ArticleJournal of neural transmission (Vienna, Austria : 1996)2026
Altered platelet function in persistent depressive disorder: a study of density subpopulations and fibrinogen binding.
Article in Journal of neural transmission (Vienna, Austria : 1996), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Persistent Depressive Disorder (PDD) is a chronic mood disorder linked to psychological and physical health burdens, including increased coronary heart disease (CHD) risk. Emerging evidence suggests platelet activation may represent a shared biological mechanism between PDD and CHD, involving inflammatory and neurovascular pathways. This study aimed to compare platelet activity and reactivity in individuals with PDD and matched controls without psychiatric disorders, using flow cytometric analysis to assess activation markers and platelet subpopulation profiles. Thirty-nine PDD patients receiving SSRI treatment and 103 controls without depressive episodes or other psychiatric disorders were recruited in Sweden. Blood samples were collected and analyzed using flow cytometry and gradient separation techniques. The first sample assessed in vivo platelet activation via fibrinogen binding to glycoprotein Ib across density-separated fractions. The second sample evaluated in vitro platelet reactivity following stimulation with ADP and TRAP-6, with fibrinogen binding as the primary outcome. Platelet counts and mean platelet volume (MPV) were also measured. Results showed no significant differences in platelet distribution across the gradient. However, PDD individuals exhibited significantly higher in vivo platelet-bound fibrinogen in high and normal density fractions (fractions 3–9) and increased platelet reactivity upon agonist stimulation compared to controls (p < 0.05). MPV was also significantly elevated in the PDD group. These findings indicate platelet hyperactivation in PDD, potentially contributing to cardiovascular risk. Heightened platelet activation in PDD without comorbid CHD indicates abnormalities intrinsic to depressive pathophysiology. Given platelet activation’s established role in CHD, these findings suggest shared platelet‑driven inflammatory and neurovascular mechanisms linking mood disorders with broader cardiometabolic risk. Further research is needed to clarify these biological links and assess platelet heterogeneity as a potential biomarker for disease progression and therapeutic response in mood and cardiovascular disorders.
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