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Medical News Today: New insights into brain inflammation may explain residual disability after stroke

Inflammation is the body’s natural response to injury or “invasion” – it summons immune system cells and agents to repair the damage or deal with the “aggressor.” But sometimes the inflammation response can be too strong and cause harm.
older lady with walking stick sitting by pond
A brain inflammation mechanism may explain why some patients experience residual disability after stroke.

In the brain, inflammation occurs when there is a stroke, or with diseases like Alzheimer’s and Parkinson’s.

Now researchers have discovered some new clues about inflammation in the brain that could lead to new treatments.

The research was led by Dr. Miguel Burguillos when he was based at the University of Lund and the Karolinska Institutet in Sweden. He is now Senior Researcher in Brain and Spinal Injury at Queen Mary University of London in the UK.

In the journal Cell Reports, Dr. Burguillos and colleagues describe new insights about the receptor TLR4 and how it interacts with a protein called galectin-3 to create a vicious cycle that keeps inflammation going.

TLR4 plays a very important role in the innate immune system – the scientists who discovered this won the Nobel Prize in 2011.

The team found that galectin-3 is secreted by microglial cells, a type of immune cell that acts as the first line of defense in the brain.

The protein is absent in healthy brains but present in brains with ongoing inflammation.

‘Self-sustaining’ cycle of brain inflammation

Senior author Tomas Deierborg, associate professor in the Department of Experimental Medical Science at Lund University, explains what they discovered about the interaction between galectin-3 and TLR4:

“The protein binds to the TLR4 receptor and amplifies the reactions that lead to inflammation. More galectin-3 is produced and binds to the immune cells, and the immune response is further intensified in a self-sustaining process.”

To explore the important connection between the receptor and the protein that triggers it, the team used lab tests, animal experiments and human trials.

For example, in one part of the study the team used mice genetically engineered to lack galectin-3 and found they had a lower inflammatory response and less brain damage after a heart attack.

In another part of the study, they found that mice with Parkinson’s disease that also lacked the gene for galectin-3 showed less sign of brain damage.

The researchers also observed how TLR4 and galectin-3 interacted in the brains of people who died of stroke.

Dr. Burguillos says they think the link between the two key players of inflammation in the brain could partly explain the residual disability that often afflicts stroke patients:

“High levels of galectin-3 remain in the brains of these patients long after the stroke, which may explain why the inflammatory response continues to cause damage and does not subside.”

Findings should help develop better drugs to reduce harmful effects of brain inflammation

Galactin-3 was already known to be involved in the brain’s inflammatory response. The protein has not been found in healthy brains – only in brains with inflammation.

Pharma companies are already developing drugs that target galectin-3 to reduce the harmful effects of inflammation in the brain. The researchers hope their new findings will help these developments, says Prof. Deierborg:

“Now that we understand the mechanism, this will make it easier to develop more effective treatments.”

Meanwhile, Medical News Today recently learned of a study that found too much sleep is linked to increased stroke risk. While the researchers did not examine the possible reasons for this, they suggest one explanation could be that a big increase in sleep need may reflect changes in blood flow in the brain.

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