An international collaboration of research scientists in Australia, the United States and Sweden has identified a molecule in the blood that holds the key to identifying the cause of suicide.

“We have known for a long time that people who attempt suicide have markers of chronic inflammation in their blood and spinal fluid. Commonly used antidepressants have only limited effect because they target serotonin – the branch of tryptophan associated with happiness – rather than quinolinic acid which is the other branch of tryptophan associated with inflammation,” said Professor of Neuroscience, Gilles Guillemin from the Faculty of Medicine and Health Sciences.

“Our latest research provides further evidence of the role of inflammation in a person’s mental state. It shows that suicidal patients have reduced activity of an enzyme called ACMSD which results in lower production of picolinic acid, an important molecule for brain protection. We now have a much clearer indication of the biological mechanics behind suicidal tendency.

“The next step will be to develop a simple blood test to detect both quinolinic and picolinic acids to determine individuals who are at risk of taking their lives.

‘With more than seven suicide attempts every hour in Australia a test like this would be a huge step forward,” finished Professor Guillemin.

In 2013, Professor Guillemin and his collaborators discovered that the over-production of the small neurotoxin quinolinic acid is directly associated with suicidal behaviour.

This breakthrough is the outcome of a longstanding partnership between teams of researchers led by Professor Guillemin and colleagues from Karolinska Institutet in Sweden and the Van Andel Research Institute in the US.

Brundin, L., Sellgren, CM., Lim, CK., Grit, J., Palsson, E., Landen, M., Samuelsson, M., Lundgren, C., Brundin, P., Fuchs, D., Postolache, TT., Träskman-Bendz, L., Guillemin, GJ., Erhardt, S. An enzyme in the kynurenine pathway that governs vulnerability to suicidal behavior by regulating excitotoxicity and neuroinflammation. Translational Psychiatry, 2 August 2016, doi: 10.1038 / TP.2016.133.

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