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Published on: May 22, 2019
Platelet surface glycoprotein expression in post-stroke depression: a preliminary study
Eugene M Cassidy1, Marie-Therese Walsh, Rory O'Connor
1Department of Psychiatry, Royal College of Surgeons in Ireland, Dublin 2, Ireland. eucass@hotmail.com
Insights
Depression and stroke patients show increased GPIb receptors on platelets compared to controls. This suggests platelet dysfunction may link depression and cerebrovascular disease.
Area of Science:
- Neuroscience
- Cardiovascular Science
- Hematology
Background:
- Depression is a known risk factor and consequence of cardiovascular disease and stroke.
- The underlying pathophysiological mechanisms connecting depression and cerebrovascular disease remain unclear.
Purpose of the Study:
- To investigate platelet surface glycoproteins involved in adhesion and aggregation in patients with depression and stroke.
- To explore the role of platelet dysfunction in the association between depression and cerebrovascular disease.
Main Methods:
- Flow cytometry was used to analyze platelet surface glycoproteins GPIb and GPIIbIIIa.
- Sample populations included depressed subjects, post-stroke subjects (depressed and non-depressed), and healthy controls.
Main Results:
- Subjects with depression and post-stroke subjects exhibited a significant increase in GPIb receptors compared to healthy controls.
- No significant difference in GPIb receptors was found between post-stroke and depressed subjects.
- No significant differences in GPIIbIIIa receptor numbers were observed across any groups.
Conclusions:
- Increased GPIb receptors suggest potential platelet dysfunction in depression and post-stroke states.
- Platelet dysfunction may play a role in the pathophysiology linking depression and cerebrovascular disease.
- Comorbid depression did not show an additive effect on GPIb or GPIIbIIIa expression in post-stroke patients.
Abstract:
Depression is a significant risk factor for and consequence of both cardiovascular disease and stroke. The pathophysiological processes underlying this association are poorly understood. This study utilised a technique for measurement of whole blood platelet surface glycoproteins involved in early adhesion and aggregation in sample populations of patients with depression and stroke, and healthy controls. We analysed the platelet surface glycoproteins GPIb and GPIIbIIIa using flow cytometry in eight depressed subjects (Hamilton depression score >17), 14 post-stroke subjects (seven depressed and seven non-depressed), and in eight healthy control subjects. The number of GPIb receptors was significantly increased in subjects with depression and in post-stroke subjects compared to control subjects. The number of GPIb receptors from post-stroke subjects was not significantly different from that of depressed subjects. There were no differences between any groups in measures of GPIIbIIIa receptor numbers. No additive effect of co-morbid depression on the surface expression level of either marker could be detected in the post-stroke subjects. Platelet dysfunction may be involved in the pathophysiological process underlying the association between depression and cerebrovascular disease.