The first session by Professor A. Sutherland looked at the role of Toxoplasma gondii, a parasite that infects 30 to 80 percent of the world’s population, and how it impacts bipolar disorder.
In infected mice, the parasite has been shown to manipulate behaviour, making them more active and willing to take risks, with a slower reaction time, ability to learn and pay attention, and a reduced fear of cats.
This adaptation of behaviour makes sense as cats are the parasite’s primary host, so increasing risky behaviours in mice increases the chance that a cat will eat them, but how do parasite-induced brain changes affect humans?
Humans infected with T. gondii have slower reaction times and cognitive performance, and increased risks of suicidal behaviour and dying in traffic accidents (which may be due to the decreased reaction times).
To work out the association with bipolar disorder, Prof Sutherland performed a meta-analysis and showed a significant association (OR 1.52, p=0.02) between T. gondii and bipolar disorder
The role of infection in bipolar disorder was further examined by Professor M. Leboyer.
Prof Leboyer opened her presentation by proposing a move away from the traditional perspective of bipolar disorder. Instead of considering bipolar as a cyclical illness characterised by full-blown manic or depressive episodes interspersed with normal euthymic periods, Prof Leboyer proposed a more holistic perspective of a subtle, chronic, progressive, multi-system disorder.
Bipolar is also associated with a lot of other conditions – obesity, diabetes, hypertension, auto-immune disorders – so Prof Leboyer proposed that this may be due to a broader multi-system inflammatory disorder.
In particular, Prof Leboyer focused on immunogenetic variety; the way that genes can influence response to pathogens. She presented data that showed that immune dysregulation due to variations in Toll-Like Receptor genes, among others, may be more common in early-onset bipolar disorder patients.
Prof Leboyer combined these aspects of her presentation together by presenting a ‘multiple hit’ model of vulnerability to bipolar disorder, where ‘hits’ throughout childhood – prenatal infection, childhood trauma – can all combine to induce an ongoing chronic mild inflammation, which is a risk factor for the subsequent development bipolar disorder.
Two fascinating talks rounded out another great morning for this correspondent. Though now Toxoplasma gondii gets added just below Ebola on my ‘Microorganisms to be terrified of’ list.
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