The search for causes of mental disorders has been keeping researchers busy for a long time. Various hypotheses have been postulated; in the 1960s, for example, scientists assumed the underlying cause to be a chemical imbalance in the brain. Is the balance of messenger substances disrupted? Do hormones play a key role?
Later, researchers discovered the so-called neuroplasticity, the brain’s ability to adapt. Contact points between neurons, namely synapses, can be regrown, but they can also disappear, new neurons form, but they also die. Such processes occur during learning and training and are perfectly normal. But they also play a role in mental disorders. As it turned out, therapies had a demonstrable impact on those processes.
A small and very recent research field is so-called psychoneuroimmunology. It focuses on the immune system’s significance in the evolution of mental disorders, and strives to use all previous approaches in combination with each other.
“Originally, the brain and the immune system were considered two separate systems,” explains Prof Dr Georg Juckel, Medical Director at the RUB’s LWL university clinic for psychiatry, psychotherapy and preventive medicine. “It was assumed that the brain operates independently from the immune system and has hardly anything to do with it. This, however, is not true.” Direct neural connections from the brain to organs of the immune system, such as the spleen, do exist. And vice versa, immune cells migrate to the brain, and local immune cells carry out various tasks there, including disposing of damaged synapses. There is yet more evidence supporting the theory that the immune system is involved in brain processes: in patients suffering from certain mental conditions, the immune parameters present characteristic mutations. A treatment with immune system mediators such as Interferon alpha, which is deployed in e.g. hepatitis C treatment, leads to depressions in 20 to 30 per cent of the patients.
Dr Astrid Friebe’s work group in the LWL clinic lab researches into the mechanisms involved in these processes (fig. 1). The researchers are mainly interested in microglial cells. These immune-competent cells, which belong to the phagocyte family, are typically responsible for repairing synaptic links, removing damaged synapses and encouraging the growth of new neurons in the brain. Moreover, they carry out various metabolic processes, some of which have not yet been fully understood. In case of a threat, microglial cells are activated and switch into the destructive mode. In this active mode, they trigger inflammation and release messengers that damage nerve cells. “We see this very clearly in patients suffering from multiple sclerosis or Alzheimer’s. The brain areas affected by inflammation or neurodegeneration are surrounded by a circle of microglial cells,” describes Georg Juckel. In schizophrenia patients, the number of microglial cells is considerably higher than in healthy individuals. Here, the cells cause synaptic links between neurons to degenerate. Those links form the so-called grey matter, which in schizophrenia patients is significantly decreased.
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