Brain Imaging and Behavior最新文献

Freezing of gait (FOG) in individuals with Parkinson's Disease is associated with a loss of gait automaticity. This loss of automaticity is demonstrated by worsening gait performance while dual tasking. Functional connectivity between the cerebellar vermis and cortex have previously been associated with spatiotemporal measures of gait in PD. The objective of this study was to determine whether this corticocerebellar connectivity is associated with gait automaticity as measured by dual task interference in PD FOG. 55 participants with PD were recruited (38 FOG, 17 non-FOG controls) to undergo a resting-state functional magnetic resonance imaging scan. Gait automaticity was quantified using spatiotemporal metrics from single and dual task time up and go trials. FOG participants demonstrated shorter step length and gait velocity compared to non-FOG PD controls. A trend toward greater dual task interference of step length in the FOG group was found. Using a seed-based connectivity approach we observed that FOG participants have greater vermis connectivity than non-FOG PD participants to several cortical regions including the superior parietal lobe, supplemental motor area, precentral gyrus and posterior cingulate (voxel threshold p < 0.01, cluster FWE corrected p < 0.05). Meanwhile, vermis connectivity to the occipital cortex was reduced in FOG participants relative to non-FOG controls. Dual task interference of step length among the FOG group correlated with the degree of vermis connectivity to the sensorimotor cortex and superior parietal cortex (voxel threshold p < 0.01, cluster FWE corrected p < 0.05). We conclude that increased corticocerebellar connectivity may be associated with loss of gait automaticity in individuals with PD FOG.

Objective: To investigate the association between plasma uric acid levels and white matter microstructural alterations in amyotrophic lateral sclerosis (ALS) patients and to explore the potential mediating role of white matter microstructural alterations in the protective effect of plasma uric acid on cognitive function in ALS patients.

Methods: 73 right-handed ALS patients were recruited for this study. Plasma uric acid levels were measured, diffusion tensor imaging scans were performed to assess white matter integrity, and cognition was evaluated using the Edinburgh Cognitive and Behavioral Screen. The relationships among plasma uric acid, white matter integrity, and cognitive function were examined through multivariate linear regression analysis. Additionally, mediation analysis was performed to investigate whether white matter integrity mediated the relationship between uric acid levels and cognitive function.

Results: The findings revealed a positive correlation between plasma uric acid levels and extensive preservation of white matter microstructure in various regions, including the fornix, cerebellar, internal capsule, frontotemporal and frontooccipital lobe bundles among ALS patients. Mediation analysis indicated that fractional anisotropy in the hippocampal portion of the cingulum fully mediated the effects of plasma uric acid levels on executive function in ALS patients.

Interpretation: Our results suggested that elevated plasma uric acid may preserve the integrity of white matter microstructure in ALS patients. Furthermore, we have identified evidence supporting the mediating influence of the hippocampal portion of the cingulum in linking plasma uric acid levels to cognitive function among ALS patients.

United States Special Operations Forces (SOF) experience neurobehavioral symptoms that can adversely affect training and combat operations. Understanding the neurobiological basis for these symptoms may guide prevention and treatment. In 29 male active-duty SOF with mean (SD) 17(4) years of service, we tested whether self-reported symptoms of apathy, disinhibition, and executive dysfunction measured by the Frontal Systems Behavior Scale, were related to functional magnetic resonance imaging and positron emission tomography biomarkers (translocator protein and tau) of the limbic, salience, and executive control networks. Higher disinhibition was associated with lower functional connectivity and higher tau signal within the salience network, though both associations diminished with age. These findings provide the basis for future multimodal studies to elucidate the relationship between neurobehavioral symptoms and neuroimaging biomarkers in the context of repeated blast exposure.

The morphological fingerprint in the brain is capable of identifying the uniqueness of an individual. However, whether such individual patterns are present in perinatal brains, and which morphological attributes or cortical regions better characterize the individual differences of neonates remain unclear. In this study, we proposed a deep learning framework that projected three-dimensional spherical meshes of three morphological features (i.e., cortical thickness, mean curvature, and sulcal depth) onto two-dimensional planes through quasi-conformal mapping, and employed the ResNet18 and contrastive learning for individual identification. We used the cross-sectional structural MRI data of 461 infants, incorporating with data augmentation, to train the model and fine-tuned the parameters based on 41 infants who had longitudinal scans. The model was validated on a fold of 20 longitudinal scanned infant data, and remarkable Top1 and Top5 accuracies of 85.90% and 92.20% were achieved, respectively. The sensorimotor and visual cortices were recognized as the most contributive regions in individual identification. Moreover, morphological fingerprints successfully predicted the long-term development of cognition and behavior. Furthermore, the folding morphology demonstrated greater discriminative capability than the cortical thickness. These findings provided evidence for the emergence of morphological fingerprints in the brain at the beginning of the third trimester, which may hold promising implications for understanding the formation of individual uniqueness, and predicting long-term neurodevelopmental risks in the brain during early development.

