In experiments involving mice, the treatment helped damaged brain tissue develop new blood vessels, supported the growth of nerve fibres and improved movement.

The researchers say the approach works partly by creating an environment that encourages the body's own immune cells to participate in the healing process.

Ischemic strokes occur when a blood clot blocks blood flow to part of the brain.

Emergency treatments can restore circulation and protect brain tissue that has not yet died. However, once brain tissue is permanently damaged, restoring blood flow cannot bring the lost tissue back.

Severe strokes can therefore leave a cavity where healthy brain tissue once existed.

Rehabilitation can help the brain's surviving circuits adapt, but it does not directly rebuild the damaged area.

To address this problem, Duke researchers developed a material known as a microporous annealed particle scaffold, or MAPS.

It is made from tiny hydrogel particles that form a porous structure, creating space where cells can enter and potentially support tissue repair.

The researchers combined the scaffold with extracellular vesicles produced by astrocytes, star-shaped cells found in the brain.

Extracellular vesicles are tiny packages released by cells that carry biological signals, including proteins, lipids and genetic material, which can influence other cells.

Rather than injecting these vesicles alone, the researchers attached them to the surface of the hydrogel particles.

This helped keep the signals concentrated in the damaged area, allowing incoming cells to interact with them.

The scientists found that a combination of two signalling molecules, IL-4 and C1q, was particularly effective at attracting immune cells to the damaged region.

Among the cells recruited were macrophages and neutrophils.

Neutrophils are commonly associated with inflammation and tissue damage during the early stages of stroke, but the study suggests they may have a different role later in recovery when exposed to the appropriate signals and environment.

When researchers reduced the population of neutrophils, the formation of new blood vessels decreased and the scaffold underwent less remodeling.

This suggested that the cells were contributing to the repair process.

The treatment also produced physical improvements in the mice. Researchers observed more axonal fibres in and around the damaged area.

Axons are structures that allow nerve cells to communicate with one another.

The treated mice also performed better on a grid-walking test that measures movement and coordination.

After eight weeks, their performance was statistically similar to that of healthy control mice, and the improvement continued for the rest of the study.

The researchers also tested the extracellular vesicles without the biomaterial scaffold.

The vesicles alone did not produce the same level of blood vessel repair, suggesting that the scaffold itself plays an important role by keeping the biological signals concentrated within the injured area.

Despite the promising results, the treatment is still at an early, preclinical stage.

The experiments so far have been conducted in mice, with the material injected directly into the damaged part of the brain.

More research is needed to determine the treatment's safety, understand how different immune cells contribute to recovery and establish whether the approach can work in larger animals and eventually humans.

The research team is also exploring the use of extracellular vesicles produced by human induced pluripotent stem cell-derived astrocytes, which could provide a more scalable and clinically relevant source of the therapeutic material.