Reported head trauma and odds of acute ischemic stroke or transient ischemic attack: A population-based study (NEDICES) DOI
Ritwik Ghosh, Félix Bermejo‐Pareja, Souvik Dubey

et al.

Journal of the Neurological Sciences, Journal Year: 2023, Volume and Issue: 456, P. 122855 - 122855

Published: Dec. 21, 2023

Language: Английский

Astrocytes, reactive astrogliosis, and glial scar formation in traumatic brain injury DOI Creative Commons

María Belén Cieri,

Alberto Javier Ramos

Neural Regeneration Research, Journal Year: 2024, Volume and Issue: 20(4), P. 973 - 989

Published: May 16, 2024

Traumatic brain injury is a global health crisis, causing significant death and disability worldwide. Neuroinflammation that follows traumatic has serious consequences for neuronal survival cognitive impairments, with astrocytes involved in this response. Following injury, rapidly become reactive, astrogliosis propagates from the core to distant regions. Homeostatic astroglial proteins are downregulated near core, while pro-inflammatory genes overexpressed. This altered gene expression considered pathological remodeling of produces recovery. In addition, glial scar formed by reactive initially necessary limit immune cell infiltration, but long term impedes axonal reconnection functional Current therapeutic strategies focused on preventing acute complications. Statins, cannabinoids, progesterone, beta-blockers, cerebrolysin demonstrate neuroprotective benefits most them have not been studied context astrocytes. review, we discuss signaling pathways activated following some potential new aimed modulate responses especially using cell-targeted miRNAs or lncRNA, viral vectors, repurposed drugs.

Language: Английский

Citations

7

Aquaporins: Gatekeepers of Fluid Dynamics in Traumatic Brain Injury DOI Open Access
Wojciech Czyżewski, Jakub Litak, Jan Sobstyl

et al.

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(12), P. 6553 - 6553

Published: June 14, 2024

Aquaporins (AQPs), particularly AQP4, play a crucial role in regulating fluid dynamics the brain, impacting development and resolution of edema following traumatic brain injury (TBI). This review examines alterations AQP expression localization post-injury, exploring their effects on overall outcomes. We discuss underlying molecular mechanisms expression, highlighting potential therapeutic strategies to modulate function. These insights provide comprehensive understanding AQPs TBI suggest novel approaches for improving clinical outcomes through targeted interventions.

Language: Английский

Citations

6

Activation of CB2R by synthetic CB2R agonist, PM289, improves brain endothelial barrier properties, decreases inflammatory response and enhances endothelial repair DOI Creative Commons

Trent A. Bullock,

Kalpani N. Udeni Galpayage Dona, Jonathan F. Hale

et al.

NeuroImmune Pharmacology and Therapeutics, Journal Year: 2023, Volume and Issue: 2(4), P. 387 - 400

Published: Oct. 13, 2023

The Cannabinoid 2 Receptor (CB2R) has been found to provide immunological modulation in different cell types. More recently, detection of CB2R the cerebral endothelium suggests a possible role resolution inflammation at level blood-brain-barrier (BBB). Here, notion that upregulation brain endothelial cells could be exploited promote vascular protection and BBB integrity was evaluated. Targeting activation accomplished by novel highly specific chromenopyrazole based agonist, PM289. This study demonstrates is induced as early 8 h cortical vasculature an experimental mouse model TBI. Unlike CB2R, CB1R marginally detected not significantly induced. In human line, hCMEC/D3 cells, similar induction observed upon stimulation with TNFα. Analysis transendothelial electrical resistance shows PM289 markedly prevented barrier-leakiness also responsible for maintaining barrier. five-fold increase ICAM1 expression stimulated diminished due activation. Utilizing wounding assays, results showed wound repair nearly half time when agonist present compared untreated control. Lastly, mechanistically, effects may explained inhibition p65 NFκB subunit. Overall, these studies support targeting activating aid context neuroinflammation.

Language: Английский

Citations

3

Reported head trauma and odds of acute ischemic stroke or transient ischemic attack: A population-based study (NEDICES) DOI
Ritwik Ghosh, Félix Bermejo‐Pareja, Souvik Dubey

et al.

Journal of the Neurological Sciences, Journal Year: 2023, Volume and Issue: 456, P. 122855 - 122855

Published: Dec. 21, 2023

Language: Английский

Citations

0