Related Experiment Video
Updated: May 5, 2026

Transient Middle Cerebral Artery Occlusion Model of Neonatal Stroke in P10 Rats
Published on: April 21, 2017
The ADMA-NO-NOX2 axis and its association with leptomeningeal collateral impairment in acute ischemic stroke
Manuela De Michele1, Angela Risitano2, Marta Iacobucci3
1Emergency Department, Stroke Unit, Umberto I Hospital, Sapienza University, Viale del Policlinico, 155, 00161, Rome, Italy. m.demichele@policlinicoumberto1.it.
Abstract:
Leptomeningeal collateral (LMC) circulation helps preserve brain tissue during acute ischemic stroke (AIS), with poor collateral status predicting worse outcomes. This study assessed the association between asymmetric dimethylarginine (ADMA), LMCs, infarct volume, and oxidative stress in 101 AIS patients with large vessel occlusion within 6 h or wake-up stroke. LMC status was graded using the Menon score (poor, intermediate, or good) on CT angiography, and recanalization was assessed by the modified Thrombolysis in Cerebral Infarction score. Serum ADMA, NADPH oxidase 2 (NOX2), and nitric oxide (NO) levels were measured at admission (< 6 h, T0), 24 h (T1), and 48 h (T2). Among patients, 43.1% had good, 35.3% intermediate, 21.6% poor LMC status. Higher admission ADMA levels were significantly associated with poor LMC at T0 (p = 0.028) and more severe neurological deficits at T1 and T2 (p = 0.005, p = 0.008). ADMA levels increased over time (p = 0.046), and correlated with NOX2 at T1 (p < 0.001). Rising NOX2 was associated with increased neutrophils (p = 0.013) and decreased lymphocytes (p = 0.006). ADMA may impair endothelial function by reducing NO availability and enhancing NOX2-driven oxidative stress. These findings support a role for the ADMA-NO-NOX2 axis in limiting collateral circulation. Targeting this axis may represent a therapeutic strategy to improve outcomes in AIS.
Related Concept Videos
Ischemic Stroke l: Introduction
Ischemic Stroke ll: Pathophysiology
Hemorrhagic Stroke l: Introduction
Hemorrhagic Stroke ll: Pathophysiology
Transient Ischemic Attack l: Introduction

