Brain Structure & Function最新文献

The claustrum is a thin gray matter structure in each brain hemisphere, characterized by exceptionally high connectivity with nearly all brain regions. Despite extensive animal studies on its anatomy and function and growing evidence of claustral deficits in neuropsychiatric disorders, its specific roles in normal and abnormal human brain function remain largely unknown. This is primarily due to its thin and complex morphology, which limits accurate anatomical delineation and neural activity isolation in conventional in vivo neuroimaging. To facilitate future neuroimaging studies, we developed a comprehensive and reliable manual segmentation protocol based on a cellular-resolution brain atlas and high-resolution (0.7 mm isotropic) MRI data. The protocols involve detailed guidelines to delineate the entire claustrum, including the inferior parts that have not been clearly described in earlier MRI studies. Additionally, we propose a geometric method to parcellate the claustrum into three subregions (the dorsal, ventral, and temporal claustrum) along the superior-to-inferior axis. The mean bilateral claustrum volume in 10 young adults was 3307.5 mm³, approximately 0.21% of total intracranial volume. Our segmentation protocol demonstrated high inter- and intra-rater reliability (ICC > 0.89, DSC > 0.85), confirming its replicability. This comprehensive and reliable manual segmentation protocol offers a robust foundation for anatomically precise neuroimaging investigations of the human claustrum.

Blindness provides a unique model for investigating brain plasticity in response to sensory deprivation. While structural changes in both gray and white matter have been widely documented, particularly in cases of early or congenital visual deprivation, gray matter studies have traditionally focused on cortical thickness, often finding cortical thickening in posterior regions. However, other aspects of gray matter integrity, such as cortical myelin content, remain underexplored. In this study, we examined the effects of visual deprivation on cortical structure in a cohort of early blind individuals who received eye surgery during adolescence, expanding beyond conventional measures to include cortical thickness, curvature, and T1-weighted signal intensity. This multi-faceted approach offers a more comprehensive view of cortical adaptations to early sensory deprivation. While blindness offers valuable insights into sensory-driven brain plasticity, an intriguing and unresolved question is whether structural plasticity reverses after sight restoration, enabling typical visual processing circuits to develop despite the initial period of deprivation. To address this, we assessed the effect of sight-recovering eye surgery on gray matter changes. Critically, individuals in this cohort received surgery after the closure of the sensitive period for visual development. We did not find evidence of gray matter changes after surgery. However, in a previous study conducted on the same cohort, we reported that notable plasticity in white matter emerged in this same population. These results suggest that white matter may potentially serve as a biomarker of structural plasticity following sight restoration, even beyond the sensitive developmental window.

Did you know that there are thousands of ways to build a connectome from diffusion MRI tractography, and the choice of approach can hugely impact the final connectome and results? To name only a few: Tractography type: deterministic or probabilistic? Parcellation resolution: coarse or fine atlas? Edge weighting: streamline count, length, or microstructural properties? These choices give rise to a daunting garden of forking paths. In this article, we revise fundamental decisions you must make when planning to build a tractography-based connectome and their impact on its network analysis.

Brain age, an estimate of biological brain aging derived from neuroimaging, has been linked to cognitive and related factors. Metrics such as the Brain Age Gap Estimate (BrainAGE), depicting the discrepancy between predicted and chronological age, are commonly used to determine the influence of variables on brain aging. This study explored how cognitive ability, musical sophistication, and social skills contribute to BrainAGE in a sample of 81 healthy participants who underwent high-resolution magnetic resonance imaging and completed cognitive, musical, and social assessments. Following statistical analyses to fit the model, structural equation modelling was used to examine the influence of cognitive ability, assessed using the Delis-Kaplan Executive Function System, California Verbal Learning Test, and Wechsler Adult Intelligence Scale; musical sophistication, measured by the Goldsmiths Musical Sophistication Index; and social skills, evaluated using the Social Skills Inventory, on BrainAGE. Our findings demonstrated no significant influence of cognitive ability, musical expertise, or social skills on BrainAGE. These findings highlight the complexity of cognitive and social influences on brain age and underscore the need for further research into their interactive effects on neurobiological aging.

