ArticleJournal of neural transmission (Vienna, Austria : 1996)2025
TMEM119-positive microglial cells in cerebrospinal fluid, a potential new marker for neuroinflammatory response after aneurysmal subarachnoid hemorrhage.
Article in Journal of neural transmission (Vienna, Austria : 1996), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed.
- The potential role of transcranial direct current stimulation in experimental ischemic stroke in adult male albino rats.Scientific reports · 2026Article
- Epigenome-wide DNA methylation profiling in aneurysmal subarachnoid hemorrhage and delayed ischemic neurologic deficit: a prospective observational study.International journal of surgery (London, England) · 2026Observational
- Increased transmembrane protein 119 (TMEM119) levels in the cerebrospinal fluid of patients with mild cognitive impairment due to Alzheimer's disease suggest early microglial involvement.Alzheimer's & dementia (Amsterdam, Netherlands)Article
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17 authors.
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Abstract
Aneurysmal subarachnoid hemorrhage (aSAH) is a debilitating condition with significant morbidity and mortality rates. Despite advancements in treatment, understanding the underlying pathophysiology, particularly the inflammatory response, remains crucial for improving patient outcomes. In this study, we investigated the presence of transmembrane protein 119 (TMEM119) of microglial cells in cerebrospinal fluid (CSF) as a potential marker for neuroinflammation following aSAH. CSF samples were collected from aSAH patients, pathological and healthy controls, processed, and analyzed using immunocytochemistry. TMEM119-positive microglial cells were consistently identified in the CSF of aSAH patients, exhibiting amoeboid morphology and intense staining. Importantly, microglial cells were detected as early as the first day post-bleeding, persisting throughout the acute phase in some cases. Analysis of consecutive samples revealed varying trends in microglial cell numbers, with a peak during the initial phase followed by a gradual decline. Our findings suggest that microglia may migrate into the CSF following aSAH, potentially serving as an early predictor of inflammatory-related CNS damage. This study underscores the importance of understanding neuroinflammatory processes in aSAH and opens avenues for further research on the role of microglia in CNS disorders by liquid biopsy.
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