Key result
The BDNF Met allele dysregulates the norepinephrine/α2A-ADR pathway, leading to platelet hyper-reactivity and increased procoagulant activity in CAD patients and mice.
Why the study?
Depression is associated with thrombotic risk, and the depression-related BDNFVal66Met polymorphism has been linked to arterial thrombosis in mice and acute myocardial infarction in humans.
Does modulation of the norepinephrine/α2A-ADR pathway reduce arterial thrombosis risk in BDNFMet/Met models?
Population
Homozygous knock-in BDNFMet/Met mice, in vitro cell models, and CAD patients with BDNFMet/Met or BDNFVal/Val
Comparison
Desipramine, rauwolscine, or BDNFMet/Met genotype vs controls or BDNFVal/Val
Design
Preclinical in vivo, in vitro, and translational human observational study
Authors
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May warrant caution selecting antidepressants in depressed CAD patients; leaves open genotype-specific thrombotic effects.
Does modulation of the norepinephrine/α2A-ADR pathway reduce arterial thrombosis risk in BDNFMet/Met models?
The BDNF Met allele dysregulates the norepinephrine/α2A-ADR pathway, predisposing to arterial thrombosis, suggesting that α2A-ADR inhibitors could be a targeted treatment for depression-associated thrombotic conditions in specific CAD patients.
Sandrini et al. (2021) studied Coronary artery disease. BDNFVal66Met polymorphism vs. BDNFVal/Val was evaluated on Platelet hyper-reactivity and procoagulant activity. The BDNF Met allele dysregulates the norepinephrine/α2A-ADR pathway, leading to platelet hyper-reactivity and increased procoagulant activity in CAD patients and mice.
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