The retrotrapezoid nucleus (RTN) of rodents is located ventral to the facial motor nucleus (7N) and consists of acid-sensitive neurons that activate breathing and mediate the central component of the ventilatory response to hypercapnia. In rodents, RTN neurons can be histologically identified by the presence of paired-like homeobox 2B positive nuclei (Phox2b +) and the absence of cytoplasmic choline acetyltransferase (ChAT-) and tyrosine hydroxylase (TH-). Up to 50% of rodent RTN neurons synthesise galanin, and 88% express pituitary adenylate cyclase activating polypeptide (PACAP). The human RTN (hRTN) has not been mapped to date. This study aimed to map the location and cytoarchitecture of the adult hRTN and compare the findings to the homologies of rodents, macaques and human infants. Formalin-fixed, paraffin-embedded tissue blocks from two adult cases, spanning the medulla-pons, were serially sectioned (10 µm thick) and every four in thirty sections was assayed for immunohistochemistry for ChAT, or double-labelled Phox2b/TH, Phox2b/galanin and Phox2b/PACAP, followed by analysis using QuPath software. hRTN neurons, identified as Phox2b + /TH-/ChAT-, were located ventral to 7N and lateral to the superior olive, overlapped with the C1 or A5 catecholaminergic population and extended rostrocaudally from Obex + 13 to + 17 mm. In the parafacial area, 90% of Phox2b immunoreactive (-ir) neurons are hRTN neurons, totaling around 5000 bilaterally, and were surrounded by numerous TH-ir fibers. Galanin- and PACAP-ir was identified in 43% and 39% of Phox2b-ir parafacial neurons, respectively. This is the first study to characterise and quantitatively map the adult human RTN using a series of neurochemical markers.

Phonological processing skills are foundational for becoming a proficient reader and have only partially been linked to genetic and shared environmental effects in twin studies. This twin difference study of 88 twin pairs (age x̄ = 16.34 ± 1.66 years; 64% female; 65% monozygotic) was designed to examine brain structure and perinatal reasons for twin differences in a measure of phonological decoding accuracy. Diffeomorphic spatial normalization was used align T1-weighted images collected from the 176 participants to a common coordinate space. Jacobian determinant images that represent the amount of volumetric displacement to spatially normalize the T1-weighted images were then examined using voxel-based analyses to determine the extent to which twin differences in voxel-wise volumetric displacement were associated with twin differences in phonological decoding accuracy. Twins with larger lateral ventricles compared to their co-twin, particularly in the left hemisphere, had significantly poorer phonological decoding accuracy. This lateral ventricle effect depended on twins with relatively large differences in phonological decoding accuracy and white matter microstructure in fiber tracts adjacent to the lateral ventricles. Perinatal risk variables, such as slow fetal growth, were hypothesized to explain these twin differences but the current data did not provide clear perinatal explanations for the lateral ventricle and phonological decoding accuracy association. Together, the results suggest that increased lateral ventricle size is a marker for phonological decoding accuracy that is lower than expected based on common genetic and environmental influences on twin brain development.

Individuals with long COVID exhibit neurological and psychiatric symptoms that often persist well beyond the initial SARS-CoV-2 infection. Studies using [18F]-FDG positron emission tomography (FDG-PET) have revealed diverse abnormalities in brain glucose metabolism during the post-acute phase of COVID-19. We conducted a systematic review and meta-analysis to assess the spatial distribution and heterogeneity of brain metabolic changes in patients in the post-acute phase of COVID-19 relative to controls. We searched the MEDLINE, EMBASE, and CENTRAL databases in June 2025 for studies reporting FDG-PET data in patients with post-acute COVID-19 who have persistent neurological symptoms. Of the 14 eligible studies (584 scans), 13 reported glucose hypometabolism across frontoparietal regions, with the frontal cortex being the most consistently affected. This finding was confirmed by meta-analysis, which revealed a large and significant effect in the frontal cortex (Hedges' g = 1.34; 95% CI: 0.79-1.88; p < 0.001), despite high heterogeneity (I² = 93.6%). The systematic review indicates that brain metabolism generally improves over time, with widely varying recovery timelines, and consistently correlates hypometabolism with neurological symptom burden. These findings underscore the clinical relevance of frontoparietal hypometabolism in post-acute COVID-19 and its association with neurocognitive deficits, highlighting the need for longitudinal, quantitative PET studies to elucidate temporal dynamics and inform therapeutic development.

