Researchers at Duke University have developed a new injectable biomaterial that shows promise in helping the brain recover after an ischemic stroke, a type of stroke caused by a blockage in a blood vessel. In experiments with mice, the material helped transform the empty space left by damaged brain tissue into a more healing-friendly environment. The treatment worked by recruiting the body's immune cells, encouraging new blood vessel growth, supporting changes in brain tissue, and improving motor function in the animals. These findings were published in the journal Cell Biomaterials. The biomaterial used in the study is called MAPS, or microporous annealed particle scaffolds. It consists of tiny hydrogel particles that assemble into a porous structure. This structure provides a framework for cells to enter and rebuild damaged neural tissue. Scientists collected extracellular vesicles (EVs) from lab-grown astrocytes, which are brain cells that support neurons. These EVs were combined with signaling molecules designed to attract immune cells, promote blood vessel repair, and improve brain function. Instead of injecting the EVs directly, the researchers chemically attached them to the hydrogel particles. This method kept the signals concentrated in the damaged area, increasing the chances that the cells would interact with them effectively. One combination of signaling molecules proved especially effective: IL-4 and C1q. These molecules were particularly good at attracting immune cells that could help repair the brain, including macrophages and a type of cell called neutrophils. Neutrophils are often linked with inflammation and damage in the early stages of a stroke, but the study found that under the right conditions, they might support tissue repair later on. When the researchers reduced the number of neutrophils, blood vessel formation dropped significantly, and the scaffold didn't remodel as effectively. The treatment also led to the growth of new blood vessels within the stroke-damaged area. Scientists observed more axonal fibers—structures that help brain cells communicate—both inside and around the injured region. These biological changes were accompanied by improved movement in the mice. When tested on a grid-walking task, the treated mice performed better, making fewer mistakes in placing their forelimbs. By eight weeks, their performance was statistically similar to that of healthy mice, and the improvement remained consistent throughout the study. The researchers also tested whether the EVs could have the same effect without the biomaterial scaffold. They found that without the scaffold, the EVs did not promote blood vessel repair. This suggests that the scaffold's structure and ability to concentrate the EV signals were crucial for the healing process. However, the treatment is still in the preclinical stage, and further research is needed to evaluate its safety, understand the role of different immune cells in recovery, and test its effectiveness in models that more closely resemble human stroke. Researchers are also working to source EVs from human-induced pluripotent stem cell-derived astrocytes, which could offer a more scalable and clinically relevant option.