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Superficial white matter tractography was performed using methodology similar to Shastin et al. (2022) in order to derive SWM segmentations. This included multi-shell multi-tissue spherical deconvolution (Jeurissen et al. 2014) to derive fiber orientation distributions (left), anatomically informed probabilistic tractography (Tournier et al. 2010) and filtering (middle), and tract segmentation (right)
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Superficial white matter (SWM) represents a significantly understudied part of the human brain, despite comprising a large portion of brain volume and making up a majority of cortico-cortical white matter connections. Using multiple, high-quality datasets with large sample sizes (N = 2421, age range 5–100) in combination with methodological advance...
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... Future work may also consider exploring alternative segmentations for comparing regional WM and GM volume changes, such as comparing cortical GM volume loss with growth of only the superficial WM volume that it encircles (Schilling et al., 2023). Doing so would make it possible to determine whether our observed changes in WM volume are primarily attributable to growth in superficial or deep WM, and to assess whether superficial WM thickening patterns mirror cortical thinning patterns. ...
A fundamental puzzle about brain development is why the volume of gray matter (GM) apparently declines as white matter (WM) grows when children enter adolescence. Since pruned synapses are too small to affect GM volume, a prevailing theory posits that an expanded distribution of myelin causes the inner edge of the GM to “whiten” while total brain volume remains steady, shifting the MRI‐measured WM:GM boundary closer to the brain's outer surface. This theory inherently predicts that GM volume loss is concurrent with WM volume growth across regions, within sexes and over time, although these predictions have yet to be explicitly tested. In this study, we test these predictions by mapping regional GM and WM volumetric changes in 2333 participants of the Adolescent Brain Cognitive Development study aged 9–14 years who each received three MRI scans 2 years apart. We show that average GM and WM volume changes follow distinct spatial, temporal, and sex‐specific patterns, indicating that GM volume loss is not balanced by WM volume growth, although cortical GM thinning is weakly correlated with WM growth in some regions. We conclude that myelin is not the main source of measured GM volume loss, and we propose alternative candidates.
... [51][52][53] The process of brain maturation pertains to distinct patterns of cortical thinning paired with microstructural changes in white matter. 54 The neonatal years encompass a critical stage for brain development, and the complex processes have previously been described. 55 The development of the brain has been shown to follow a general pattern from inferior to superior and from posterior to anterior regions. ...
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that is increasingly affecting pediatric and adult populations. Neuropsychiatric manifestations (ie, cognitive dysfunction and mood disorders) appear to occur with greater severity and poorer prognosis in childhood‐onset SLE (cSLE) versus adult‐onset SLE, negatively impacting school function, self‐management, and psychosocial health, as well as lifelong health‐related quality of life. In this review, we describe pathogenic mechanisms active in cSLE, such as maladaptive inflammatory processes and ischemia, which are hypothesized to underpin central phenotypes in patients with cSLE, and the role of alterations in protective central nervous system (CNS) barriers (ie, the blood–brain barrier) are also discussed. Recent findings derived from novel neuroimaging approaches are highlighted because the methods employed in these studies hold potential for identifying CNS abnormalities that would otherwise remain undetected with conventional multiple resonance imaging studies (eg, T2‐weighted or fluid‐attenuated inversion recovery sequences). Furthermore, we propose that a more robust presentation of neuropsychiatric symptoms in cSLE is in part due to the harmful impact of a chronic inflammatory insult on a developing CNS. Although the immature status of the CNS may leave patients with cSLE more vulnerable to harboring neuropsychiatric manifestations, the same property may represent a greater urgency to reverse the maladaptive effects associated with a proneuroinflammatory state, provided that effective diagnostic tools and treatment strategies are available. Finally, considering the crosstalk among the CNS and other organ systems affected in cSLE, we postulate that a finer understanding of this interconnectivity and its role in the clinical presentation in cSLE is warranted.
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... This relation was observed only in the white matter. The gray and white matter undergo distinct morphological alterations during the lifespan [90,91]. The gray matter volume tends to increase until around middle childhood (approximately 6 years), after which it starts to decline from young adulthood onwards. ...
... In contrast, the white matter achieves its maximum volume in adulthood (between 20 and 40 years), stabilizing and subsequently decreasing in late adulthood. Both gray and white matter exhibit accelerated atrophy during the late stages of adulthood [91][92][93][94]. ...
