Matter Of Brain Research Articles

Attenuation coefficient as a tool to detect changes in the white matter of the rat brain caused by different types of gliomas and irradiation

In the present work, we carried out a comparative study of the attenuation coefficient of the white matter of the rat brain during the growth of glial tumors characterized by different degrees of malignancy (glioblastoma 101/8, astrocytoma 10-17-2, glioma C6) and during irradiation. We demonstrated that some tumor models cause a pronounced decrease in white matter attenuation coefficient values due to infiltration of tumor cells, myelinated fiber destruction, and edema. In contrast, other tumors cause compression of the myelinated fibers of the corpus callosum without their ruptures and prominent invasion of tumor cells, which preserved the attenuation coefficient values changeless. In addition, for the first time, the possibility of using the attenuation coefficient to detect late radiation-induced changes in white matter characterized by focal development of edema, disruption of the integrity of myelinated fibers, and a decrease in the amount of oligodendrocytes and differentiation of these areas from tumor tissue and healthy white matter has been demonstrated. The results indicate the promise of using the attenuation coefficient estimated from OCT data for in vivo assessment of the degree of destruction of peritumoral white matter or its compression, which makes this method useful not only in primary resections but also in repeated surgical interventions for recurrent tumors.

Gray matter based spatial statistics framework in the 1-month brain: insights into gray matter microstructure in infancy.

The neurodevelopmental epoch from fetal stages to early life embodies a critical window of peak growth and plasticity in which differences believed to be associated with many neurodevelopmental and psychiatric disorders first emerge. Obtaining a detailed understanding of the developmental trajectories of the cortical gray matter microstructure is necessary to characterize differential patterns of neurodevelopment that may subserve future intellectual, behavioral, and psychiatric challenges. The neurite orientation dispersion density imaging (NODDI) Gray-Matter Based Spatial Statistics (GBSS) framework leverages information from the NODDI model to enable sensitive characterization of the gray matter microstructure while limiting partial volume contamination and misregistration errors between images collected in different spaces. However, limited contrast of the underdeveloped brain poses challenges for implementing this framework with infant diffusion MRI (dMRI) data. In this work, we aim to examine the development of cortical microstructure in infants. We utilize the NODDI GBSS framework and propose refinements to the original framework that aim to improve the delineation and characterization of gray matter in the infant brain. Taking this approach, we cross-sectionally investigate age relationships in the developing gray matter microstructural organization in infants within the first month of life and reveal widespread relationships with the gray matter architecture.

Differences in Grey Matter Concentrations and Functional Connectivity between Young Carriers and Non-Carriers of the APOE ε4 Genotype.

Background: The pathophysiology of Alzheimer's disease (AD) may begin developing years or even decades prior to the manifestation of its first symptoms. The APOE ε4 genotype is a prominent genetic risk for AD that has been found to be associated with brain changes across the lifespan since early adulthood. Thus, studying brain changes that may occur in young adults with an APOE ε4 status is highly relevant. Objective: Examine potential differences in grey matter (GM) and functional connectivity (FC) in brains of cognitively healthy young APOE ε4 carriers and non-carriers, denoted here as ε4(+) and ε4(-), respectively. Methods: Three Tesla magnetic resonance imaging (MRI) brain scans were acquired from cognitively healthy young participants aged approximately 20 years (n = 151). Voxel-based morphometry (VBM) analysis was employed to identify potential structural differences in GM between ε4(+) and ε4(-). In a subsequent seed-based connectivity (SBC) analysis, brain regions that structurally differed in the VBM analysis were considered as seeds and correlated with all the remaining voxels across the brains to then measure the differences in FC between groups. Results: The VBM analysis suggested that ε4(+) (n = 28) had greater GM densities relative to ε4(-) (n = 123) in the left hippocampus and the left posterior insula (puncorr < 0.001). However, the effect did not survive the correction for multiple comparisons, suggesting minimal structural differences in this age range. In contrast, the SBC analysis indicated that ε4(+) exhibited significantly decreased FC between the left hippocampus and areas of the left middle temporal gyrus (n = 27) compared to ε4(-) (n = 102). These results remained significant after multiple comparisons (pFDR < 0.05). Lastly, no statistically significant differences in FC between groups were observed for the left insular seed (pFDR > 0.05). Discussion: These results suggest early structural and functional brain changes associated with the APOE ε4 genotype on young adults. Yet, they must be cautiously interpreted and contrasted with both older adults with genetic risk for AD and patients diagnosed with AD.

