Could an inflamed brain be behind mental health disorders such as depression and schizophrenia? It’s one of the hottest ideas in psychiatry, but now it seems it’s only part of the picture: blocking inflammation in mice only relieved some of the signs of depression.
Inflammation is one of the body’s ways of fighting infection and recovering from injury. The characteristic red, hot swelling we associate with inflammation is a result of the immune system recruiting a range of molecules, such as cytokines, to sites of damage where they clear out debris and kick-start repair.
Intriguingly, about a third of people with depression have higher than normal levels of cytokines in their blood. What’s more, several studies suggest that some people with schizophrenia seem to have more active microglia – immune cells found in the brain – than people without the condition.
Results like these have prompted research into whether taking anti-inflammatory drugs alongside antidepressants could help treat depression.
To explore their effect, Jonathan Godbout at Ohio State University in Columbus and his colleagues put mice under stress for six days by placing a more aggressive mouse in their cage once a day. The mice began behaving anxiously, cowering in dark corners, and having memory problems – something that also affects people with depression.
No new brain cells
As expected, the mice had more microglia activation and other inflammation-causing immune cells in their brains. They also stopped making new brain cells, something that has also been seen in other animal models of depression.
Giving the animals an anti-inflammatory drug when the bully mouse was put into their cage reduced the anxiety and memory problems, but had no effect on brain cell production.
“The worst symptoms seem to be linked to inflammation,” says Godbout, but if it were the only contributing mechanism, we might have expected the drug to restart neurogenesis. The fact that it didn’t suggests that “inflammation is not the be-all and end-all”, he says.
Carmine Pariante at King’s College London disagrees. He thinks inflammation could be responsible for the lack of new neurons and suggests that perhaps the particular drug that Godbout used didn’t have a broad enough effect to restart neurogenesis.
Pariante and his colleagues have just started a trial using both standard antidepressants and anti-inflammatory drugs to treat people with depression and raised levels of inflammation. He cautions against people taking both types of drug together at this stage as each can increase the risk of gastric bleeding – combined, the risk could be even greater.
In the meantime, there are other ways to reduce inflammation, says Pariante, such as eating healthily and getting plenty of exercise.
This article first appeared on ‘New Scientist’ on 2 March 2016.