Scientists have for the first time explained mechanisms behind the brain's ability to protect itself from damage due to stroke.
The Oxford University researchers hope that harnessing this inbuilt biological mechanism, identified in rats, could help in treating stroke and preventing other neurodegenerative diseases in the future.
"We have shown for the first time that the brain has mechanisms that it can use to protect itself and keep brain cells alive," said lead researcher Professor Alastair Buchan in a statement.
Stroke occurs when the blood supply to part of the brain is cut off. When this happens, brain cells are deprived of the oxygen and nutrients they need to function properly, and they begin to die.
This explains why treatment for stroke is so dependent on speed. The faster someone can reach hospital, be scanned and have drugs administered to dissolve any blood clot and get the blood flow re-started, the less damage to brain cells there will be.
The Oxford University research group have now identified the first example of the brain having its own built-in form of neuroprotection, so-called 'endogenous neuroprotection'.
They did this by going back to an observation first made over 85 years ago. It has been known since 1926 that neurons in one area of the hippocampus, the part of the brain that controls memory, are able to survive being starved of oxygen, while others in a different area of the hippocampus die.
However, what protected that one set of cells from damage had remained a puzzle until now.
"Previous studies have focused on understanding how cells die after being depleted of oxygen and glucose. We considered a more direct approach by investigating the endogenous mechanisms that have evolved to make these cells in the hippocampus resistant," explained first author Dr Michalis Papadakis.
Working in rats, the researchers found that production of a specific protein called hamartin allowed the cells to survive being starved of oxygen and glucose, as would happen after a stroke.
They showed that the neurons die in the other part of the hippocampus because of a lack of the hamartin response. The team was then able to show that stimulating production of hamartin offered greater protection for the neurons.
The researchers were also able to identify the biological pathway through which hamartin acts to enable the nerve cells to cope with damage when starved of energy and oxygen.
The group pointed out that knowing the natural biological mechanism that leads to neuroprotection opens up the possibility of developing drugs that mimic hamartin's effect.
The study was published in the journal Nature Medicine.