Canavan disease: a rare case report

Canavan disease is a very rare, fatal, autosomal recessive neurodegenerative disorder. It usually manifests during infancy. Mutations in the aspartoacylase (ASPA) gene (17p13.3), which code for the aspartoacylase enzyme, cause this disease. It is a leukodystrophy and affects white matter of the brain. This disease is associated with deficiency of an essential enzyme, aspartoacylase. The deficiency leads to loss of white matter in brain, leading to defective transmission of nerve signals. This disorder affects all ethnic groups, but occurs with greater frequency, in individuals of Ashkenazi Jewish descent.

Quantitation of the physicochemical properties of myelin using Nile Red fluorescence spectroscopy.

Myelin is a vital structure that is key to rapid saltatory conduction in the central and peripheral nervous systems. Much work has been done over the decades examining the biochemical composition and morphology of myelin at the light and electron microscopic levels. Here we report a method to study myelin based on the fluorescent probe Nile Red. This lipophilic dye readily partitions into live and chemicallyfixed myelin producing bright, well-resolved images of the sheath. Using spectral confocal microscopy, a complete emission spectrum of Nile Red fluorescence can be acquired for each pixel in an image. The solvatochromic properties of Nile Red cause its emission spectrum to change depending on the polarity of its local environment. Therefore, measuring spectral shifts can report subtle changes in the physicochemical properties of myelin. We show differences in myelin polarity in central versus peripheral nervous system and in different regions of central nervous system white matter of the mouse brain, together with developmental and sex variations. This technique is also well suited for measuring subtle changes in myelin properties in live exvivo white matter specimens. We also demonstrate how light deprivation induces a myelin polarity change in adult mouse optic nerve underscoring a continuing myelin plasticity in response to axonal activity well into adulthood. The Nile Red spectroscopic method allows measurement of subtle physicochemical changes in myelin that can importantly influence its electrical properties and by extension, conduction velocities in axons.

Numerical modelling of multiple sclerosis: A tissue-scale model of brain lesions

Multiple Sclerosis (MS) is an autoimmune condition leading to the degeneration of brain tissue, occurring when the immune system attacks the myelin sheath surrounding axons of white brain matter thereby disrupting brain signals. This study aimed to evaluate how MS lesions alter stress distribution through grey and white brain matter with lesions (active, chronic, and inactive). A linear viscoelastic model represents the tissue-scale dynamic deformation and time dependency of brain tissue. A Prony series expansion was used to model viscous effects including stress relaxation. An elastic modulus, within the viscoelastic model, was either reduced by 11 % for active lesions, or increased by 35 % increase for inactive lesions. These material properties were then implemented to model healthy tissue, active, chronically inflamed, and inactive lesions. Finite element analysis enabled stress evaluation in response to a peak cyclic displacement of 0.5 mm (1 % strain) with the healthy model acting as a control model. Chronic lesions had the largest effect on stress induced, in terms of high (171 Pa) and low stress (108 Pa). Inactive lesions induced an increase in stress of 11 Pa with areas of low stress (105 Pa). Active lesions caused the least deviation in peak induced stress (7 Pa). In conclusion, a hierarchy in stress induced across the lesion types has been found, from highest to lowest: chronic, inactive and active, with potential implications for lesion progression. In conclusion, MS lesions within brain tissue should model lesions, avoid assuming homogeneity during degeneration, and should distinguish between active and passive lesions.

Visual Impairment, Eye Conditions, and Diagnoses of Neurodegeneration and Dementia

