Cut your finger, and after a few hours the wound swells a little, reddens, and hurts. This is inflammation, and it’s an essential part of healing.  It’s the result of activation of special cells from the immune system; they respond to tissue damage and even more vigorously if the wound becomes infected with foreign organisms, such as bacteria. One result is an increase, in the blood, of substances secreted by these immunity cells that activate other cells and result in full-blown inflammation.

 It’s well-known that a deficient immune system puts you at risk of serious illness, but also that an overactive one can cause auto-immune disorders such as certain types of arthritis, bowel disease or diabetes.  This is because the immunity cells, instead of attacking or destroying dead tissue or invading organisms, assault and destroy normal cells.

The brain needs a very special environment to work properly. It is separated from the rest of the body by a barrier that regulates entry of substances and cells from the blood, so that large but temporary changes in blood composition – after a meal, for example – do not disturb brain function.  It was once thought that the body’s immune system did not involve the brain: this is now known not to be entirely correct.  But the brain does have its own immune-type cells, called microglia.  These normally sit around the brain in an inactive state: but if they are activated, then they begin to attack other cells, including nerve cells – particularly those that may be in a vulnerable condition by reason of other events (for example, the presence of toxins).  So brain inflammation is largely a matter of microglial activation. 

Inflammatory changes in the brain, sometimes accompanied by equivalent signs in the blood, are now being discovered in several neurological conditions.  After a stroke, damage to the brain may be worsened by microglial activation, and by partially damaged nerve cells emitting ‘eat-me’ signals that attract microglial attention.  Parkinsons’s disease has been suggested to result from inflammatory changes in cells in the brain containing dopamine. So has schizophrenia. Some of the damaging effects of cocaine on cognition may be because it increases inflammation in the brain. One of the most interesting ideas follows the finding that the brain’s of Alzheimer patients show clear signs of inflammation, particularly around the characteristic blobs of amyloid that are typical of this disease.  Is Alzheimer’s disease caused by abnormal inflammation of the brain, or is inflammation a response to the presence of amyloid?  There are still arguments over this.  But signs of inflammation in the blood are associated with cognitive decline in older people, and there has been some success in reducing this by giving substances that reduce inflammation (non-steroidal anti-inflammatory drugs).

Depression, or at least some cases of depression (depression is certainly not a single disorder) is also being associated with inflammation. A longitudinal study in the UK on 5000 subjects showed that those with signs of increased inflammation in their blood at aged 9 predicted depressive symptoms 9 years later (much depression starts in adolescence); they also predicted more persistent forms of depression.  Chronic or recurrent depression is a risk for later Alzheimer’s disease, so it’s intriguing to wonder whether persistent, low-grade inflammation in the brain might be the link between them. If it is, then we may have a clue for developing effective prevention.

All this focuses attention on the microglia, cells that were largely ignored for many years, but which have now become the subject of intense research. Luckily, the immense amount of knowledge we have acquired over the years about inflammation in the rest of the body may very well help us to understand the role of these cells in human neurological and mental disorders, and offer ways of recognizing and treating these conditions. As so often in medical research, a new door opens in an unexpected place.

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