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Periventricular injury is frequently noted as one aspect of severe traumatic brain injury (TBI) and the presence of the ventricles has been hypothesized to be a primary pathogenesis associated with the prevalence of periventricular injury in patients with TBI. Although substantial endeavors have been made to elucidate the potential mechanism, a thorough explanation for this hypothesis appears lacking. In this study, a three-dimensional (3D) finite element (FE) model of the human head with an accurate representation of the cerebral ventricles is developed accounting for the fluid properties of the intraventricular cerebrospinal fluid (CSF) as well as its interaction with the brain. An additional model is developed by replacing the intraventricular CSF with a substitute with brain material. Both models are subjected to rotational accelerations with magnitudes suspected to induce severe diffuse axonal injury. The results reveal that the presence of the ventricles leads to increased strain in the periventricular region, providing a plausible explanation for the vulnerability of the periventricular region. In addition, the strain-exacerbation effect associated with the presence of the ventricles is also noted in the paraventricular region, although less pronounced than that in the periventricular region. The current study advances the understanding of the periventricular injury mechanism as well as the detrimental effects that the ventricles exert on the periventricular and paraventricular brain tissue.

The brain ventricular system (BVS) consists of brain ventricles and channels connecting ventricles filled with cerebrospinal fluid (CSF). The disturbance of CSF flow has been linked to neurodegenerative disease including hydrocephalus, which manifests itself as an abnormal expansion of BVS. This relatively common developmental disorder has been observed in human and domesticated animals and linked to functional deficiency of various cells lineages facing BVS, including the choroid plexus or ependymal cells that generate CSF or the ciliated cells that cilia beating generates CSF flow. To understand the underlying causes of hydrocephalus, several animal models were developed, including rodents (mice, rat, and hamster) and zebrafish. At another side of a spectrum of BVS anomalies there is the “slit-ventricle” syndrome, which develops due to insufficient inflation of BVS. Recent advances in functional genetics of zebrafish brought to light novel genetic elements involved in development of BVS and circulation of CSF. This review aims to reveal common elements of morphologically different BVS of zebrafish as a typical representative of teleosts and other vertebrates and illustrate useful features of the zebrafish model for studies of BVS. Along this line, recent analyses of the two novel zebrafish mutants affecting different subunits of the potassium voltage-gated channels allowed to emphasize an important functional convergence of the evolutionarily conserved elements of protein transport essential for BVS development, which were revealed by the zebrafish and mouse studies.

Normal pressure hydrocephalus (NPH) is an intracranial disease characterized by an abnormal accumulation of cerebrospinal fluid (CSF) in brain ventricles within the normal range of intracranial pressure. Most NPH in aged patients is idiopathic (iNPH) and without any prior history of intracranial diseases. Although an abnormal increase of CSF stroke volume (hyper-dynamic CSF flow) in the aqueduct between the third and fourth ventricles has received much attention as a clinical evaluation index in iNPH patients, the biomechanical effects of this flow on iNPH pathophysiology are poorly understood. This study aimed to clarify the potential biomechanical effects of hyper-dynamic CSF flow through the aqueduct of iNPH patients using magnetic resonance imaging-based computational simulations. Ventricular geometries and CSF flow rates through aqueducts of 10 iNPH patients and 10 healthy control subjects were obtained from multimodal magnetic resonance images, and these CSF flow fields were simulated using computational fluid dynamics. As biomechanical factors, we evaluated wall shear stress on the ventricular wall and the extent of flow mixing, which potentially disturbs the CSF composition in each ventricle. The results showed that the relatively high CSF flow rate and large and irregular shapes of the aqueduct in iNPH resulted in large wall shear stresses localized in relatively narrow regions. Furthermore, the resulting CSF flow showed a stable cyclic motion in control subjects, whereas strong mixing during transport through the aqueduct was found in patients with iNPH. These findings provide further insights into the clinical and biomechanical correlates of NPH pathophysiology.