Vision and eye conditions are associated with increased risk for Alzheimer disease and related dementias (ADRDs), but the nature of the association and the underlying biological pathways remain unclear. If causal, vision would be an important modifiable risk factor with viable population-level interventions. To evaluate potentially causal associations between visual acuity, eye conditions (specifically cataracts and myopia), neuroimaging outcomes, and ADRDs. A cohort and 2-sample bidirectional mendelian randomization (MR) study was conducted using UK Biobank participants and summary statistics from previously published genome-wide association studies on cataract, myopia, and AD. The participants included in the analysis were aged 55 to 70 years without dementia at baseline (calendar years 2006 to 2010), underwent genotyping, and reported on eye conditions; a subset completed visual acuity examinations (n = 69 852-71 429) or brain imaging (n = 36 591-36 855). Data were analyzed from August 15, 2022, through November 28, 2023. Self-reported cataracts, visual acuity, and myopia measured by refraction error. ADRD, AD, and vascular dementia were identified from electronic medical records. Total and regional brain volumes were determined using magnetic resonance imaging. The sample included 304 953 participants (mean [SD] age, 62.1 (4.1) years; 163 825 women [53.72%]); 14 295 (4.69%) had cataracts and 2754 (3.86%) had worse than 20/40 vision. Cataracts (hazard ratio [HR], 1.18; 95% CI, 1.07-1.29) and myopia (HR, 1.35; 95% CI, 1.06-1.70) were associated with a higher hazard of ADRD. In MR analyses to estimate potential causal effects, cataracts were associated with increased risk of vascular dementia (inverse variance-weighted odds ratio [OR], 1.92; 95% CI, 1.26-2.92) but were not associated with increased dementia (OR, 1.21; 95% CI, 0.98-1.50). There were no associations between myopia and dementia. In MR for potential reverse causality, AD was not associated with cataracts (inverse variance-weighted OR, 0.99; 95% CI, 0.96-1.01). Genetic risk for cataracts was associated with smaller total brain (β = -597.43 mm3; 95% CI, -1077.87 to -117.00 mm3) and gray matter (β = -375.17 mm3; 95% CI, -680.10 to -70.24 mm3) volumes, but not other brain regions. In this cohort and MR study of UK Biobank participants, cataracts were associated with increased risk of dementia, especially vascular dementia, and reduced total brain volumes. These findings lend further support to the hypothesis that cataract extraction may reduce the risk for dementia.

Effects of growth hormone and sex steroid therapy on brain structure and pituitary function in turner syndrome

Introduction: Turner syndrome (TS) is a chromosomal disorder affecting approximately 1 in 2,500 live female births, characterized by the partial or complete absence of one X chromosome. This genetic anomaly leads to physical, cognitive, and endocrine abnormalities, including short stature, gonadal dysgenesis, and structural brain anomalies. Cognitive deficits in TS involve visuospatial processing, memory, and executive function, often linked to structural brain changes. Magnetic resonance imaging (MRI) has revealed significant alterations in gray and white matter volumes in various brain regions. Growth hormone (GH) and sex steroid therapies, such as estrogen and progesterone, are used to address growth and developmental delays in TS. However, their impact on brain structure and pituitary function remains an area of active research. Aim of the Review: To systematically review and synthesize findings on the effects of GH and sex steroid therapy on brain structure and pituitary function in patients with Turner syndrome. Methods: A comprehensive literature review was conducted to identify studies examining the effects of GH and sex steroid therapy on brain structure and pituitary function in TS. Data from various sources were compiled, focusing on MRI-based structural brain changes. Key parameters analyzed included sample size, findings from MRI and fMRI studies, and clinical associations. Studies were summarized and presented in a structured table format. Results: Estrogen-progesterone treatment was found to suppress pituitary gonadotropin release more effectively than estrogen alone, indicating a feedback interaction between pituitary gonadotropin release and sex steroids. MRI studies showed that TS patients exhibit smaller volumes in the hippocampus, caudate, lenticular, thalamic nuclei, and parieto-occipital brain matter, correlating with cognitive deficits. GH-IGF axis abnormalities are modulated by body composition and physical fitness, with sex hormone replacement normalizing the GH-IGF axis and improving body composition. Although GH therapy alone did not significantly improve cognitive functions, the combination of GH with oxandrolone improved working memory. Estrogen deficiency and TS are associated with slower growth in parieto-occipital regions and enhanced volume growth in basal ganglia and cerebellar areas during adolescence, underscoring the importance of estrogen replacement in brain development. Discussion: GH and sex steroid therapies significantly impact brain structure, pituitary function, and clinical outcomes in TS. GH therapy, often combined with sex steroids, improves growth and cognitive functions, particularly working memory. However, GH alone does not significantly impact overall cognitive function. The timing and combination of these therapies are crucial for optimizing outcomes. Regular monitoring and individualized treatment plans are essential to address the complex needs of TS patients. Further research is needed to explore the long-term impacts of these therapies and develop optimal treatment regimens. Conclusion: GH and sex steroid therapies are vital in managing TS contributing to improved growth, body composition, and cognitive enhancements. A multifaceted therapeutic approach and regular monitoring are crucial for optimizing treatment outcomes and quality of life for TS patients.

Transferring Adult-like Phase Images for Robust Multi-view Isointense Infant Brain Segmentation.

