Growing evidence suggests that inflammation is of importance for the pathophysiology of psychiatric disorders. The major aim of this project is to increase the knowledge of the aetiology of psychiatric disorders by studying the influence of the immune system on different aspects of brain functions.
In depression, elevated levels of pro-inflammatory cytokines and acute phase proteins in serum have been found. Little is known about the pathophysiological mechanisms underlying the association between psychiatric disorders and inflammation – is an activation of the immune system increasing the vulnerability to develop depression and anxiety or vice versa?
The traditional and most favoured hypothesis is that the signs of inflammation observed in depression and anxiety are the result of mental stress inducing a peripheral inflammatory response; thus, this view suggests that the disturbance in mood is the primary event. Intriguingly, a more direct involvement of the immune system in the aetiology of psychiatric disorders however cannot be excluded. This suggestion gains support e.g. by data from our group showing that genetic variations in genes associated with the innate immune system (and thereby with inflammation) are influencing personality traits. Also, just recently we showed associations between cognitive parameters and polymorphisms in genes related to inflammation. These associations imply that the immune system is indeed modulating human behaviour. Animal studies have suggested an influence of immune-related substances in synaptic function including long-term potentiation and neurogenesis but the role for inflammation in the human, normal brain needs to be clarified.
Of interest is also the enhanced mortality in cardiovascular diseases (CVD) in patients with depression and panic disorder since both groups of disorders are associated with signs of e.g. low-grade inflammation. Likewise, both CVD and depression are associated with certain personality traits, such as anger and hostility. It is possible that depression and panic anxiety may trigger CVD, but one also cannot rule out the possibility that these disorders are epiphenomena; i.e., they may occur independently of each other due to e.g. a dysregulation of the immune system. We are investigating the role of inflammation in this context by means of studying cardiovascular parameters in a study including controls as well as patients with depression and panic disorder.
Agneta Ekman, associate professor
Box 431, 405 30 Göteborg
031-786 00 00 (växel)
031-786 31 64