Early life adversity, defined as exposure to stressful events during childhood, is a significant risk factor for the development of psychiatric disorders. Diffusion tensor imaging studies employing tract-based spatial statistics have shown microstructural abnormalities in white matter among individuals exposed to early life adversity; however, robust conclusions are yet to be drawn. This systematic review synthesizes findings of previous tract-based spatial statistics studies to identify the white matter alterations in adult brains exposed to early life adversity, in papers with methodological consistency. The literature search (April 2024) was conducted to identify tract-based spatial statistics studies that compared diffusion metrics between adults exposed to early life adversity and adults not. Embase, Pubmed, and PsycInfo were searched, retrieving 2458 articles. Following deduplication, 1739 titles and/or abstracts were screened. 1699 articles were excluded, and 40 full texts were reviewed. Seven articles, reporting on 764 subjects, met the inclusion criteria and were included in the narrative synthesis. Compared to controls, adults exposed to early life adversity showed lower fractional anisotropy values in white matter tracts of the limbic and visual processing systems, specifically the anterior thalamic radiation, inferior longitudinal fasciculus, corona radiata, uncinate fasciculus, inferior fronto-occipital fasciculus, and cingulum bundle. This systematic review highlights that early life adversity may underlie emotional dysregulation and contribute to an increased risk of psychopathology in later life and explores the potential neurobiological mechanisms that underpin these structural changes. Understanding these associations is crucial for developing targeted interventions aimed at mitigating the long-term impact of early life adversity.

Previous literature has indicated that individuals with high trait anxiety have negative bias in forecasting future emotions, but the neural mechanisms underlying this remain unclear. Individuals with high trait anxiety (HTA; n = 38) and individuals with low trait anxiety (LTA; n = 38) were recruited. All participants completed the Social Affective Forecasting task and underwent resting-state fMRI scanning. Compared with the LTA group, the HTA group anticipated lower levels of arousal for future positive events but showed comparable performance for anticipated valence for future positive events. Moreover, the HTA group demonstrated intact performance in reporting anticipated valence and anticipated arousal for future negative events. In addition, the HTA group demonstrated increased functional connectivity between the left ventromedial prefrontal cortex (vmPFC) and left lingual gyrus relative to the LTA group. Besides, the HTA group also showed increased functional connectivity between the dorsal anterior insula and right posterior cingulate cortex compared to the LTA group. No significant associations were found between the altered functional connectivity and affective forecasting performance. Increased functional connectivity observed in the HTA group suggested that HTA individuals may devote more efforts when anticipating future events, to maintain intact in anticipating valence for future events.

Numerous previous studies have classified brain regions related to social processing into the "social brain" regions. Recent genetic studies showed that gene expression has a crucial effect on both brain functions and behavioral social performance. However, studies still lack a clear understanding of the organization of the social gene expression (SocGene) network. This study aimed to distinguish the difference between the SocGene network and the social brain network (SBN) and further explored their deficits in schizophrenia (SCZ) patients. The SocGene network was constructed by generating the gene expression maps of six social neuropeptide receptors from the Allen Human Brain Atlas. Then, we recruited a general population sample of 37 participants and a clinical sample including 26 SCZ and 25 Healthy controls (HCs) successively to construct the resting-state SocGene and SBN at the individual level. The integration (global efficiency, GE) and segregation (local efficiency, LE) of these brain networks were calculated using the graphic analysis. Results showed that the GE and LE of the SocGene network were significantly higher than those of the SBN in both two cohorts. The SCZ patients showed significantly diminished LE of the two brain networks compared to HCs, especially in the SocGene network. These findings implied that the SocGene network strengthened the integration and segregation compared to the SBN. SCZ patients mainly exhibited deficits in the segregation of these two brain networks. The current findings provide a new perspective on combining genetic expression and brain function in understanding the psychopathology of social functioning.

