Thursday 21 February 2013

The Neurobiology of Suicidality: development of a blood test?

A blood test to determine if a person is suicidal may sound like science-fiction, but if recent research in Australia is anything to go by, such a technology may be within reach of medical practitioners sooner than you think.

According to the Australian Bureau of Statistics, suicide is the most common cause of death for young Australians, aged between 15 and 40. Consequently, research in the early detection of suicidality is vital. While there are several observable behavioural warning signs of suicide, a growing number of studies have looked at the neurobiology of suicidality, in an attempt to determine reliable chemical warning signs. According to Dr. Guilemin from the University of New South Wales, most studies in the area have so far looked at the imbalances of a neurotransmitter called Serotonin in the brain. However, after decades of research the link between Serotonin and suicidal behaviour remains unclear.

More recently, another neurotransmitter in the brain, known as quinolinic acid, has come to the attention of researchers. In a study recently published in Neuropsychopharmacology, higher levels of quinolinic acid were found in individuals hospitalised after a suicide attempt compared to a healthy control group. Moreover, high levels of quinolinic acid were also related to higher scores on a self-report and assessor-report scale assessing suicide intent.

Importantly, the hospitalised patients in the study underwent a ‘washout period,’ where they did not receive any antipsychotic or antidepressant medication, which was argued to rule out the possibility that different levels of the neurotransmitter were due to differences in medication between the groups. Furthermore, the authors noted that quinolinic acid was high in all suicide attempt patients, regardless of whether they were given a diagnosis of depression or not. Consequently, this may suggest that higher levels of the neurotransmitter may be specifically linked to suicidality rather than more general depressive symptoms (Serotonin, on the other hand, is more reliably linked to depression). Interestingly, quinolinic acid in the suicide attempt group normalised to that of the control group six months later.

Previously, it has been suggested that abnormal activation of N-methyl-D-aspartate (NMDA) receptors in the brain may be in some way responsible for suicidal behaviour, consistent with the general findings that medications that blocks NMDA receptors appear to alleviate such symptoms. Quinolinic acid may therefore be an important part of this mechanism, given that this neurotransmitter is known to trigger and activate NMDA-Receptors.

Of course, even if an excess of quinolinic acid is found to be a reliable indicator of suicidality it does not necessarily make it in any way a direct cause, and future research is required to determine how effective medication that manipulates this neurotransmitter will be in reducing suicidality. As the authors of the study point out, suicidality is a complex phenomenon and such things as psychological factors may in fact be a more immediate cause, with the observed excess of quinolinic acid being a secondary trigger. Consequently, psychological therapies would continue to play a critical role in treatment.

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