A domestic research team reveals a new mechanism for how brain damage progresses after a stroke and identifies a candidate drug that can prevent it through animal testing./Courtesy of pixabay

Stroke strikes out of the blue, threatens life and, even if a person recovers, can leave aftereffects such as paralysis or speech disorders. In particular, ischemic stroke—cerebral infarction—occurs when a blood vessel in the brain is blocked; the faster the treatment, the better the prognosis, but in the field the golden time is often missed.

Lee Chang-jun, head of the Memory and Astrocyte Research Center at the Institute for Basic Science (IBS), said on the 28th that the team, together with researchers at Eulji University, uncovered a new mechanism for how brain damage progresses after stroke and, through animal experiments, identified a potential new drug candidate that can block it. The findings were published the same day in the international journal "Cell Metabolism."

Astrocytes are a type of glial cell that account for a large portion of the brain. True to their name, they are star-shaped and ordinarily help neurons and keep the brain environment stable. When a stroke occurs, they are known to form a "glial scar" around the damaged area to prevent the lesion from spreading further.

However, this study showed that this barrier does not always act protectively. When hydrogen peroxide surges after a stroke, astrocytes are stimulated to produce type I collagen. Collagen is well known as a protein that makes up skin, bone and connective tissue, but in stroke conditions it can accumulate around astrocytes, encase neurons and act as a factor that worsens damage.

Based on this mechanism, the researchers tested their self-developed drug candidate "KDS12025." The compound is designed to reduce hydrogen peroxide and suppress collagen production.

When KDS12025 was administered to a mouse model of stroke, formation of the glial scar and neuronal cell death were greatly reduced. Motor function, which had declined due to stroke, recovered to near-normal levels within a week. Notably, neurological recovery was observed even when the drug was given two days after stroke onset.

The team also confirmed the effects of KDS12025 in a primate model. Three days after administration, lesion size decreased, and after a week, the previously paralyzed hand function recovered. In a test of picking up and eating fruit, the treated monkey succeeded in all 10 attempts.

Yu Seung-jun, a professor at Eulji University, said, "It is meaningful in that hydrogen peroxide and collagen are presented as new targets for stroke treatment," and added, "Given that we confirmed therapeutic effects in a primate model, we expect the work could lead to follow-up clinical studies."

Lee Chang-jun, Director General of IBS, said, "Through research that linked basic research, new drug development and preclinical validation, we presented both the cause of stroke damage and the potential for treatment."

References

Cell Metabolism (2026), DOI: https://doi.org/10.1016/j.cmet.2026.04.001

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