Related Experiment Video
Updated: Jan 22, 2026
09:21
Optimized Management of Endovascular Treatment for Acute Ischemic Stroke
Published on: January 18, 2018
12.5K
Antiphospholipid antibodies predict post-stroke depression after acute ischemic stroke.
Guangli Wang1, Yiting Zhou1, Xiaoqing Bu2
1Department of Epidemiology, School of Public Health and Jiangsu Key Laboratory of Preventive and Translational Medicine for Geriatric Diseases, Medical College of Soochow University, 199 Renai Road, Industrial Park District, Suzhou, Jiangsu Province 215123, China.
Journal of Affective Disorders
|July 14, 2019
Summary
Elevated antiphosphatidylserine (aPS) and anticardiolipin (aCL) antibodies increase the risk of post-stroke depression (PSD). These antiphospholipid antibodies (aPLs) may aid in predicting PSD after acute ischemic stroke.
Area of Science:
- Neurology
- Immunology
- Psychiatry
Background:
- Antiphospholipid activity is linked to depression.
- The role of antiphospholipid antibodies (aPLs) in post-stroke depression (PSD) remains unclear.
Purpose of the Study:
- Investigate the association between aPLs, specifically antiphosphatidylserine (aPS) and anticardiolipin (aCL) antibodies, and depression following acute ischemic stroke.
Main Methods:
- Measured aPS and aCL in 497 ischemic stroke patients.
- Assessed PSD using the 24-item Hamilton Depression Rating Scale at 3 months post-stroke.
Main Results:
- aPS-positive and aCL-positive patients had higher odds of PSD (ORs 1.77 and 2.06, respectively).
- Increased aPS and aCL levels correlated with higher PSD risk (ORs 1.29 and 1.30, respectively).
- aPLs significantly improved PSD risk prediction models.
Conclusions:
- Higher baseline aPS and aCL levels are associated with an increased risk of 3-month PSD.
- aPLs show potential as predictors for post-stroke depression.
Related Concept Videos
01:27Regulation of Stroke Volume
4.8K
The regulation of stroke volume, which is the amount of blood the heart pumps out during each heartbeat, is critical for maintaining a healthy circulatory system. Stroke volume is influenced by three main factors: preload, contractility, and afterload.
Preload refers to the degree of stretch on the heart before it contracts. It's analogous to the stretching of a rubber band; the more it's stretched, the more forcefully it snaps back. This concept is encapsulated in the Frank-Starling law of the...
Preload refers to the degree of stretch on the heart before it contracts. It's analogous to the stretching of a rubber band; the more it's stretched, the more forcefully it snaps back. This concept is encapsulated in the Frank-Starling law of the...
4.8K
01:11Cardiac Output and Stroke Volume
4.5K
Cardiac output (CO) is an integral aspect of human physiology, reflecting the heart's efficiency and responsiveness to the body's needs. It represents the volume of blood that the left or right ventricle ejects into the aorta or pulmonary trunk each minute. The CO is calculated by multiplying the heart rate (HR)—the number of heartbeats per minute—by the stroke volume (SV)—the amount of blood pumped out with each heartbeat.
In an average resting adult male, the typical cardiac...
In an average resting adult male, the typical cardiac...
4.5K
01:22Cardiac Output II: Effect of Stroke Volume on Cardiac Output
3.2K
Cardiac output (CO), the amount of blood the heart pumps per minute, is a parameter in cardiovascular physiology determined by stroke volume and heart rate. Stroke volume, the amount of blood pushed from one of the ventricles per heartbeat, is influenced by preload, afterload, and contractility.
Preload
Preload refers to the initial elongation of the cardiac myocytes before contraction and is related to the volume of blood filling the heart at the end of diastole, or end-diastolic volume. The...
Preload
Preload refers to the initial elongation of the cardiac myocytes before contraction and is related to the volume of blood filling the heart at the end of diastole, or end-diastolic volume. The...
3.2K
01:05Long-term Depression
33.2K
Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
33.2K
01:03Long-term Depression
3.1K
Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
Calcium Ion Concentration Mechanism
If over...
Calcium Ion Concentration Mechanism
If over...
3.1K
03:12Freezing Point Depression and Boiling Point Elevation
39.6K
Boiling Point Elevation
The boiling point of a liquid is the temperature at which its vapor pressure is equal to ambient atmospheric pressure. Since the vapor pressure of a solution is lowered due to the presence of nonvolatile solutes, it stands to reason that the solution’s boiling point will subsequently be increased. Vapor pressure increases with temperature, and so a solution will require a higher temperature than will pure solvent to achieve any given vapor pressure, including one...
The boiling point of a liquid is the temperature at which its vapor pressure is equal to ambient atmospheric pressure. Since the vapor pressure of a solution is lowered due to the presence of nonvolatile solutes, it stands to reason that the solution’s boiling point will subsequently be increased. Vapor pressure increases with temperature, and so a solution will require a higher temperature than will pure solvent to achieve any given vapor pressure, including one...
39.6K