Background: Chronically re-experiencing the memory of a traumatic event might cause a glial response. This study examined whether glial activation would be associated with PTSD in a study of responders present after the 9/11 World Trade Center attacks without comorbid cerebrovascular disease.
Methods: Plasma was retrieved from 1,520 WTC responders and stored for a cross-sectional sample of responders of varying levels of exposure and PTSD. Plasma levels (pg/ml) of glial fibrillary acidic protein (GFAP) were assayed. Because stroke and other cerebrovascular diseases cause distributional shifts in GFAP levels, multivariable-adjusted finite mixture models analyzed GFAP distributions in responders with and without possible cerebrovascular disease.
Results: Responders were aged 56.3 years and primarily male; 11.07% (n = 154) had chronic PTSD. Older age was associated with increased GFAP, whereas higher body mass was associated with decreased GFAP. Multivariable-adjusted finite mixture models revealed that severe re-experiencing trauma from 9/11 was associated with lower GFAP (B = -0.558, p = 0.003).
Conclusion: This study presents evidence of reduced plasma GFAP levels among WTC responders with PTSD. Results suggest re-experiencing traumatic events might cause glial suppression.
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http://dx.doi.org/10.1016/j.bbih.2023.100631 | DOI Listing |
Mol Med
December 2024
Department of Ophthalmology, Ruijin Hospital Affiliated Medical School, Shanghai Jiaotong University, 197 Ruijin er Road, Shanghai, 200025, China.
Background: Glaucoma is a group of heterogeneous neurodegenerative diseases with abnormal energy metabolism and imbalanced neuroinflammation in the retina. Thioredoxin-interacting protein (TXNIP) is involved in glucose and lipid metabolism, and associated with oxidative stress and inflammation, however, not known whether to be involved in glaucoma neuropathy and its underlying mechanisms.
Methods: To establish the chronic ocular hypertension (COH) mice model.
Neurochem Int
December 2024
Master and PhD Programs in Pharmacology and Toxicology, School of Medicine, Tzu Chi University, Hualien, Taiwan 970; Department of Pharmacology, School of Medicine, Tzu Chi University, Hualien, Taiwan 970. Electronic address:
Previous studies have shown that celecoxib or NSAID may paradoxically induce cyclooxygenase-2 (COX-2) expression and trigger inflammation-like responses in airway smooth muscle cells and renal mesangial cells. Despite the extensive research on celecoxib, its atypical biological effect on the induction of COX-2 in astroglial cells within the central nervous system (CNS) remains unexplored. In the present study, we investigated the impact of celecoxib on COX-2 and Glial Fibrillary Acidic Protein (GFAP) expression and explored the mechanisms underlying celecoxib-regulated COX-2 expression in cortical astrocytes of rats.
View Article and Find Full Text PDFBrain Res Bull
December 2024
Department of Neurology, the First Affiliated Hospital of Hainan Medical University, Haikou 570102, China. Electronic address:
Neuroinflammation mediated by glial cells plays a crucial role in demyelination in experimental autoimmune encephalomyelitis (EAE), a multiple sclerosis (MS) model. Forsythoside B (FTS·B), a natural phenylethanoid glycoside isolated from the dried fruits and leaves of Forsythia suspensa (Thunb.) Vahl, has been found to have antioxidant, anti-apoptotic, and anti-inflammatory properties.
View Article and Find Full Text PDFTransl Neurodegener
December 2024
Department of Neurosciences, Hengyang Medical School, University of South China, Hengyang, 421009, China.
Background: Neurological complications are a significant concern of Coronavirus Disease 2019 (COVID-19). However, the pathogenic mechanism of neurological symptoms associated with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is poorly understood.
Methods: We used Drosophila as a model to systematically analyze SARS-CoV-2 genes encoding structural and accessory proteins and identified the membrane protein (M) that disrupted mitochondrial functions in vivo.
Brain Behav Immun
December 2024
Department of Anesthesiology, the Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong Province 510630, China. Electronic address:
Glial cell-induced neuroinflammation in the spinal cord is the critical pathology underlying complete Freund's adjuvant (CFA)-induced inflammatory pain. Previously, we showed that spinal glial cells undergo ferroptosis after CFA injection, which may contribute to the development of neuroinflammation and inflammatory pain. However, the mechanism underlying the occurrence of ferroptosis during inflammatory pain remains unclear.
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