Accurate tissue segmentation of infant brain in magnetic resonance (MR) images is crucial for charting early brain development and identifying biomarkers. Due to ongoing myelination and maturation, in the isointense phase (6-9 months of age), the gray and white matters of infant brain exhibit similar intensity levels in MR images, posing significant challenges for tissue segmentation. Meanwhile, in the adult-like phase around 12 months of age, the MR images show high tissue contrast and can be easily segmented. In this paper, we propose to effectively exploit adult-like phase images to achieve robustmulti-view isointense infant brain segmentation. Specifically, in one way, we transfer adult-like phase images to the isointense view, which have similar tissue contrast as the isointense phase images, and use the transferred images to train an isointense-view segmentation network. On the other way, we transfer isointense phase images to the adult-like view, which have enhanced tissue contrast, for training a segmentation network in the adult-like view. The segmentation networks of different views form a multi-path architecture that performs multi-view learning to further boost the segmentation performance. Since anatomy-preserving style transfer is key to the downstream segmentation task, we develop a Disentangled Cycle-consistent Adversarial Network (DCAN) with strong regularization terms to accurately transfer realistic tissue contrast between isointense and adult-like phase images while still maintaining their structural consistency. Experiments on both NDAR and iSeg-2019 datasets demonstrate a significant superior performance of our method over the state-of-the-art methods.

Techniques and Surgical Nuances of Management of Comminuted Fronto-Orbital Depressed Fractures: A Single-Surgeon Experience

AbstractCompound fronto-orbital depressed fractures (FODFs) are complex fractures involving the frontal and orbital bones, with associated lacerated wounds on the skin. Repairing such fractures is challenging and requires a multidisciplinary approach. Surgical indications include cerebrospinal fluid rhinorrhea, exposed brain matter, frontal sinus fractures, vision impairment, and cosmetic disfigurement. The repair is typically done using titanium implants (low-profile plates [LPPs] and screws) for a good functional outcome.In this case series of 10 patients operated by a single surgeon (RG), we present different techniques for repairing FODF. Early surgery (&lt; 48 hours) was performed to minimize infection risk.Surgical steps included elevation of depressed fragments, dural repair, and reconstruction of orbital walls using LPP. Some cases required inside-out fixation or suture fixation for better alignment of fragments. Autograft was used for severe bone loss.The results showed good functional outcomes with minimal infection rates. Primary single-stage repair using titanium implants provided satisfactory cosmesis. The use of inside-out repair and sutures was beneficial in specific cases.In conclusion, primary repair of FODF with titanium implants is safe and effective, reducing morbidity and cost. Early surgery and proper techniques are crucial for successful outcomes. Longer follow-up is needed to assess long-term viability and bone resorption.

Lung Function and Brain MRI Outcomes in the Atherosclerosis Risk in Communities Neurocognitive Study.

Brain imaging studies may provide etiologic insight into observed links between lung function and dementia and stroke. We evaluated associations of lung function measures with brain MRI markers of vascular and neurodegenerative disease in the ARIC Neurocognitive Study, as few studies have examined the associations. Lung function was measured at participants' midlife in 1990-1992 (mean age = 56±5 years) and later-life in 2011-2013 (mean age = 76±5 years), and brain MRI was performed in 2011-2013. Linear regression models were used to examine the associations of lung function with brain and white matter hyperintensity (WMH) volumes, and logistic regression models were used for cerebral infarcts and microbleeds, adjusting for potential confounders. In cross-sectional analysis (i.e., examining later-life lung function and MRI markers, n = 1,223), higher forced-expiratory volume in one second (FEV1) and forced vital capacity (FVC) were associated with larger brain and lower WMH volumes [e.g., 8.62 (95% CI:2.54-14.71) cm3 greater total brain volume per one-liter higher FEV1]. No association was seen with microbleeds in the overall sample, but higher FVC was associated with lower odds of microbleeds in never-smokers and higher odds in ever-smokers. In the cross-temporal analysis (i.e., associations with midlife lung function, n = 1,787), higher FVC levels were significantly associated with lower later-life brain volumes. Our results support modest associations of better lung function with less neurodegenerative and cerebrovascular pathology, although findings for microbleeds were unexpected in ever-smokers.

