Neurological manifestations of encephalitic alphaviruses, traumatic brain injuries, and organophosphorus nerve agent exposure DOI Creative Commons

Morgen VanderGiessen,

Caroline de Jager,

Jessica Leighton

и другие.

Frontiers in Neuroscience, Год журнала: 2024, Номер 18

Опубликована: Дек. 13, 2024

Encephalitic alphaviruses (EEVs), Traumatic Brain Injuries (TBI), and organophosphorus nerve agents (NAs) are three diverse biological, physical, chemical injuries that can lead to long-term neurological deficits in humans. EEVs include Venezuelan, eastern, western equine encephalitis viruses. This review describes the current understanding of pathology during these conditions, provides a comparative case studies vs. animal models, summarizes therapeutics. While epidemiological data on clinical pathological manifestations conditions known humans, much our mechanistic relies upon models. Here we models findings for EEVs, TBIs, NAs compare with what is from human studies. Additionally, research limited due their classification as high-risk pathogens (BSL-3) and/or select agents; therefore, leverage commonalities TBI develop further mechanisms damage. Furthermore, discuss overlapping damage between TBI, NAs, highlight novel medical countermeasure opportunities. We describe treatment methods reducing induced by individual general neuroprotective options. Finally, perspectives future drug development against sequelae NAs.

Язык: Английский

Glial Cell Reprogramming in Ischemic Stroke: A Review of Recent Advancements and Translational Challenges DOI
Andrei Greșiță, Dirk M. Hermann, Ianis Kevyn Stefan Boboc

и другие.

Translational Stroke Research, Год журнала: 2025, Номер unknown

Опубликована: Фев. 4, 2025

Язык: Английский

Процитировано

1
Neurodegenerative diseases and neuroinflammation-induced apoptosis DOI Creative Commons

Shi Huang,

Yaxin Lu,

Wenjun Fang

и другие.

Open Life Sciences, Год журнала: 2025, Номер 20(1)

Опубликована: Янв. 1, 2025

Abstract Neuroinflammation represents a critical pathway in the brain for clearance of foreign bodies and maintenance homeostasis. When neuroinflammatory process is dysregulate, such as over-activation microglia, which results excessive accumulation free oxygen inflammatory factors brain, among other factors, it can lead to an imbalance homeostasis development various diseases. Recent research has indicated that numerous neurodegenerative diseases closely associated with neuroinflammation. The pathogenesis neuroinflammation intricate, involving alterations genes proteins, well activation inhibition signaling pathways. Furthermore, inflammation result neuronal cell apoptosis, further exacerbate extent disease. This article presents summary recent studies on relationship between apoptosis caused by aim identify link two provide new ideas targets exploring pathogenesis, prevention treatment

Язык: Английский

Процитировано

0
Interrogating mediators of single-cell transcriptional changes in the acute damaged cerebral cortex: Insights into endothelial-astrocyte interactions DOI
Caroline de Jager, Eman Soliman, Michelle H. Theus

и другие.

Molecular and Cellular Neuroscience, Год журнала: 2025, Номер unknown, С. 104003 - 104003

Опубликована: Март 1, 2025

Язык: Английский

Процитировано

0
The Janus Face of Astrocytes in Multiple Sclerosis: Balancing Protection and Pathology DOI Creative Commons
Ahmad Abulaban, Hayder M. Al‐kuraishy, Ali I. Al‐Gareeb

и другие.

Brain Research Bulletin, Год журнала: 2025, Номер unknown, С. 111356 - 111356

Опубликована: Апрель 1, 2025

Multiple sclerosis (MS) is a chronic autoimmune disorder characterized by demyelination and neurodegeneration in the central nervous system (CNS), predominantly affecting young adults with notable female predominance. While pathogenesis of MS involves complex interactions between peripheral immune cells CNS glia, astrocytes-the most abundant glial cells-play dual role disease progression. Traditionally classified into pro-inflammatory A1 neuroprotective A2 phenotypes, recent single-cell spatial transcriptomics reveal that human astrocytes exhibit continuum states beyond this binary paradigm. In MS, reactive contribute to neurotoxicity disrupting blood-brain barrier (BBB), promoting glutamate excitotoxicity, presenting antigens autoreactive T cells. Conversely, they also support repair through neurotrophic factor release (e.g., BDNF, CNTF) remyelination. Emerging therapies like dimethyl fumarate (DMF) fingolimod modulate astrocyte reactivity, targeting oxidative stress sphingosine-1-phosphate receptors mitigate neuroinflammation. However, challenges persist translating murine A1/A2 concepts as display heterogeneous, context-dependent responses influenced regional microenvironments stages. Advanced techniques, including multi-omics, highlight astrocyte-microglia crosstalk metabolic reprogramming key drivers pathology. This review synthesizes current evidence on heterogeneity, their Janus-faced roles therapeutic potential astrocyte-targeted strategies, advocating for precision approaches account human-specific biology. Future research must priorities human-centric biomarkers dynamic modelling bridge gap experimental findings clinical applications.

Язык: Английский

Процитировано

0
Body weight-supported treadmill training reduces glial scar overgrowth in SCI rats by decreasing the reactivity of astrocytes during the subacute phase DOI Creative Commons

Jili Cai,

Yu Wang,

Chenyuan Zhai

и другие.

