Whole brain fluorescence imaging in Drosophila reveals spreading depolarization and its initiation, propagation, and resilience dynamics.

Frontal brain injury alters human risky choices in self and other contexts.

Ceftriaxone has a similar effect on astrocytic and neuronal GLT-1 distribution after mild traumatic brain injury.

The complement cascade contributes to secondary brain injury after intracerebral hemorrhage (ICH). However, research remains scarce on the initiation characteristics of proximal complement pathways and the expression of complement inhibitors in the hemorrhagic brain. In this study, we used collagenase VII-S, thrombin, and hemoglobin injections into mouse brains to establish an ICH model and stimulate the coagulation cascade and hemolysis. Our findings highlighted notable discrepancies in the gene and protein expression profiles of proximal complement components and complement inhibitors within the hemorrhagic brain post ICH. At the mRNA level, the coagulation cascade and hemolysis were linked to potential complement initiation and neuroinflammation via the alternative pathway. In contrast, the hemorrhagic brain showed pronounced upregulation of proteins across all three proximal complement pathways, along with concurrent increases in certain complement inhibitors. If these proximal complement pathways are activated, targeting a single pathway may not be sufficient to inhibit the complement cascade in ICH. To further assess the potential for comprehensive inhibition of the complement cascade, we closely examined the expression of previously identified complement-inhibitory proteins. Our exploration of the distribution and functional roles of CD55, a prominent complement inhibitor, revealed its localization in microglia/macrophages, neurons, and endothelial cells, but not in astrocytes. Notably, we demonstrated that adeno-associated virus vector-mediated overexpression of CD55 significantly suppressed the complement cascade, mitigated neuroinflammation, and enhanced outcomes following ICH. This study provides previously unrecognized preclinical evidence that warrants further investigation into strategies to inhibit the complement cascade in the hemorrhagic brain.

Electroacupuncture modulates P300-mediated STAT6/PPARγ binding to promote M2 polarization of microglia following cerebral ischemic injury.

Lipidized deferoxamine nanomedicines (DFOsomes) against iron overload.

Patients with severe traumatic brain injury (TBI) are at risk of developing nonneurologic organ dysfunction. Acute kidney injury (AKI) has been associated with morbidity and mortality in adults with TBI, but the prevalence in children is poorly described. The objective of this study was to determine the prevalence of AKI among a multiinstitutional, international cohort of children with severe TBI and to explore the association of AKI with outcomes. An unplanned, secondary exploratory analysis of the Approaches and Decisions for Acute Pediatric TBI (ADAPT) study. Fifty-one institutions participating in ADAPT. Children with severe TBI who underwent intracranial pressure monitoring and were admitted to a participating institution from 2014 to 2017. None. AKI was considered to have occurred when a patient met either the ADAPT definition of AKI or the Kidney Disease: Improving Global Outcomes (KDIGO) AKI criteria. The daily urine output and worst creatinine within the first 12 hours of admission were reviewed to determine who met KDIGO criteria. One thousand children were included and 160 children (16%) had AKI. Of these, stage 1 AKI occurred in 78 of 160 patients (48%), stage 2 in 65 of 160 patients (41%), and stage 3 AKI in 17 of 160 patients (11%). After adjusting for covariates in regression analyses, AKI was associated with an increase in hospital length of stay (LOS) and a worse Glasgow Outcome Scale Extended-Pediatrics score, but we failed to identify an association with longer PICU LOS or prevalence of mortality. In the ADAPT cohort, AKI was present in 16% of cases. Although we found an association between AKI and two clinically important secondary outcomes, more contemporary studies are needed to better characterize AKI in children with severe TBI and to determine whether strategies aimed at preventing AKI can improve patient-centered outcomes.

Clinical applications of EEG connectivity in acute brain injuries: A systematic review.

Association of blood pressure variability with clinical and biomarker outcomes in moderate to severe TBI: A TRACK-TBI study.