Sport, neurodegenerative illness and the social determinants of health

ABSTRACT This article proposes a Social Determinants of Health framework as a counter to the prominence of bio-determinist tropes in understandings of the relationship between concussion and later life neurodegenerative conditions in athletic populations. It is argued that debates about concussion (or repetitive head impacts) causing CTE have been particularly influenced by broader social trends towards neuro-essentialism. This paradigm reduces complex social behaviour to brain matter and continues to dominate the field despite the recent diversification of evidence from autopsy-based studies of neuropathology to epidemiological studies comparing recorded causes of death among former elite athletes. In contrast, this article explores the ‘causes of causes’ of neurodegenerative conditions. It outlines the ways in which the distinct dynamics of: a) employment, b) education, income and wealth, c) health systems and services, and d) social environment and public safety relate to the specific occupational conditions of elite sport and likely negatively shape health outcomes of athletic populations. The article concludes by arguing that to more effectively address these particular health harms we must move beyond narrow, mono-causal models and evoke a cultural change that extends beyond making rule changes and adjusting psychological attitudes and behavioural norms, to redress the social structural parameters of elite sports participation. The continuation of narrower, neuro-centric and reductionist paradigms obscures the causes of the causes of neurodegenerative decline and limits the scope for change.

Modeling of periodical shearing flow in a fibrous space with applications in shear-induced brain injury

This paper presents a theoretical model examining the interaction between a fibrous network and viscous fluid flow driven by an oscillating boundary. The aim is to understand how oscillating impacts are transmitted from the skull, through the arachnoid trabeculae network filled with cerebrospinal fluid, as observed in shaken baby syndrome. The model uses an effective medium approach to determine the fluid velocity field while each fiber is treated as a soft string undergoing deformation. Results indicate that the frequency of oscillation, fiber stiffness, and porous structure resistance significantly influence the oscillating shearing flow, as indicated by the Womersley (Wo), Brinkman (α), and Bingham (Bm) numbers. Application of the model to shaken baby syndrome suggests that oscillations in the cerebrospinal fluid and arachnoid trabeculae can significantly surpass those on the skull, leading to intense shear stress penetration to the brain. This model is the first study to integrate the dynamic response of string-like fibrous networks in fluid flows with oscillating boundaries and offers a quantitative framework for predicting the transmission of shearing forces from the skull to the brain matter.

Life-course neighbourhood deprivation and brain structure in older adults: the Lothian Birth Cohort 1936.

Neighbourhood disadvantage may be associated with brain health but the importance of exposure at different stages of the life course is poorly understood. Utilising the Lothian Birth Cohort 1936, we explored the relationship between residential neighbourhood deprivation from birth to late adulthood, and global and local neuroimaging measures at age 73. A total of 689 participants had at least one valid brain measures (53% male); to maximise the sample size structural equation models with fullinformation maximum likelihood were conducted. Residing in disadvantaged neighbourhoods in mid- to late adulthood was associated with smaller total brain (β = -0.06; SE = 0.02; sample size[N] = 658; number of pairwise complete observations[n]=390), grey matter (β = -0.11; SE = 0.03; N = 658; n = 390), and normal-appearing white matter volumes (β = -0.07; SE = 0.03; N = 658; n = 390), thinner cortex (β = -0.14; SE = 0.06; N = 636; n = 379), and lower general white matter fractional anisotropy (β = -0.19; SE = 0.06; N = 665; n = 388). We also found some evidence on the accumulating impact of neighbourhood deprivation from birth to late adulthood on age 73 total brain (β = -0.06; SE = 0.02; N = 658; n = 276) and grey matter volumes (β = -0.10; SE = 0.04; N = 658; n = 276). Local analysis identified affected focal cortical areas and specific white matter tracts. Among individuals belonging to lower social classes, the brain-neighbourhood associations were particularly strong, with the impact of neighbourhood deprivation on total brain and grey matter volumes, and general white matter fractional anisotropy accumulating across the life course. Our findings suggest that living in deprived neighbourhoods across the life course, but especially in mid- to late adulthood, is associated with adverse brain morphologies, with lower social class amplifying the vulnerability.