Conduct problems (CP) encompass a wide array of behavioral difficulties in youths, including aggression, defiance, and rule-breaking, resulting in interpersonal conflicts. CP comprises various psychiatric conditions, constituting a significant public health burden. This study performed a whole-brain coordinate-based meta-analysis (CBMA) that synthesized findings from diffusion tensor imaging (DTI), voxel-based morphometry (VBM), and surface-based morphometry (SBM) studies to investigate consistent structural brain abnormalities in children and adolescents with CP. A total of 35 studies were eventually included. Altered white matter integrity in the right lenticular nucleus and the right inferior longitudinal fasciculus (ILF) were observed. Gray matter volume (GMV) alterations included increased volume in the right superior frontal gyrus, as well as reduced volume in the right supramarginal gyrus and left amygdala. Cortical thickness reductions were detected in the left precentral gyrus and right superior frontal gyrus. These findings underscored the intricate neurobiological basis of CP, and the meta-regression analysis revealed age-related variations in structural brain alterations, further highlighting the need for early and personalized interventions. This comprehensive study advanced our understanding of the neural underpinnings of CP, and future research and interdisciplinary collaboration to translate our findings into meaningful interventions for individuals with CP should be further explored.

Aerobic exercise has been proved to reduce the risk of major depression in subthreshold depression (StD) individuals effectively, yet previous studies ignored the different functions of amygdala subregions. In this study, 44 StD individuals and 34 healthy controls (HCs) underwent resting-state functional magnetic resonance imaging before and after eight weeks of aerobic exercise respectively. Transverse and longitudinal analyses were conducted based on the seed-based functional connectivity (FC) analysis between amygdala subregions and the whole brain of the two groups. The transverse analyses showed that compared to HCs, StD individuals showed abnormal FC between the right dorsal amygdala (DA) and right superior frontal gyrus, the left medial amygdala (MA) and left gyrus rectus, right caudate, as well as the right ventrolateral amygdala (VA) and right angular gyrus before the exercise intervention, while increased FC between the right DA and left supramarginal gyrus after the exercise intervention. The longitudinal analysis showed decreased FC between the left DA and left caudate, left middle frontal gyrus, while increased FC between the right MA and posterior central gyrus in StD individuals after exercise intervention. As for HCs, the DA showed FC differences with the insula, frontal lobe, parietal lobe, temporal lobe and thalamus. The MA showed FC differences with the central posterior gyrus, occipital lobe and thalamus. The VA showed FC differences with the calcarine cortex and parietal lobe. The findings demonstrated the alleviative effect of aerobic exercise on depression from the perspective of brain function.

Magnetic resonance imaging (MRI) is frequently used to monitor disease progression in multiple sclerosis (MS). This study aims to systematically evaluate the correlation between MRI measures and histopathological changes, including demyelination, axonal loss, and gliosis, in the central nervous system of MS patients. We systematically reviewed post-mortem histological studies evaluating myelin density, axonal loss, and gliosis using quantitative imaging in MS. Relevant studies were identified through searches in PubMed, EMBASE, and Web of Science. A total of 38 studies involving 1782 regions of interest from 229 subjects were included. Pooled random-effects models were used to calculate the correlation between demyelination, axonal loss, gliosis, and various MRI parameters, including magnetization transfer ratio (MTR), T1 and T2 relaxation times, myelin water fraction (MWF), proton density (PD), and diffusivities. Pair-wise analyses compared results between lesioned and non-lesioned tissues. Our results demonstrated moderate to strong correlations between MRI parameters and myelin density in MS, with correlation coefficients: T1 (0.72), T2 (0.72), MTR (-0.73), FA (-0.73), RD (0.70), MD (0.70), MWF (-0.82), and PD (0.73). Interestingly, stronger correlations were found in lesioned tissues compared to non-lesioned tissues (P < 0.001). Moderate correlations were found between MRI parameters and axonal loss and gliosis. Our study reveals significant correlations between MRI techniques and histological assessments of myelin, axonal damage, and gliosis in MS. MRI metrics exhibited a more robust association with demyelination in lesioned areas than in non-lesioned brain tissue, highlighting the pronounced degree of myelin degradation in MS lesions. Further investigation is warranted to corroborate these results and refine MRI-based monitoring of MS pathology.