BMC Neuroscience, Год журнала: 2025, Номер 26(1)

Опубликована: Апрель 28, 2025

Spinal cord injury is followed by glial scar formation, which was long seen mainly as a physical barrier preventing axonal regeneration. Glial astrocytes lead to formation and produce inhibitory factors prevent axons from growing through the scar, while inhibiting conversion of reactive into scar-forming may represent an ideal treatment for CNS injury. Exercise non-invasive effective therapeutic intervention clinical rehabilitation spinal However, its precise mechanisms still need be continuously explored. 30 rats were randomly assigned three groups (Sham, SCI, SCI + BWSTT; n = 10 per group). In this study, we employed BBB scales gait analysis system examine behavioral functions in each group. Furthermore, utilized immunoblotting tissue at site, addition histological staining immunofluorescence staining, explore aggregation regeneration group rats. Our results revealed that hindlimb motor function significantly improved after sustained subacute period BWSTT, accompanied promotion repair nerve Subsequent showed diminished astrocyte reactivity region surrounding well reduced expression distribution collagen fibers near lesion BWSTT. Additionally, significant decrease MMP-2/9, closely related migration, observed vicinity lesions. study demonstrates BWSTT during phase can effectively reduce scarring overgrowth, thereby facilitating functional recovery SCI.

Язык: Английский

Процитировано

0
Astrocyte-mediated inflammatory responses in traumatic brain injury: mechanisms and potential interventions DOI Creative Commons
Haifeng Zhang, Xian Zhang, Yan Chai

и другие.

Frontiers in Immunology, Год журнала: 2025, Номер 16

Опубликована: Май 8, 2025

Astrocytes play a pivotal role in the inflammatory response triggered by traumatic brain injury (TBI). They are not only involved initial following but also significantly contribute to Astrocyte activation and inflammasome release key processes pathophysiology of TBI, affecting progression secondary long-term outcomes. This comprehensive review explores complex triggering mechanisms astrocyte intricate pathways controlling inflammasomes from activated astrocytes, subsequent neuroinflammatory cascade its multifaceted roles after injury. The exploration these deepens our understanding highlights potential astrocytes as critical therapeutic targets for TBI interventions. We then evaluate cutting-edge research aimed at targeted approaches modulate pro-inflammatory discuss emerging pharmacological interventions their efficacy preclinical models. Given that there has yet be relevant elucidating specific intracellular targeting substances, this aims provide nuanced astrocyte-mediated neuroinflammation elucidate promising avenues could fundamentally change management improve patient development neurological sequelae. By releasing variety cytokines chemokines, regulate neuroinflammation, thereby influencing survival function surrounding cells. In recent years, researchers have concentrated efforts on signaling crosstalk between other cells under various conditions, while exploring paper which produce mediators during acute phase post-TBI, including signaling, blood-brain barrier integrity, neuronal protection. Additionally, we current clinical intervention strategies mitigate damage enhance recovery TBI. Finally, explore feasibility pharmacologically assessing activity post-TBI biomarker predicting acute-phase changes.

Язык: Английский

Процитировано

0
Impact of galanin receptors 2 and 3 double-knockout on neuroinflammation and functional recovery following traumatic brain injury DOI Creative Commons
Susanne M. Brunner,

Stefanie Gaisbauer,

Patrick N. Pallier

и другие.

Peptides, Год журнала: 2025, Номер unknown, С. 171415 - 171415

Опубликована: Май 1, 2025

Traumatic brain injury (TBI) is one of the world's leading causes death and disability in young individuals mechanism underlying TBI-associated neuroinflammation poorly understood. The regulatory neuropeptide galanin (GAL) its three receptors (GAL1-3R) are assumed to modulate neuroinflammatory response following TBI, especially by signalling via GAL2R GAL3R. Therefore, role GALRs acute functional recovery moderate Controlled Cortical Impact TBI was studied using GAL2/3R-double-KO (GAL2/3R-KO) mice. Brains cerebrospinal fluid (CSF) were collected at day 1 30 days post TBI. Functional assessed modified Neurological Severity Score (mNSS), Elevated Plus Maze (EPM) Morris Water (MWM) test. Post (day 28 injury), neurological dysfunction more severe GAL2/3R-KO mice than WT At inflammatory markers several nerve growth factors significantly increased ipsilateral hemisphere, compared contralateral hemisphere both 4 surgery, entered frequent open-arms EPM Sham-operated mice, suggestive exploratory behaviour immunostaining sections revealed significant differences vascularisation glial scarring cortex when comparing but genotypes similar. In summary, results indicate that and/or GAL3R have a neuroprotective as severity lower their presence absence.

Язык: Английский

Процитировано

0
Neurological manifestations of encephalitic alphaviruses, traumatic brain injuries, and organophosphorus nerve agent exposure DOI Creative Commons

Morgen VanderGiessen,

Caroline de Jager,

Jessica Leighton

и другие.

Frontiers in Neuroscience, Год журнала: 2024, Номер 18

Опубликована: Дек. 13, 2024

Encephalitic alphaviruses (EEVs), Traumatic Brain Injuries (TBI), and organophosphorus nerve agents (NAs) are three diverse biological, physical, chemical injuries that can lead to long-term neurological deficits in humans. EEVs include Venezuelan, eastern, western equine encephalitis viruses. This review describes the current understanding of pathology during these conditions, provides a comparative case studies vs. animal models, summarizes therapeutics. While epidemiological data on clinical pathological manifestations conditions known humans, much our mechanistic relies upon models. Here we models findings for EEVs, TBIs, NAs compare with what is from human studies. Additionally, research limited due their classification as high-risk pathogens (BSL-3) and/or select agents; therefore, leverage commonalities TBI develop further mechanisms damage. Furthermore, discuss overlapping damage between TBI, NAs, highlight novel medical countermeasure opportunities. We describe treatment methods reducing induced by individual general neuroprotective options. Finally, perspectives future drug development against sequelae NAs.

Язык: Английский

Процитировано

1