Physiological aging and inflammation-induced cellular senescence may contribute to oligodendroglial dysfunction in MS

Aging affects all cell types in the CNS and plays an important role in CNS diseases. However, the underlying molecular mechanisms driving these age-associated changes and their contribution to diseases are only poorly understood. The white matter in the aging brain as well as in diseases, such as Multiple sclerosis is characterized by subtle abnormalities in myelin sheaths and paranodes, suggesting that oligodendrocytes, the myelin-maintaining cells of the CNS, lose the capacity to preserve a proper myelin structure and potentially function in age and certain diseases. Here, we made use of directly converted oligodendrocytes (dchiOL) from young, adult and old human donors to study age-associated changes. dchiOL from all three age groups differentiated in an comparable manner into O4 + immature oligodendrocytes, but the proportion of MBP + mature dchiOL decreased with increasing donor age. This was associated with an increased ROS production and upregulation of cellular senescence markers such as CDKN1A, CDKN2A in old dchiOL. Comparison of the transcriptomic profiles of dchiOL from adult and old donors revealed 1324 differentially regulated genes with limited overlap with transcriptomic profiles of the donors’ fibroblasts or published data sets from directly converted human neurons or primary rodent oligodendroglial lineage cells. Methylome analyses of dchiOL and human white matter tissue samples demonstrate that chronological and epigenetic age correlate in CNS white matter as well as in dchiOL and resulted in the identification of an age-specific epigenetic signature. Furthermore, we observed an accelerated epigenetic aging of the myelinated, normal appearing white matter of multiple sclerosis (MS) patients compared to healthy individuals. Impaired differentiation and upregulation of cellular senescence markers could be induced in young dchiOL in vitro using supernatants from pro-inflammatory microglia. In summary, our data suggest that physiological aging as well as inflammation-induced cellular senescence contribute to oligodendroglial pathology in inflammatory demyelinating diseases such as MS.

In vivo 3-photon fluorescence microscopy of white matter in mouse brain excited at the 1700 nm window

White matter, a densely packed collection of myelinated axons, plays an essential part in neural networks. With high spatial resolution and deep penetration, multi-photon microscopy (MPM) is promising for white matter imaging in animal models in vivo. The third harmonic generation (THG) signal can be generated from white matter, but the bottom part of the white matter layer generates weak THG due to its high scattering. Here, we demonstrate an in vivo labeling and imaging technology, capable of visualizing the white matter layer in the mouse brain, combining fluorescence labeling with MitoTracker Red and three-photon fluorescence (3PF) microscopy excited at the 1700 nm window. 3PF signals are several times higher than THG signals, resulting in deeper imaging of the white matter layer with the former. Our results indicate that 3PF microscopy is a promising technology for white matter imaging in the deep brain in vivo.

Depth-Specific Hypoxic Responses to Spreading Depolarizations in Gyrencephalic Swine Cortex Unveiled by Photoacoustic Imaging.

Spreading depolarizations (SDs) are a marker of brain injury and have a causative effect on ischemic lesion progression. The hemodynamic responses elicited by SDs are contingent upon the metabolic integrity of the affected tissue, with vasoconstrictive reactions leading to pronounced hypoxia often indicating poor outcomes. The stratification of hemodynamic responses within different cortical layers remains poorly characterized. This pilot study sought to elucidate the depth-specific hemodynamic changes in response to SDs within the gray matter of the gyrencephalic swine brain. Employing a potassium chloride-induced SD model, we utilized multispectral photoacoustic imaging (PAI) to estimate regional cerebral oxygen saturation (rcSO2%) changes consequent to potassium chloride-induced SDs. Regions of interest were demarcated at three cortical depths covering up to 4mm. Electrocorticography (ECoG) strips were placed to validate the presence of SDs. Through PAI, we detected 12 distinct rcSO2% responses, which corresponded with SDs detected in ECoG. Notably, a higher frequency of hypoxic responses was observed in the deeper cortical layers compared to superficial layers, where hyperoxic and mixed responses predominated (p < 0.001). This data provides novel insights into the differential oxygenation patterns across cortical layers in response to SDs, underlining the complexity of cerebral hemodynamics post-injury.

Association between dietary magnesium intake, inflammation, and neurodegeneration