The brain lacks a classic lymphatic drainage system. How it is cleansed of damaged proteins, cellular debris, and molecular by-products has remained a mystery for decades. Recent discoveries have identified a hybrid system that includes cerebrospinal fluid (CSF)-filled perivascular spaces and classic lymph vessels in the dural covering of the brain and spinal cord that functionally cooperate to remove toxic and non-functional trash from the brain. These two components functioning together are referred to as the glymphatic system. We propose that the high levels of melatonin secreted by the pineal gland directly into the CSF play a role in flushing pathological molecules such as amyloid-β peptide (Aβ) from the brain via this network. Melatonin is a sleep-promoting agent, with waste clearance from the CNS being highest especially during slow wave sleep. Melatonin is also a potent and versatile antioxidant that prevents neural accumulation of oxidatively-damaged molecules which contribute to neurological decline. Due to its feedback actions on the suprachiasmatic nucleus, CSF melatonin rhythm functions to maintain optimal circadian rhythmicity, which is also critical for preserving neurocognitive health. Melatonin levels drop dramatically in the frail aged, potentially contributing to neurological failure and dementia. Melatonin supplementation in animal models of Alzheimer’s disease (AD) defers Aβ accumulation, enhances its clearance from the CNS, and prolongs animal survival. In AD patients, preliminary data show that melatonin use reduces neurobehavioral signs such as sundowning. Finally, melatonin controls the mitotic activity of neural stem cells in the subventricular zone, suggesting its involvement in neuronal renewal.

Cerebrospinal fluid (CSF) is integral to brain function. CSF provides mechanical support for the brain and helps distribute nutrients, neurotransmitters and metabolites throughout the central nervous system. CSF flow is driven by several processes, including the beating of motile cilia located on the walls of the brain ventricles. Despite the physiological importance of CSF, the underlying mechanisms of CSF flow and solute transport in the brain ventricles remain to be comprehensively resolved. This study analyzes and evaluates specifically the role of motile cilia in CSF flow and transport. We developed finite element methods for modeling flow and transport using the geometry of embryonic zebrafish brain ventricles, for which we have detailed knowledge of cilia properties and CSF motion. The computational model is validated by in vivo experiments that monitor transport of a photoconvertible protein secreted in the brain ventricles. Our results show that while cilia contribute to advection of large particles, diffusion plays a significant role in the transport of small solutes. We also demonstrate how cilia location and the geometry of the ventricular system impact solute distribution. Altogether, this work presents a computational framework that can be applied to other ventricular systems, together with new concepts of how molecules are transported within the brain and its ventricles.

Enlargement of the choroidal-ventricular system occurs in aging and Alzheimer's disease (AD), but emerging evidence links these abnormalities to amyloid beta (Aβ) aggregation. We tested this hypothesis by assessing associations between AD pathophysiology and choroidal-ventricular system measures across the AD continuum. Ventricular volume, choroid-plexus volume, and ventricular radioactivity after positron emission tomography (PET) tracer injections were analyzed in 385 Translational Biomarkers in Aging and Dementia (TRIAD) and 282 Alzheimer's Disease Neuroimaging Initiative (ADNI) participants using linear models and partial correlations. A composite score combining these measures was also tested against established AD biomarkers. With advancing AD stages, ventricular and choroid-plexus volumes increased while ventricular radioactivity declined. These measures were interrelated, and abnormalities appeared even in amyloid-negative elderly. Across cohorts, they correlated with amyloid- and tau-PET, cerebrospinal fluid (CSF) and plasma p-tau isoforms, glial fibrillary acidic protein (GFAP), and cognition. Voxel-wise analyses showed strong associations with cortical Aβ, mediating downstream tau effects. Changes in the choroidal-ventricular system are mutually correlated and carry an additive-effect on cortical Aβ load.

