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BDNFVal66met polymorphism: a potential bridge between depression and thrombosis.

Patrizia Amadio1, Gualtiero I Colombo1, Eva Tarantino2

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The BDNFVal66Met gene variant linked to depression promotes thrombosis and cardiovascular disease risk. SIRT1 activation mitigates these prothrombotic effects, suggesting therapeutic potential for heart attack prevention.

Keywords:
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Area of Science:

  • Cardiovascular Biology
  • Neurogenetics
  • Thrombosis Research

Background:

  • Stress, depression, and cardiovascular diseases (CVDs) are linked, but mechanisms are unclear.
  • The BDNFVal66Met gene polymorphism, associated with depression, is a potential CVD genetic risk factor.
  • Investigating this polymorphism's impact on thrombosis is crucial for understanding CVD pathogenesis.

Purpose of the Study:

  • To investigate the impact of the BDNFVal66Met single-nucleotide polymorphism on thrombosis.
  • To explore the mechanistic link between the BDNF Met allele, depression, and hypercoagulability.
  • To evaluate SIRT1 activation as a potential therapeutic strategy against BDNFMet-associated thrombosis.

Main Methods:

  • Utilized a knock-in mouse model (BDNFMet/Met) mimicking human BDNFVal66Met polymorphism.
  • Performed proteomic analysis of aorta secretome to identify differential protein expression.
  • Induced thrombosis using FeCl3 and collagen/epinephrine challenges; assessed SIRT1 activation effects.

Main Results:

  • BDNFMet/Met mice exhibited depressive-like behavior, hypercoagulability, and platelet hyperreactivity.
  • The BDNF Met allele predisposed to arterial thrombosis and mortality.
  • SIRT1 activation by resveratrol/CAY10591 inhibited thrombus formation and restored physiological markers.

Conclusions:

  • BDNFMet/Met mice display features mirroring anxiety/depression-related vascular changes.
  • The BDNFVal66Met polymorphism contributes to arterial thrombosis propensity and acute myocardial infarction (AMI) risk.
  • SIRT1 activation emerges as a promising therapeutic target for preventing thrombosis in individuals with the BDNF Met allele.