BackgroundConsistent evidence shows that magnesium (Mg) intake is associated with lower blood pressure (BP), and that lower BP is associated with improved cerebral health. However, recent findings indicate that the positive effect of dietary Mg intake on cerebral health is not mediated by a decrease in BP. As Mg’s anti-inflammatory action is a plausible alternative mechanism, the objective of this study was to investigate the associations between Mg intake and inflammation to determine whether it mediates any neuroprotective effect.MethodsParticipants from the UK Biobank (n = 5775, aged 40–73 years, 54.7% female) were assessed for dietary magnesium using an online food questionnaire, brain and white matter lesion (WML) volumes were segmented with FreeSurfer software, and inflammation markers including high-sensitivity C-reactive protein (hs-CRP), leukocyte, erythrocyte count, and Glycoprotein acetylation (GlycA) were measured using specific laboratory techniques such as immunoturbidimetry, automated cell counting, and nuclear magnetic resonance. Hierarchical linear regression models were performed to investigate the association between dietary Mg, and inflammatory markers and between dietary Mg, brain and WMLs volumes. Mediation analysis was performed to test a possible mediation role of inflammation on the association between dietary Mg and brain and WMLs volumes.ResultsHigher dietary Mg intake was associated with lower inflammation: hs-CRP level (− 0.0497%; 95% confidence interval [CI] − 0.0497%, − 0.0199%) leukocytes count (− 0.0015%; 95%CI − 0.00151%, − 0.0011%), and GlycA (− 0.0519%; 95%CI − 0.1298%, − 0.0129%). Moreover, higher dietary Mg intake was associated with larger grey matter volume (0.010%; 95%CI 0.004%, 0.017%), white matter volume (0.012%; 95%CI 0.003, 0.022) and right hippocampal volume (0.002%; 95%CI 0.0007, –0.0025%). Lower hs-CRP levels mediated the positive association between higher dietary Mg intake and larger grey matter volume.ConclusionsThe anti-inflammatory effects of dietary Mg intake in the general population, appears to mediate its neuroprotective effect.

Mathematical model of the dependence between cerebral ventricular size and capillary pressure in laboratory animals

Aim: To adapt a mathematical model describing the interaction between fluid media and brain matter for the purpose of definition of the dependence between brain ventricle size and capillary pressure in laboratory animals of two genotypes, BALB/c and C57BL/6. Material and methods. The study included 4 male mice of each inbred strain C57BL/6 and BALB/c at the age of 12 weeks. The brain and cerebrospinal fluid system images were obtained using an 11.7 T horizontal MR scanner (Bruker, BioSpec 117/16 USR, Germany). An axial section at the level of -0.5 mm from bregma was chosen as the geometry for mathematical modelling. To describe the data obtained, the mathematical model was adapted by selecting a scale factor based on the known values of the cerebrospinal fluid formation rate for humans and mice. Results and discussion. The same qualitative pattern of relationship between capillary pressure and mean ventricular wall displacement was observed for all animals considered. Although the selected genetic strains of BALB/c and C57Bl mice differ significantly in terms of cerebral ventricle size, these differences in animal genotype did not affect the nature of this relationship. Changing the parameters of the fluid media interaction in the area of compression or moderate ventricular dilation almost does not lead to an exit from the physiologically acceptable capillary pressure value. In this case, the size of the ventricles changes significantly. In the area of large ventricular dilation, in contrast, there is little change in ventricular size, and this is accompanied by a dramatic increase in capillary pressure far beyond physiologic limits. Thus, the change in ventricular size is an adaptive process associated with pressure fluctuations caused by changes in intracranial fluid flow. The mere fact that some of the values reach the zone of physiologically unacceptable pressures associated, in fact, with death, provided that there is practically no change in ventricular size indicates that such a situation is rarely realized and is possible in case of violation of intracranial fluid media flows associated with the fact that the increase in ventricular size limits adaptive capabilities. Conclusions. The presented animal model will further increase the understanding of the pattern we have established and allow us to move on to attempts at prediction.

Two Uncommon Cases of Pediatric Transethmoidal–Transnasal Encephaloceles with a Review of Literature

AbstractEncephaloceles are defined as the herniation of brain matter beyond the confines of the skull bone through a defect on the cranium or face. The encephaloceles are classified into different categories as per onset as congenital or traumatic, as per contents as meningocele, meningoencephalocele, and hydromeningoencephalocele, and as per anatomical location into frontoethmoid, basal, occipital, and cranial vault. Transethmoidal encephalocele is a rare type of encephalocele with a very few patients reported in the literature to date. We are presenting two cases of transethmoidal–transnasal encephalocele in the pediatric age group with one being congenital and other traumatic in onset. The first child presented with a mass visible inside the nasal cavity since birth with nasal obstruction. The second child presented with a history of trauma 5 years back followed by occasional cerebrospinal fluid leak, fever, and nasal stuffiness. Both patients underwent craniotomy and excision of the encephalocele with repair of the defect in the cribriform plate. These two uncommon cases highlight the different onsets of the disease successfully managed surgically.