BACKGROUND: The Evans index (EI) is a practical radiological tool used to assess ventricular size; however, normative reference values remain insufficiently defined across diverse populations. This study aimed to establish normative EI values in a healthy North Indian adult population and to investigate age- and sex-related variations in ventricular morphometry. MATERIALS AND METHODS: A cross-sectional magnetic resonance imaging (MRI)-based study was conducted on 142 neurologically healthy North Indian adults (79 females and 63 males; age range: 18–72 years). Axial T2-weighted images acquired on a 1.5 Tesla MRI system were analysed to measure the frontal horn width (FHW) and the transverse inner diameter of the skull (TIDS). The EI was calculated as the ratio of FHW to TIDS. Statistical analyses were performed using SPSS version 29.0. Welch’s t-tests were applied to assess sex differences, Spearman’s correlation was used to examine associations between cranial measurements and age, and binary logistic regression was employed to identify predictors of biological sex. RESULTS: The mean age of the participants was 37.4 years. The overall average measurements were FHW = 31.5 mm, TIDS = 122.4 mm, and EI = 0.257. Males exhibited significantly higher mean EI values than females (0.265 vs 0.251; p < 0.001). Correlation analysis revealed a strong positive association between FHW and EI (rho = 0.866; p < 0.001). Logistic regression analysis identified FHW as the strongest predictor of sex (OR: 1.82, p < 0.001). The model demonstrated a sensitivity of 0.746, a specificity of 0.861, and an AUC of 0.81. CONCLUSIONS: This study establishes normative EI values for healthy North Indian adults and demonstrates significant sex differences in cranial morphometric parameters. FHW and EI are useful predictors of biological sex, with potential implications for clinical neuroimaging and anthropometric assessments.

Long-duration spaceflight induces changes to the brain and cerebrospinal fluid compartments and visual acuity problems known as spaceflight-associated neuro-ocular syndrome (SANS). The clinical relevance of these changes and whether they equally affect crews of different space agencies remain unknown. We used MRI to analyze the alterations occurring in the perivascular spaces (PVS) in NASA and European Space Agency astronauts and Roscosmos cosmonauts after a 6-mo spaceflight on the International Space Station (ISS). We found increased volume of basal ganglia PVS and white matter PVS (WM-PVS) after spaceflight, which was more prominent in the NASA crew than the Roscosmos crew. Moreover, both crews demonstrated a similar degree of lateral ventricle enlargement and decreased subarachnoid space at the vertex, which was correlated with WM-PVS enlargement. As all crews experienced the same environment aboard the ISS, the differences in WM-PVS enlargement may have been due to, among other factors, differences in the use of countermeasures and high-resistive exercise regimes, which can influence brain fluid redistribution. Moreover, NASA astronauts who developed SANS had greater pre- and postflight WM-PVS volumes than those unaffected. These results provide evidence for a potential link between WM-PVS fluid and SANS.

The cerebrospinal fluid (CSF) fills the brain ventricles and the subarachnoid space surrounding the brain and spinal cord. The fluid compartment of the brain ventricles communicates with the interstitial fluid of the brain across the ependyma. In comparison to blood, the CSF contains very little protein to buffer acid–base challenges. Nevertheless, the CSF responds efficiently to changes in systemic pH by mechanisms that are dependent on the CO2/HCO3− buffer system. This is evident from early studies showing that the CSF secretion is sensitive to inhibitors of acid/base transporters and carbonic anhydrase. The CSF is primarily generated by the choroid plexus, which is a well-vascularized structure arising from the pial lining of the brain ventricles. The epithelial cells of the choroid plexus host a range of acid/base transporters, many of which participate in CSF secretion and most likely contribute to the transport of acid/base equivalents into the ventricles. This review describes the current understanding of the molecular mechanisms in choroid plexus acid/base regulation and the possible role in CSF pH regulation.

Hippocampal injury is common in traumatic brain injury (TBI) patients, but the underlying pathogenesis remains elusive. In this study, we hypothesize that the presence of the adjacent fluid-containing temporal horn exacerbates the biomechanical vulnerability of the hippocampus. Two finite element models of the human head were used to investigate this hypothesis, one with and one without the temporal horn, and both including a detailed hippocampal subfield delineation. A fluid-structure interaction coupling approach was used to simulate the brain-ventricle interface, in which the intraventricular cerebrospinal fluid was represented by an arbitrary Lagrangian-Eulerian multi-material formation to account for its fluid behavior. By comparing the response of these two models under identical loadings, the model that included the temporal horn predicted increased magnitudes of strain and strain rate in the hippocampus with respect to its counterpart without the temporal horn. This specifically affected cornu ammonis (CA) 1 (CA1), CA2/3, hippocampal tail, subiculum, and the adjacent amygdala and ventral diencephalon. These computational results suggest that the presence of the temporal horn exacerbate the vulnerability of the hippocampus, highlighting the mechanobiological dependency of the hippocampus on the temporal horn.