I think Brian Dickie must have planned the early morning slot of the International Symposium in Brussels as a talk that would make delegates sit up and take note. Southampton based Professor Hugh Perry’s presentation certainly made me do that on Sunday morning, the last day of the meeting.
His presentation was on the role of inflammation in neurodegenerative disease. ‘Most of what I’m going to talk about is not about MND’, he commented, ‘but I hope that it will have some resonance for you’. He started off talking about prion disease. In particular he is interested in cells that are called microglia that exist in the brain and spinal cord.
Perhaps about ten years ago the MND research world found out that it wasn’t just motor neurones we should be paying attention to in MND. There are cells called glial cells that support the function of motor neurones and come in all shapes and sizes in different parts of the brain. The whole set of talks in this session were dedicated to discussing their role in MND.
What, where and how?
Just like any good detective story (or news story) Professor Perry started with some basic questions – what do the microglia do in the brain of his mouse model (he was using prion disease as an example of neurodegenerative disease), where do the microglia come from and how do they contribute to neurodegeneration? He found the presence of more microglia in the brain of mice with neurodegenerative disease compared to unaffected mice. This higher number of microglia is also seen in the brains of people with prion disease and also in people with Alzheimer’s Disease.
Microglia and infection
From the time someone is born they are exposed to all manner of different infections – from colds to urinary infections. Depending on the nature of the infection explained Prof Perry, there will be short term (‘acute’) signs, eg fever and more long term (‘chronic’) signs of infection such as permanent tissue damage. ‘But what happens to microglia when someone with neurodegenerative disease gets an infection?’ asked Prof Perry, pulling together the two themes of his talk.
He showed a series of experiments tracking the body’s reaction to infection (sometimes described as inflammation) to the passage of these inflammation signals through the blood brain barrier (the brain’s protective covering) to interact with the microglia. As explained above, we know that the levels of microglia are already raised in neurodegenerative disease. Infection seems to exaggerate the damaging role of microglia – speeding up the loss of nerve cells. The chemical TNF alpha is well known in the medical field for being involved in inflammation. In the prion mouse the effects of microglia can be reduced by blocking TNF alpha. Crucially to MND research, the same chemical block, given to (the SOD1) mouse model of MND delayed onset of symptoms and slightly extended their survival. So its possible that a similar approach might help in people with MND.
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