Alzheimer’s disease (AD) is the leading cause of dementia and is characterized by a progressive decline in cognitive abilities. A pathological hallmark of AD is a region-specific accumulation of the amyloid-beta protein (Aβ). Here, we explored the association between regional Aβ deposition, sociodemographic, and local biochemical factors. We quantified the Aβ burden in postmortem cortical samples from parietal (PCx) and temporal (TCx) regions of 27 cognitively unimpaired (CU) and 15 AD donors, aged 78–100 + years. Histological images of Aβ immunohistochemistry and local concentrations of pathological and inflammatory proteins were obtained at the “Aging, Dementia and TBI Study” open database. We used the area fraction fractionator stereological methodology to quantify the Aβ burden in the gray and white matter within each cortical region. We found higher Aβ burdens in the TCx of AD octogenarians compared to CU ones. We also found higher Aβ loads in the PCx of AD nonagenarians than in AD octogenarians. Moreover, AD women exhibited increased Aβ deposition compared to CU women. Interestingly, we observed a negative correlation between education years and Aβ burden in the white matter of both cortices in CU samples. In AD brains, the Aβ40, Aβ42, and pTau181 isoforms of Aβ and Tau proteins were positively correlated with the Aβ burden. Additionally, in the TCx of AD donors, the proinflammatory cytokine TNFα showed a positive correlation with the Aβ load. These novel findings contribute to understanding the interplay between sociodemographic characteristics, local inflammatory signaling, and the development of AD-related pathology in the cerebral cortex.
... In this section, we discuss potential anatomical mechanisms contributing to the relationship between sulcal depth and behavior in two main ways. First, long-range white matter fibers have a gyral bias, while short-range white matter fibers have a sulcal bias in which some fibers project directly from the deepest points of a sulcus (Cottaar et al., 2021 ;Reveley et al., 2015 ;Schilling et al., 2018Schilling et al., , 2023Van Essen et al., 2014 ). As such, recent work hypothesized a close link between sulcal depth and short-range white matter properties (Bodin et al., 2021 ;Pron et al., 2021 ;Voorhies et al., 2021 ;Willbrand et al., 2023b ;Yao et al., 2022 ): deeper sulci would reflect even shorter short-range white matter fibers, which would result in faster communication between local, cortical regions and in turn, contribute to improved cognitive performance. ...
Recent work has uncovered relationships between evolutionarily new small and shallow cerebral indentations, or sulci, and human behavior. Yet, this relationship remains unexplored in the lateral parietal cortex (LPC) and the lateral parieto-occipital junction (LPOJ). After defining thousands of sulci in a young adult cohort, we uncovered four previously unidentified small and shallow LPC/LOPJ sulci—one of which (ventral supralateral occipital sulcus, slocs-v) is present in nearly every hemisphere, and is morphologically, architecturally, and functionally dissociable from neighboring regions. A data-driven, model-based approach relating sulcal depth to behavior revealed that the morphology of only a subset of LPC/LPOJ sulci, including the slocs-v, is related to performance on a spatial orientation, but not a relational reasoning task. Our findings build on classic neuroanatomical theories and identify new neuroanatomical targets for future “precision imaging” studies exploring the relationship among brain structure, brain function, and cognitive abilities in individual participants.
... In this section, we discuss potential anatomical mechanisms contributing to the relationship between sulcal depth and behavior in two main ways. First, long-range white matter fibers have a gyral bias, while short-range white matter fibers have a sulcal bias in which some fibers project directly from the deepest points of a sulcus (Cottaar et al., 2021 ;Reveley et al., 2015 ;Schilling et al., 2018Schilling et al., , 2023Van Essen et al., 2014 ). As such, recent work hypothesized a close link between sulcal depth and short-range white matter properties (Bodin et al., 2021 ;Pron et al., 2021 ;Voorhies et al., 2021 ;Willbrand et al., 2023b ;Yao et al., 2022 ): deeper sulci would reflect even shorter short-range white matter fibers, which would result in faster communication between local, cortical regions and in turn, contribute to improved cognitive performance. ...
Recent work has uncovered relationships between evolutionarily new small and shallow cerebral indentations, or sulci, and human behavior. Yet, this relationship remains unexplored in the lateral parietal cortex (LPC) and the lateral parieto-occipital junction (LPOJ). After defining thousands of sulci in a young adult cohort, we uncovered four previously unidentified small and shallow LPC/LOPJ sulci—one of which (ventral supralateral occipital sulcus, slocs-v) is present in nearly every hemisphere, and is morphologically, architecturally, and functionally dissociable from neighboring regions. A data-driven, model-based approach relating sulcal depth to behavior revealed that the morphology of only a subset of LPC/LPOJ sulci, including the slocs-v, is related to performance on a spatial orientation, but not a relational reasoning task. Our findings build on classic neuroanatomical theories and identify new neuroanatomical targets for future “precision imaging” studies exploring the relationship among brain structure, brain function, and cognitive abilities in individual participants.