In the adult mammalian nervous system, sex differences can be manifested independently or in concert with sex-specific hormone cycles, such as the rat estrous cycle. Biological sex and related cycles influence neuronal properties in many brain regions, including the striatum, encompassing the nucleus accumbens (NAc) core, NAc shell, and caudate-putamen (CPu). While neuron soma size and density are commonly assessed in the context of biological sex, these attributes have never been investigated in the striatal regions of adult gonad-intact rodents disaggregated by sex and estrous cycle phase. Thus, we tested the hypothesis that neuron soma size and density would vary by striatal region, sex, and estrous cycle phase. Neuron soma size and density were measured in NAc core, NAc shell, and CPu from adult male rats and female rats in diestrus, proestrus, and estrus phases. Overall, neuron soma size was larger in the CPu than the NAc core and shell. Neuron density was greatest in the NAc shell, followed by the NAc core and CPu. Regarding sex, soma size was larger in male than female NAc shell and did not differ in other regions. Soma density did not sexually differ. Neither soma size nor density differed across estrous cycle phases. These results provide, for the first time, striatal neuron size and density measurements disaggregated by sex and estrous cycle phase and an indication of a sex difference in NAc shell soma size. In contrast, the estrous cycle appears to influence striatal function via other mechanisms than neuronal soma attributes.

Anatomical asymmetry is a hallmark of the human brain and may reflect hemispheric differences in its functional organization. Widely used software like FreeSurfer can automate neuroanatomical measurements and facilitate studies of hemispheric asymmetry. However, patterns of surface area lateralization measured using FreeSurfer are curiously consistent across diverse samples. Here, we demonstrate systematic biases in these measurements obtained from the default processing pipeline. We compared surface area asymmetry measured from reconstructions of original brains vs. the same scans after flipping their left-right orientation. The default pipeline returned implausible asymmetry patterns between the original and flipped brains: Many structures were always left- or right-lateralized. Notably, these biases occur prominently in key speech and language regions. In contrast, manual labeling and curvature-based parcellations of key structures both yielded the expected reversals of left/right lateralization in flipped brains. We determined that these biases result from discrepancies in how regional labels are defined between the cortical parcellation atlases' left and right hemispheres. These biases are carried into individual parcellations because the parcellation algorithm prioritizes vertex correspondence to the template over individual neuroanatomical variation, meaning such biases could exist in any asymmetric atlas-based parcellation. We further demonstrate several straightforward, bias-free approaches to measuring surface area asymmetry, including using symmetric registration templates and parcellation atlases, vertex-wise analyses, and within-subject curvature-based parcellations. These results highlight theoretical concerns about using only atlas-based parcellations to make inferences about population-level brain asymmetry and underscore the need for validating bias-free neuroanatomical measurements, particularly to better examine how structural lateralization underlies functional lateralization.

This study aims to investigate potential changes in network controllability and structural-function coupling in cerebral small vessel disease (CSVD). Fifty-one CSVD patients and forty-one elderly controls underwent diffusion tensor imaging and resting-state functional magnetic resonance imaging. Average controllability and modal controllability were calculated using network control theory. Structural connectivity and functional connectivity were constructed respectively. Structural-functional coupling in each region was assessed using Spearman's rank correlation. Cognitive function was assessed using the Mini-Mental Scale Examination (MMSE) and the Trail Making Test (TMT). CSVD patients showed higher global average controllability but lower average controllability within the left prefrontal cortex. Additionally, they exhibited lower modular controllability at the global scale and within the Sensorimotor Network, while showing higher modular controllability in the left prefrontal cortex. Global average controllability was negatively correlated with MMSE scores and positively correlated with TMT-A and TMT-B scores. Global modal controllability was positively correlated with MMSE scores and negatively correlated with TMT-A and TMT-B scores. Global and regional changes in average controllability and modular controllability were linked to the severity of white matter injury. Moreover, regional structural-functional coupling was positively correlated with TMT-A scores at the global level, left sensorimotor cortex, and temporal cortex. Positive relationships were observed between TMT-B scores and the global and regional structural-functional coupling of several sub-networks. The integration of control theory and structural-function coupling may provide a comprehensive framework for elucidating the complex dynamics of CSVD and its association with cognitive impairment.