Plasma Human Cartilage Glycoprotein-39 and Cognitive Impairment After Acute Ischemic Stroke

Ziyi Wang1, Kaixin Zhang2,3, Chongke Zhong3

  • 1Department of Neurology, Affiliated Hospital of Nantong University Medical School of Nantong University Nantong China.

Insights

Elevated levels of human cartilage glycoprotein-39 (YKL-40) are linked to a higher risk of cognitive impairment after acute ischemic stroke. This finding suggests YKL-40 may be a useful biomarker for post-stroke cognitive decline.

Area of Science:

  • Biomarkers
  • Neurology
  • Cardiovascular Research

Background:

  • Acute ischemic stroke poses a significant risk for developing cognitive impairment.
  • Human cartilage glycoprotein-39 (YKL-40) is a potential inflammatory biomarker.
  • The association between YKL-40 and post-stroke cognitive impairment requires further investigation.

Purpose of the Study:

  • To evaluate the association between plasma YKL-40 levels and cognitive impairment at 3 months post-acute ischemic stroke.
  • To determine if YKL-40 can serve as a predictive biomarker for cognitive decline after stroke.

Main Methods:

  • Plasma YKL-40 levels were measured in 604 patients from the China Antihypertensive Trial in Acute Ischemic Stroke.
  • Cognitive function was assessed at 3 months using the Mini-Mental State Examination and Montreal Cognitive Assessment.
  • Statistical analyses included quartile comparisons, regression models, and ROC curve analysis.

Main Results:

  • Patients in the highest quartile of YKL-40 had a 2.01-fold increased risk of cognitive impairment (MMSE score).
  • Each 1 SD increase in YKL-40 was associated with a 28% increased risk of cognitive impairment.
  • YKL-40 improved the discriminatory power of conventional risk factors for predicting cognitive impairment.

Conclusions:

  • Elevated plasma YKL-40 levels are significantly associated with an increased risk of cognitive impairment 3 months after acute ischemic stroke.
  • YKL-40 may serve as a valuable biomarker for identifying patients at higher risk of post-stroke cognitive impairment.
Abstract

Related Concept Videos

Ischemic Stroke l: Introduction01:15

Ischemic Stroke l: Introduction

Ischemic stroke is an acute cerebrovascular condition in which blood flow to a brain region is suddenly interrupted, leading to tissue infarction. Neurons depend on continuous oxygen and glucose supply, so even brief reductions in perfusion cause energy failure, ionic imbalance, and irreversible injury. Ischemic strokes are classified into thrombotic and embolic types based on their underlying mechanisms.Thrombotic MechanismsThrombotic stroke develops when a clot forms within a cerebral artery.
Ischemic Stroke ll: Pathophysiology01:15

Ischemic Stroke ll: Pathophysiology

An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...
Hemorrhagic Stroke l: Introduction01:17

Hemorrhagic Stroke l: Introduction

A hemorrhagic stroke is an acute neurological event that occurs when a weakened cerebral blood vessel ruptures, allowing blood to accumulate within or around the brain. The sudden release of blood forms a focal hematoma that increases intracranial pressure, displaces neural tissue, and can obstruct cerebrospinal fluid pathways. These effects may be compounded by intraventricular extension of the hemorrhage, cerebral edema, or compression of adjacent structures, all of which contribute to...
Hemorrhagic Stroke ll: Pathophysiology01:29

Hemorrhagic Stroke ll: Pathophysiology

A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...
Transient Ischemic Attack l: Introduction01:26

Transient Ischemic Attack l: Introduction

A transient ischemic attack (TIA) is a brief episode of neurological dysfunction caused by a temporary, focal reduction in cerebral blood flow. Although symptoms resemble those of an ischemic stroke, the interruption in perfusion is short-lived and does not cause permanent infarction. TIAs are clinically important because they often serve as early warning events for future stroke.Mechanisms of Transient Cerebral IschemiaTransient cerebral ischemia may arise through several mechanisms. One...