Lingering Brain Inflammation Prolongs Disability After Stroke

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Researchers have identified a mechanism that perpetuates inflammation in the brain of victims of stroke or neurodegenerative diseases like Alzheimer’s and Parkinson’s disease.

The receptor TLR4, which plays an important role in the innate immune system, interacts with protein galectin-3 to continue creating inflammation in the brain. Galectin-3 is not found in healthy brains, as it is the brain’s first line of defense in trauma.

Researchers from the University of Lund and the Karolinska Institutet in Sweden found that the protein binds to the TLR4 receptor and enhances the reaction that leads to inflammation, creating a self-sustaining immune response process. This constant level of inflammation can continue to cause damage, like the residual kind that is seen in stroke patients.

In lab tests and animal models, the researchers found that those who lack galectin-3 have a lower inflammatory response and less brain damage after heart attack; a similar response was observed in mice with Parkinson’s disease.

Pharmaceutical companies are already at work developing drugs that target galectin-3 in hopes of reducing inflammation in the brain. 

Epilepsy drug for stroke
Lingering Brain Inflammation Prolongs 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. 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.

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