A recent study suggests that the key to preventing brain damage associated with stroke lies in the hibernation habits of our favorite park denizens: squirrels.
A recent study published in the Foundation of American Societies for Experimental Biology (FASEB) journal by researchers from the United States suggests that hibernating ground squirrels may provide clues to preventing brain damage related to stroke.
During hibernation, a squirrel’s brain experiences dramatically reduced blood flow. It’s the same scenario experienced by human patients after suffering from a particular type of stroke. However, unlike humans, squirrels have the capability to emerge unscathed from their extended naps.
In humans, interrupted or reduced blood supply to the brain usually causes irreversible damage such as paralysis, brain damage, and at the worst, even death.
In the United States alone, 800,000 people suffer from stroke every year, killing nearly 130,000. According to the American Heart Association, stroke is the number five cause of death in the country and one of the leading cause of long-term disability.Researchers found that #squirrels could be the key to prevent brain damage!Click To Tweet
How Squirrels Could Lead to new Treatments in Preventing Brain Damage
The squirrels’ capability to reduce blood flow to their brains during hibernation was deemed similar by scientists from the National Institute of Neurological Disorders and Stroke (NINDS) to the ischemic stroke in humans.
Ischemic stroke is a kind of stroke that causes blood supply containing sugar and oxygen to be cut off to the brain. Such event causes cells to die which often leads to speech impairments and paralysis.
Joshua Bernstock, the first author of the study, said:
“If we could only turn on the process hibernators appear to use to protect their brains, we could help protect the brain during a stroke and ultimately help people recover.”
To date, preventing brain damage caused by cell death during a stroke is done by removing the blood clot from the brain as quickly as possible.
However, John Hallenbeck who led the team of researchers from NINDS found that a certain type of squirrels has a cellular brain process known as SUMOylation that goes into overdrive during hibernation. Hallenbeck suspects that this enables these squirrels’ brains to survive the reduced blood flow. Subsequently, experiments conducted in the cells of mice confirmed his discovery.
SUMOylation normally occurs when an enzyme attaches a molecular tag known as Small Ubiquitin-like Modifier (SUMO) to a protein which alters its activity and location in the cell.
In a report from Doctor NDTV, Bernstock and his colleagues allegedly examined if any of the over 4,000 molecules from the NCATS small molecule collection could boost SUMOYlaytion by blocking SENP called SENP2. In theory, such a procedure could protect cells from a shortage of life-sustaining substances and eventually prevent brain damage.
The researchers were said to use an automated process to examine whether the compounds could indeed prevent SENP2 from blocking the connection between a tiny metal bead and artificial SUMO protein created in the lab of Duke University associate professor and another co-author of the study, Dr. Wei Yang.
“This system, along with computer modeling and further tests performed both in and outside of cells, whittled the thousands of candidate molecules down to eight that could bind to SENP2 in cells and were non-toxic. Two of those – ebselen and 6-thioguanine – were then found to both boost SUMOylation in rat cells and keep them alive in the absence of oxygen and glucose,” Doctor NDTV further reported.
The final experiment suggests that the ebselen boosted SUMOylation in the brains of mice. The researchers are now planning to test if ebselen could protect the brains of animal models of stroke.
Bernstock and the whole team believe that this similar approach could be used in preventing brain damage in humans. Dr. Francesca Bosetti went on to say:
“For decades scientists have been searching for an effective brain-protecting stroke therapy to no avail. If the compound identified in this study successfully reduces tissue death and improves recovery in further experiments, it could lead to new approaches for preserving brain cells after an ischemic stroke.”