UCLA neuroscientists first to show that adult brains turn back developmental clock to repair damage

A new study by UCLA neuroscientists shows for the first time that a unique pattern of cellular activity found in early brain development also triggers repairs to damaged adult brains. The findings, appearing in the July 15 edition of the peer-reviewed Journal of Neuroscience, hold implications for treating brain damage caused by stroke and other disorders.

Researchers in the Department of Neurology and Brain Research Institute at UCLA used rat models to show how cells in brains damaged with stroke-like lesions, caused by interruption of blood flow, develop slow synchronous activity. This activity triggers cells to sprout new connections into areas of the brain disconnected by the lesion.

"Our research shows for the first time that this activity works to trigger repairs in adult brains," said Dr. Marie-Francoise Chesselet, professor of neurology at the David Geffen School of Medicine at UCLA and study co-author. "Previously this activity has been identified as a key component of brain development."

Scientists and clinicians had recognized this pattern of activity for many years after brain injury in humans, but its function remained unknown. This new research suggests that these cellular rhythms may be signaling a repair process in the human brain after injury.

"On its own, a damaged brain has a limited ability to repair itself. Recovery is partial," said Dr. S. Thomas Carmichael, assistant professor of neurology at UCLA and study co-author. "A better understanding of how the brain recovers from injury will allow us to manipulate the repair process and to maximize recovery from brain damage caused by stroke and other disorders."

The researchers made their discovery using a model of brain injury that allowed them to isolate signals specific to the sprouting of new connections from other changes that occur because of damage. They then measured the frequency, power and synchroneity of brain activity in a model that induced sprouti

Contact: Dan Page
University of California - Los Angeles

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