Squirrels could hold the key to helping stroke patients avoid brain damage, according to scientists.
Researchers in the US have discovered that in hibernating squirrels, a protective process occurs in cells, which allows their brain to function even with reduced blood flow and oxygen.
On awakening the animals do not suffer any ill-effects despite being deprived of essential nutrients.
During an ischemic stroke the blood supply, which supplies sugar and oxygen, to the brain gets cut off, causing cells to die, which often leads to paralysis and speech problems.
According to scientists from the National Institute of Neurological Disorders and Stroke (NINDS), by creating a drug, which could trigger the same cellular changes of hibernating squirrels, it may be possible to prevent brain damage.
"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," said first author Joshua Bernstock, a graduate student at NINDS, The Telegraph reported.
Around 100,000 people suffer strokes each year in the UK, and 85 per cent suffer ischemic strokes, leaving almost two thirds of the survivors with a disability. There are 1.2 million people in the UK who are suffering the after-effects of a stroke.
''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,'' said researcher Francesca Bosetti.
The researchers led by John Hallenbeck found that a cellular process called SUMOylation goes into overdrive in a certain species of ground squirrel during hibernation. Hallenbeck suspected that the animals' brains survived the reduced blood flow caused by hibernation due to the process. This was confirmed in subsequent experiments in cells and mice confirmed his suspicions.
In SUMOylation, an enzyme attaches a molecular tag called a Small Ubiquitin-like Modifier (SUMO) to a protein, which alters its activity and location in the cell. Other enzymes called SUMO-specific proteases (SENPs) then detach those tags, thereby decreasing SUMOylation. First author Bernstock and his colleagues studied more than 4,000 molecules from the NCATS small molecule collections for the ability to boost SUMOylation by blocking a SENP called SENP2, which would theoretically protect cells from a shortage of life-sustaining substances.
The researchers found that of the thousands of molecules, two ebselen and 6-thioguanine could both boost SUMOylation in rat cells and keep them alive in the absence of oxygen and glucose.