A research team led by Professor Kyoungho Suk from the Department of Pharmacology at the School of Medicine, Kyungpook National University, published findings on May 21, 2026, in the journal Brain Network Disorders. The research details how glial cells interact and communicate during traumatic brain injury.
Traumatic brain injury affects millions of people worldwide every year and remains a major cause of long-term disability, cognitive decline, and neurological complications. Glial cells are non-neuronal cells, including microglia, astrocytes, and oligodendrocytes.
Suk's team conducted a comprehensive examination of how these cells interact, adapt, and communicate during different stages of traumatic brain injury. "Glial cells are remarkably plastic and multifunctional. They can either protect or damage the brain depending on the surrounding microenvironment and injury stage," Suk said.
The research describes how activated microglia release inflammatory molecules that can transform astrocytes into neurotoxic states. Conversely, astrocytes can promote anti-inflammatory microglial responses and support neuronal survival. Oligodendrocytes are responsible for producing myelin around axons; they are vulnerable to traumatic injury and inflammatory stress. Damage to these cells can lead to white matter degeneration and impaired neural signaling.
Acute inflammatory responses following traumatic brain injury help clear debris and initiate repair. However, excessive or persistent activation of inflammation can worsen neuronal death, demyelination, and chronic neurodegeneration. "Understanding these dynamic transitions is critical for developing therapies that preserve beneficial responses while limiting pathological activation," Suk said.
Clemastine fumarate, an FDA-approved antihistamine, is being investigated for its promyelinating effects. "Traumatic brain injury should not be viewed solely as neuronal damage, but as a complex disorder involving coordinated interactions between brain cells and systemic responses," Suk said. "Future therapeutic success will likely depend on combination strategies that integrate glial modulation, regenerative medicine, and personalized interventions," he said. The study's reference is Suk, K. (2026). Neuroglia in traumatic brain injury: Pathophysiology and therapeutic targeting. Brain Network Disorders. DOI: 10.1016/j.bnd.2026.03.002.
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