. Although male/female brain differentiation may vary in pattern and scale, nonetheless, in some respects (e.g., relative local gray matter volumes) it can be substantial, taking the form of sexual dimorphism and involving large areas of the brain (the cortex in particular). A significant part of this review is devoted to arguing that some sex differences in the brain may serve to prevent (in the case where they are maladaptive), rather than to produce, differences at the behavioral/skill level. Specifically, some differences might result from compensatory mechanisms aimed at maintaining similar intellectual capacities across the sexes, despite the smaller average volume of the brain in females compared with males. © 2016 Wiley Periodicals, Inc.