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How the circadian clock helps the brain recover after injury – Neuroscience News

Summary: NG2-glia, a newly discovered type of brain cell that can renew itself is regulated by circadian rhythms. The findings shed new light on how the body’s circadian clock may promote healing after traumatic brain injury.

Source: National Children’s Hospital

A type of brain cell that can renew itself is regulated by circadian rhythms, providing important insights into how the body’s internal clock can promote healing after traumatic brain injury (TBI), new research from Children’s National suggests. Hospital.

Published in the latest issue of in Euro, the results open new avenues of investigation for future TBI therapies. These injuries are currently only managed with supportive and rehabilitative care, rather than targeted drug treatment options.

The findings also underscore the importance of addressing circadian disruptions to help injured brains heal.

Many cells in the body follow a 24-hour rhythm driven by their genes known as the circadian clock. The Children’s National research team found that a relatively new type of brain cell — known as NG2-glia, or oligodendrocyte precursor cells — also follows a circadian rhythm. This type of cell is one of the few cells to continually self-renew throughout adulthood and is notably proliferative during the first week after brain injury.

“We found evidence for the role of this well-known molecular pathway – the molecular circadian clock – in regulating the ability of these NG2-glia to proliferate, both at rest and after injury,” said Terry Dean. , MD, Ph.D., critical care specialist at Children’s National and senior author of the article.

“This will serve as a starting point to further study the pathways controlling cell regeneration and optimizing recovery after injury.”

Sometimes called the “silent epidemic,” TBI affects an estimated 69 million people worldwide each year, with injuries ranging from mild concussions to severe injuries that result in death or lifelong disability.

Many cells in the body follow a 24-hour rhythm driven by their genes known as the circadian clock. Image is in public domain

In the United States alone, approximately 2.8 million people experience TBI each year, including 630,000 children. TBI is the leading cause of death in people under the age of 45, and those who survive are often left with persistent physical, cognitive, and psychological disabilities.

Yet no targeted therapy exists for TBI, creating a critical need to discover the mechanisms that could unlock the regeneration of these NG2-glia cells, which are the most common type of brain cells known to proliferate and self-renewing in adult brains.

“Knowing that cell turnover is coordinated with time of day is critical for researchers,” said Vittorio Gallo, Ph.D., acting academic director and acting director of the Children’s National Research Institute. “With this knowledge, we can dig deeper into the body’s genetic healing process to understand how cells regulate and regenerate themselves.”

About This TBI Research News

Author: Katie Shader
Source: National Children’s Hospital
Contact: Katie Shrader – National Children’s Hospital
Image: Image is in public domain

Original research: Access closed.
“Endogenous circadian clock machinery in cortical NG2-glia regulates cell proliferation” by Terry Dean et al. in Euro

See also

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Summary

Endogenous circadian clock machinery in cortical NG2-glia regulates cell proliferation

The molecular circadian clock is found throughout the body and is essential for synchronizing cellular physiology with the 24-hour day. However, the role of the clock in regulating the regenerative potential of the brain has not been explored.

Here, we report that murine NG2-glia, the largest population of proliferating cells in the mature central nervous system, rhythmically express circadian clock genes over a 24-hour period, including the critical clock component Bmal1 BMAL1 RNA and protein.

Interestingly, daily NG2-glia proliferation occurs preferentially during the time of day when Bmal1 expression is elevated, while conditional knockout (CKO) of Bmal1 decreases both cortical NG2-glia density and cell proliferation.

Additionally, in a neurotrauma model, we show that pathology-induced NG2-glia proliferation also depends on Bmal1 expression.

Since circadian rhythm disturbances are common in neurological disorders across the lifespan, including head trauma, these findings have important implications for cellular regeneration in brain injury and disease.

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