How brain connectivity is disrupted by inflammation after a stroke

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When people suffer from conditions like stroke or Alzheimer’s, their brains often become inflamed.

This inflammation is damaging and can lead to severe cognitive problems and even death.

While it’s been known for a long time that intense inflammation can destroy brain cells (neurons), new research from the University of California, San Francisco (UCSF) shows that even mild inflammation can be harmful.

The study, published recently in Cell Reports, revealed that mild inflammation doesn’t necessarily kill neurons. Instead, it damages the neuron’s extensions, known as neurites.

These neurites are crucial as they connect neurons to each other, facilitating brain functions such as learning and memory.

This discovery opens up a new understanding of brain damage, showing a specific way inflammation disrupts brain function.

The research conducted by Dr. Raymond Swanson and his team at UCSF and the San Francisco Veterans Affairs Medical Center focuses on the subtle yet harmful effects of inflammation.

They found that in diseases like Alzheimer’s and after a stroke, inflammation doesn’t kill the brain cells directly but damages the neurites. These are like the wiring that connects different parts of a machine—if the wiring is damaged, the machine can’t operate properly.

This understanding came from studies involving laboratory mice. The researchers induced inflammation in parts of the mice’s brains that control movement.

They noticed that while the mice struggled with motor skills, the neurons were not dead; instead, the neurites were severely damaged. This left the neurons isolated, unable to communicate effectively, which was enough to impair the mice’s ability to move properly.

Further experiments showed that the inflammation made immune cells release a chemical called superoxide, which caused proteins inside the neurites—specifically cofilin and actin—to clump together into structures known as cofilactin rods (CARs).

These CARs block the normal function of neurites. By manipulating levels of superoxide or cofilin, the researchers were able to protect neurites from damage and preserve the mice’s motor functions.

This new pathway from inflammation to neurite damage presents a potential target for new treatments. Many neurological diseases, such as multiple sclerosis, traumatic brain injury, and ALS, involve inflammation.

Understanding how this inflammation leads to neurite damage provides a crucial insight for developing drugs that could interrupt these processes.

Dr. Swanson highlighted that there are several promising drugs now entering clinical trials that target these inflammatory processes. These findings underscore the importance of looking at how these drugs can protect neurites in patients with neurological conditions.

This research offers hope for treating and possibly preventing the damage caused by various neurological diseases.

By targeting the specific mechanisms of inflammation-induced damage to neurites, new therapies might better protect brain function, especially in aging populations where inflammation tends to have a more pronounced effect.

If you care about stroke, please read studies about how to eat to prevent stroke, and diets high in flavonoids could help reduce stroke risk.

For more information about health, please see recent studies about how Mediterranean diet could protect your brain health, and wild blueberries can benefit your heart and brain.

The research findings can be found in Cell Reports.

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