Aneurysmal subarachnoid hemorrhage (aSAH) triggers a robust inflammatory response, which has been associated with brain injury and poor outcome. The complement system is an integral part of the innate immune system activated after acute brain injury. The early complement proteins C1q and C3 have roles in glial-neuronal interactions and synaptic pruning. The objective of this study was to determine whether changes in CSF complement proteins over time after aSAH are associated with neurologic outcome. We performed an exploratory retrospective case-control study investigating the association of CSF levels and clearance of C1q and C3 with outcome in patients with aSAH and compared with controls with normal CSF. Clearance was defined as the percent change of complement protein levels between 2 time points corresponding to peaks of early (<72 hours) and delayed (5-7 days) brain injury after aSAH. The primary endpoint was functional outcome, assessed by Glasgow Outcome Scale (GOS; range 1-5 with higher scores denoting better outcome), at the time of discharge. Good functional outcome was defined as GOS 4-5. Complement protein clearance was adjusted by baseline differences, and receiver operating characteristic analysis was performed. Early after aSAH, there was a robust increase in C1q (median 89.10 vs 6.42 ng/mL, p < 0.0001) and C3 (78.00 vs 8.72 µg/mL, p = 0.0001) in CSF of 20 patients with aSAH compared with 11 controls. Between early and late time points, both C1q (97.38 vs 47.85 ng/mL, p = 0.0326) and C3 (85.23 vs 23.10 µg/mL, p = 0.0004) decreased in those with good outcome. Percent clearance of C3 from CSF was larger in those with good vs poor neurologic outcome (median 74.85% vs 11.43% reduction over time, p = 0.0159). C3 clearance, particularly when adjusted by baseline Glasgow coma scale on admission, was a highly sensitive and specific marker of neurologic outcome after aSAH (area under curve = 0.990, 95% confidence interval 0.958-1.000, sensitivity 90.9%, specificity 100.0%). Increased CSF clearance of C3 within the first week after aSAH appears to be associated with improved neurologic outcome. Future strategies to promote clearance of inflammatory mediators such as early complement proteins from CSF may, therefore, improve outcomes after aSAH.

Unraveling the link between brain injury and enhanced artistic skills.

The first week of postnatal life is a period of transition for both pulmonary and systemic vascular flow patterns. Owing to associated shunts and altered systemic/pulmonary blood flow, neonates with congenital heart defect (CHD) are at particular risk for disrupted end-organ perfusion and oxygen delivery, including that of the brain. Near-infrared spectroscopy (NIRS) measures venous-weighted cerebral oxygen saturation (CSat) at the frontal cortex, serving as an indirect reflection of cerebral blood flow. CSat is impacted by factors such as tissue perfusion, systemic oxygenation, regional oxygen extraction and haemoglobin levels, all of which are affected by cardiac function and vascular supply [1, 2]. Cerebral fractional tissue oxygen extraction (cFTOE) reflects the balance between cerebral oxygen utilisation and oxygen delivery, and it is operationally defined as (preductal SpO2—CSat)/preductal SpO2. As such, cFTOE can provide insight into cerebral oxygen utilisation. Increased cFTOE can be due to decreased oxygen delivery or increased oxygen consumption not met by associated increase in delivery. Likewise, decreased cFTOE can indicate that the brain is using less oxygen or that oxygen delivery has increased relative to utilisation [3]. Data on CSat and cFTOE as cerebrovascular metrics in neonates with CHD during the period of postnatal adaptation are limited. Elements of anterior cerebral artery (ACA) Doppler such as resistive index (RI) and pulsatility index (PI) assess vascular resistance and flow characteristics in the frontal cortex and have been shown to correspond to cerebral perfusion pressure [4]. Abnormal RI is a recognised indicator of such newborn pathologies as increased intracranial pressure, brain injury and diastolic steal [5-7]. This study has made a notable contribution to the literature by applying these established bedside tools to a vulnerable and complex group of patients (neonates with CHD) during a time of critical transitional physiology (postnatal adaptation). The authors recruited 34 neonates with various types of CHD and analysed 142 concomitant data measurements of NIRS and daily ultrasound Doppler over the first 7 days of life. They used mixed-effects models to evaluate the relationship between CSat/cFTOE and RI/PI-ACA, adjusting for time since birth, pCO2 and haemoglobin levels. The authors found a decline in CSat and rise in cFTOE throughout the first week of life in neonates with CHD, which aligns with findings from prior research [8]. RI and PI both increased over the time period, indicating increased resistance to flow velocities. The authors also reported statistically significant associations between CSat/cFTOE and simultaneous RI/PI values. The findings suggest a progressive increase in oxygen extraction, possibly related to diminished blood flow, impaired oxygen delivery or increased metabolic demand during postnatal transition. The authors theorise that this may be partly owing to altered adaptation due to shunts and abnormal anatomy. Despite the variability of the study population, the findings supported consistent directional trends in NIRS and ultrasound. While these results are meaningful, an even greater impact will be gained in translating the findings to earlier detection/management of cerebral hypoperfusion in order to improve neurodevelopmental outcomes. URL LINK: https://ebneo.org/ebneo-commentary-cerebral-saturation-and-fractional-tissue-oxygen-extraction-and-anterior-cerebral-artery-doppler. Ashley L. Lynch: conceptualization, writing – original draft. Ethan L. Gillett: writing – review and editing. The authors have nothing to report. The authors declare no conflicts of interest. Data sharing not applicable to this article as no datasets were generated or analysed during the current study.

