Elevated 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.
Serum NSE levels and prevalence of high NSE increased significantly across tertiles of log2-transformed NLR in AIS patients.
Each unit increase in log2(NLR) was associated with a 38% increased risk of high NSE after full adjustment for covariates.
NLR demonstrated modest discriminatory ability for identifying patients with high NSE as assessed by ROC analysis.
The study design was cross-sectional, precluding causal inference about the relationship between systemic inflammation and neuronal injury.
The association between NLR and serum NSE in AIS supports a link between the systemic inflammatory response and the extent of central neuronal injury.
This research suggests that in patients experiencing acute ischemic stroke (a type of stroke caused by a blocked blood vessel in the brain), higher levels of systemic (whole-body) inflammation are linked to greater damage to brain cells. The researchers measured inflammation using a simple blood test ratio called the neutrophil-to-lymphocyte ratio (NLR), which compares two types of white blood cells. They also measured a protein called neuron-specific enolase (NSE) in the blood, which is released when brain nerve cells are damaged. Analyzing data from 4,272 stroke patients, they found that patients with higher NLR values were significantly more likely to have elevated NSE levels, with each doubling of NLR associated with a 38% higher odds of having high NSE. The relationship between NLR and NSE was linear, meaning that as inflammation increased, markers of brain cell damage tended to increase proportionally. However, when researchers tested how well NLR alone could identify patients with high brain cell damage, it performed only modestly (AUC of 0.62 out of a maximum of 1.0), suggesting it would not be reliable enough on its own as a clinical diagnostic tool. This research suggests there may be an important interaction between the body's inflammatory response and the degree of brain injury during ischemic stroke, which could have implications for understanding why some stroke patients experience worse outcomes than others. Because the study was cross-sectional (a single snapshot in time rather than following patients over time), it is not possible to determine whether inflammation causes more brain damage, whether brain damage drives more inflammation, or whether both are driven by some other factor. Future studies following patients over time would be needed to clarify this relationship.
Rong N, Li H, Qian S, Ya Y, Tian H, Wang N, et al.. (2026). 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. https://doi.org/10.1002/iid3.70456