ArticleImmunity, inflammation and disease2026
Systemic Inflammation and Central Neuronal Damage: The Relationship Between Neutrophil-to-Lymphocyte Ratio and Neuron-Specific Enolase in Acute Ischemic Stroke.
Article in Immunity, inflammation and disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Systemic Inflammation and Central Neuronal Damage: The Relationship Between Neutrophil-to-Lymphocyte Ratio and Neuron-Specific Enolase in Acute Ischemic Stroke.Immunity, inflammation and disease · 2026Article
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Authors and funding
9 authors.
Funding
Abstract
background and purposeThe systemic inflammatory response, quantified by the neutrophil-to-lymphocyte ratio (NLR), and central neuronal injury, reflected by serum neuron-specific enolase (NSE), are implicated in the pathogenesis of acute ischemic stroke (AIS). However, the association between these two processes remains inadequately explored at the population level. This study aimed to investigate the relationship between NLR and neuronal injury via circulating biomarkers in AIS.
methodsIn this cross-sectional study, 4272 consecutively enrolled AIS patients from a single center in China were included. Serum NSE levels were measured, and NLR was calculated from peripheral blood counts and log₂-transformed for analysis. The association between log
resultsSerum NSE levels and the prevalence of high NSE both increased significantly across tertiles of log
conclusionElevated NLR is independently associated with higher levels of serum NSE in patients with AIS, supporting a link between systemic inflammation and the extent of central neuronal injury. These findings provide epidemiological evidence for an interaction between circulatory inflammatory responses and brain damage following ischemic stroke. However, due to the cross-sectional design, causality cannot be inferred, and the modest discriminatory ability of NLR limits its potential as a standalone clinical marker.
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