A multidisciplinary, symptom-targeted approach to rehabilitation in pediatric concussion.

Dexterous hand motor functions are highly flexible and finely controlled by complex neural commands from the motor cortex. However, in patients with brain injuries such as stroke, restoring fine motor control from the perilesional cortex remains extremely challenging. A major obstacle is the absence of appropriate non-human primate models to elucidate the behavioral and neural signatures of hand motor function during recovery following treatments. Here, we present a new non-human primate model that reflects the motor function recovery processes following lesion-induced hand paralysis after contralateral C7 nerve transfer (CC7) surgery, which establishes a new neural pathway from the ipsilateral cortex to control the paralyzed hand. By developing a hand reach-to-pinch task and quantifying finger kinematics, we established systematic, objective profiles of fine motor recovery in human patients and monkey models following CC7 treatment. Furthermore, when considering behavioral aspects, spontaneous recovery of hand motor skills was notably limited in human patients and monkey models, as indicated by the consistently abnormal "thumb-in-palm" patterns observed in finger kinematic analysis. However, the CC7 surgery gradually restored the finger kinematic patterns during hand-pinch actions to nearly identical patterns to those of the healthy hand. In addition, the human functional MRI and macaque electrophysiology results revealed, on a neural level, the emergence of a new command area and its spiking-based motor-command refinements specifically for the paralyzed hand in the contralesional M1 and premotor cortex (PMC) after CC7 treatment. Thus, our findings strongly support the notion that modifying peripheral nerve pathways greatly promotes the recovery of dexterous motor function in a paralyzed hand by reconstructing new motor-control neural mechanisms within the ipsilateral healthy motor cortex.

Mechanistic insights into glufosinate-ammonium (GLA)-Induced brain injury revealed by LC-MS/MS-based metabolomics.

A review on cellular ferroptosis in traumatic brain injury: Mechanisms and therapeutic implications.

BackgroundTraumatic brain injury (TBI) and post-traumatic stress disorder (PTSD) are emerging contributors to the development and progression of dementia.ObjectiveThis study examined how traumatic brain injury and post-traumatic stress disorder relate to cognitive function and neuroimaging markers in U.S. veterans from the Department of Defense Alzheimer's Disease Neuroimaging Initiative (ADNI-DOD).MethodsTBI severity was quantified with a new scoring system, and PTSD symptoms and combat exposure were assessed using the Clinician-Administered PTSD Scale (CAPS) and Combat Exposure Scale (CES). Cognitive performance was evaluated with the Mini-Mental State Examination (MMSE), Alzheimer's Disease Assessment Scale-Cognitive Subscale (ADAS-Cog), and Clinical Dementia Rating Sum of Boxes (CDR-SOB). Neuroimaging included amyloid-β (Aβ) and tau positron emission tomography (PET), diffusion tensor imaging (DTI), vascular imaging, and resting-state functional MRI (rs-fMRI).ResultsAs expected, higher Aβ and tau burden were significantly associated with worse cognitive performance on the MMSE, ADAS-Cog, and CDR-SOB. Greater PTSD symptom severity was also linked to poorer cognition measured by all three tests, and higher TBI severity correlated with lower MMSE scores. However, neither TBI severity nor PTSD symptoms were associated with neuroimaging biomarkers of neurodegeneration or vascular damage.ConclusionsThese findings suggest that cognitive impairment in veterans is related to the prior history of TBI and PTSD, but these risk factors may not affect the cognition directly through the accumulation of AD pathologies or vascular injuries. Although these results need further validation by other cohorts who have more recent trauma and wider range of cognitive impairment.

