People with schizophrenia, a type of psychosis, have much higher levels of immune system activity within the brain, a recent study finds. The research conducted by Peter Bloomfield and teams at both Kings College and Imperial College London investigated the activity of immune cells in 56 participants who already had a diagnosis of schizophrenia, were at high risk of developing the condition, or were at low risk of developing the condition.

Using PET scans (positron emission tomography) they looked at the activity of a very particular type of cell; a microglia. These cells respond to signs of damage or disease through mediating the inflammatory response within the brain and are also responsible for the ‘pruning’ process, whereby connections between neurons are removed when they are not used. Pruning happens naturally to everybody during childhood as it makes the brain more efficient and helps us to learn.

The research found that microglial activity was significantly greater for people who had schizophrenia compared to those that didn’t, and the severity of their symptoms was positively correlated with the amount of activity in these cells. In other words, there was a very strong link between an the occurrence of a neurological immune response and severe schizophrenic symptoms.

One major component of any immune response is a large amount of inflammation which is, in part, mediated by microglia. When you get a cut on your leg, you may notice that the skin around the injured area becomes red, inflamed and swollen; this is your immune response kicking into action.

Inflammation helps the body to attack antigens which may cause the body harm, and helps to heal damaged cells. The inflammatory response can often go into overdrive however, which seems to be happening in the brains of people with schizophrenia. What’s more, this activity was found in the brains of ‘at risk’ participants, suggesting that inflammation comes before schizophrenia. In other words, the large amount of microglial activity which triggers inflammation may be causing some of the symptoms of the illness.

As lead author Peter Bloomfield suggests, this is very exciting news:

“Our findings are particularly exciting because it was previously unknown whether these cells become active before or after onset of the disease. Now we have shown this early involvement, mechanisms of the disease and new medications can hopefully be uncovered.”

There are, of course, some problems with the study. The sample size of 56 participants is very small, particularly when you take into consideration that within each of the three groups (those with schizophrenia, those at risk and healthy participants) there were less than 20 people. The study also fails to suggest why the inflammation might occur in the first place. Correlation, after all, is not causation. Is schizophrenia the cause of the inflammation, or is inflammation the cause of the schizophrenia? Despite the results leaning towards the latter, they have not established anything conclusive.

Nevertheless, the research has not only unveiled a mechanism by which schizophrenia may develop, but it may also suggest new treatment options, as outlined by Dr Oliver Howes, head of the psychiatric imaging group at the MRC Clinical Sciences Centre:

“This is a promising study as it suggests that inflammation may lead to schizophrenia and other psychotic disorders. We now aim to test whether anti-inflammatory treatments can target these. This could lead to new treatments or even prevention of the disorders altogether.”

To find out more about the study see the original journal article and medical research council press release.