Residual mechanical stresses, also known as solid stresses, emerge during rapid differential growth or remodeling of tissues, as observed in morphogenesis and tumor growth. While residual stresses typically dissipate in most healthy adult organs, as the growth rate decreases, high residual stresses have been reported in mature, healthy brains. However, the origins and consequences of residual mechanical stresses in the brain across health, aging, and disease remain poorly understood. Here, we utilized and validated a previously developed method to map residual mechanical stresses in the brains of mice across three age groups: 5–7 days, 8–12 weeks, and 22 months. We found that residual solid stress rapidly increases from 5–7 days to 8–12 weeks and remains high in mature 22 months mice brains. Three-dimensional mapping revealed unevenly distributed residual stresses from the anterior to posterior coronal brain sections. Since the brain is rich in negatively charged hyaluronic acid, we evaluated the contribution of charged extracellular matrix (ECM) constituents in maintaining solid stress levels. We found that lower ionic strength leads to elevated solid stresses, consistent with its unshielding effect and the subsequent expansion of charged ECM components. Lastly, we demonstrated that hemorrhagic stroke, accompanied by loss of cellular density, resulted in decreased residual stress in the murine brain. Our findings contribute to a better understanding of spatiotemporal alterations of residual solid stresses in healthy and diseased brains, a crucial step toward uncovering the biological and immunological consequences of this understudied mechanical phenotype in the brain.
Characterizing how, when and where the human brain changes across the lifespan is fundamental to our understanding of developmental processes of childhood and adolescence, degenerative processes of aging, and divergence from normal patterns in disease and disorders. We aimed to provide detailed descriptions of white matter pathways across the lifespan by thoroughly characterizing white matter microstructure, white matter macrostructure, and morphology of the cortex associated with white matter pathways. We analyzed 4 large, high-quality, cross-sectional datasets comprising 2789 total imaging sessions, and participants ranging from 0 to 100 years old, using advanced tractography and diffusion modeling. We first find that all microstructural, macrostructural, and cortical features of white matter bundles show unique lifespan trajectories, with rates and timing of development and degradation that vary across pathways— describing differences between types of pathways and locations in the brain, and developmental milestones of maturation of each feature. Second, we show cross-sectional relationships between different features that may help elucidate biological differences at different stages of the lifespan. Third, we show unique trajectories of age-associations across features. Finally, we find that age associations during development are strongly related to those during aging. Overall, this study reports normative data for several features of white matter pathways of the human brain that are expected to be useful for studying normal and abnormal white matter development and degeneration.
Characterizing how, when and where the human brain changes across the lifespan is fundamental to our understanding of developmental processes of childhood and adolescence, degenerative processes of aging, and divergence from normal patterns in disease and disorders. We aimed to provide detailed descriptions of white matter pathways across the lifespan by thoroughly characterizing white matter microstructure, white matter macrostructure, and morphology of the cortex associated with white matter pathways. We analyzed 4 large, high-quality, publicly-available datasets comprising 2789 total imaging sessions, and participants ranging from 0 to 100 years old, using advanced tractography and diffusion modeling. We first find that all microstructural, macrostructural, and cortical features of white matter bundles show unique lifespan trajectories, with rates and timing of development and degradation that vary across pathways - describing differences between types of pathways and locations in the brain, and developmental milestones of maturation of each feature. Second, we show cross-sectional relationships between different features that may help elucidate biological changes occurring during different stages of the lifespan. Third, we show unique trajectories of age-associations across features. Finally, we find that age associations during development are strongly related to those during aging. Overall, this study reports normative data for several features of white matter pathways of the human brain that will be useful for studying normal and abnormal white matter development and degeneration.
Extra temporal lobe epilepsy (eTLE) may involve heterogenous widespread cerebral networks. We investigated the structural network of an eTLE cohort, at the postulated epileptogenic zone later surgically removed, as a network node; the resection zone (RZ). We hypothesised patients with an abnormal connection to/from the RZ, to have proportionally increased abnormalities based on topological proximity to the RZ, in addition to poorer post-operative seizure outcome. Structural and diffusion MRI were collected for 22 eTLE patients pre- and post-surgery, and for 29 healthy controls. The structural connectivity of the RZ prior to surgery, measured via generalised fractional anisotropy (gFA), was compared to healthy controls. Abnormal connections were identified as those with substantially reduced gFA (z < −1.96). For patients with one or more abnormal connections to/from the RZ, connections with closer topological distance to the RZ had higher proportion of abnormalities. The minority of the seizure-free patients (3/11) had one or more abnormal connections, whilst most non-seizure free patients (8/11) had abnormal connections to the RZ. Our data suggest eTLE patients with one or more abnormal structural connections to/from the RZ had more proportional abnormal connections based on topological distance to the RZ and associated with reduced chance of seizure freedom post-surgery.