Excessive alcohol consumption contributes substantially to the global burden of disease, yet population-level evidence on disparities in high-risk drinking among people with disabilities remains limited. We aimed to estimate and compare trends in the prevalence of high-risk drinking and all-cause mortality associated with drinking behavior among men with disabilities and those without disabilities. Nation-wide serial cross-sectional study. South Korea, using linked administrative national health check-up and mortality databases. A total of 7 551 340 adult men who participated in the National Health Insurance Service health check-up program in 2017, including 450 536 men with registered disabilities and 7 100 804 men without disabilities. High-risk drinking was defined as consumption of seven or more standard drinks per occasion at least twice per week, based on self-reported health check-up questionnaires. Age-standardized prevalence of high-risk drinking was estimated annually from 2009 to 2017. Associations between disability characteristics and high-risk drinking were estimated using multivariable logistic regression in 2017. All-cause mortality occurring within 2017 was ascertained through deterministic linkage to the national death registry using unique personal identifiers. In 2017, age-standardized prevalence of high-risk drinking was 17 141 per 100 000 among men with disabilities and 23 226 per 100 000 among men without disabilities. Among men aged 20-49 years, prevalence was 29 710 per 100 000 in those with mild disabilities and 26 332 per 100 000 in those without disabilities. In 2017, compared with men without disabilities, mild disability was associated with higher odds of high-risk drinking [adjusted odds ratio (aOR) = 1.12, 95% confidence interval (CI) = 1.11-1.13], whereas brain injury was associated with lower odds (aOR = 0.61, 95% CI = 0.58-0.65). In 2017, age-standardized mortality rates were 131.4 per 100 000 among non-drinkers, 99.2 among high-risk drinkers, 77.3 among moderate drinkers and 59.9 among low-risk drinkers. Across drinking categories, several disability groups had adjusted odds ratios greater than 1.0 for all-cause mortality compared with those for men without disabilities within the same drinking category. High-risk drinking prevalence among South Korean men was lower among those with disabilities than among those without disabilities from 2009 to 2017, with declining trends in both groups. High-risk drinking prevalence among South Korean men appears to differ by disability characteristics. Mortality odds ratios within drinking categories vary by disability type and severity when compared with men without disabilities in the same drinking category.

Acrylamide (ACR), an environmental neurotoxicant prevalent in thermally processed foods, contributes to brain injury via oxidative stress and neuroinflammation. The cumulative effects of long-term low-dose exposure are particularly alarming. As a traditional food ingredient, the inflorescence of Coreopsis tinctoria Nutt. is rich in polyphenolic compounds that exhibit significant anti-inflammatory and antioxidant properties. This study systematically evaluated the neuroprotective potential of Coreopsis tinctoria Nutt. polyphenols (CTNP) against chronic low-dose ACR exposure in mice. Behavioral analyses demonstrated that CTNP (0.25-1.00 g kg-1) significantly ameliorated ACR-induced gait abnormalities and restored voluntary activity. CTNP mitigated neuronal misalignment and loss of synaptic density in the hippocampal CA1/CA3 regions and markedly reduced serum levels of brain injury markers MBP and GFAP by 30.6% and 41.7%, respectively. Mechanistic investigations revealed that CTNP attenuated oxidative damage via activation of the Nrf2/HO-1 pathway, leading to decreased brain reactive oxygen species and malondialdehyde levels while enhancing catalase, superoxide dismutase and glutathione peroxidase activities. Furthermore, CTNP suppressed MAPK pathway-mediated neuroinflammation, reducing pro-inflammatory factors such as COX-2, TNF-α and IL-1β. These findings demonstrate that CTNP, as diet-derived bioactives, mitigate ACR neurotoxicity through coordinated modulation of Nrf2/HO-1 antioxidant and MAPK anti-inflammatory pathways, supporting their potential as a functional food component for preventing environmental toxicant-associated neural damage. © 2026 Society of Chemical Industry.

Quantitative measures of autonomic cardiorespiratory maturation in preterm infants are associated with brain volumes at term age.