Researchers in Norway have discovered the HCAR1 gene can help repair brain damage caused by a lack of oxygen at birth. Scientists from the University of Oslo (UIO) found when mice had their HCAR1 gene removed, they showed little regeneration of cells compared to unaffected mice.
Hypoxic-ischemic brain damage is the most common cause of death and injury in newborn babies and is caused when the supply of blood and oxygen to the brain is blocked. “The lack of blood and nutrients causes brain cells to die. These babies can then suffer from neurological disorders such as cerebral palsy”, said researcher and associate professor at UIO, Johanne Egge Rinholm.
In a recently published essay, Rinholm and her team at the Institute of Basic Medical Sciences at UIO and Oslo University Hospital, outline the findings of their experiments with the HCAR1 gene receptor. A receptor is a protein that activates a response inside a cell, and it was discovered that the HCAR1 receptor helped to repair brain damage.
How the research was conducted
The researchers experimented on a group of newborn mice whose HCAR1 gene had been removed and another group of unaltered mice. They found the brain tissue in the unaffected mice was partly restored over the 42 days following the brain damage. The mice lacking the HCAR1 gene showed little or no sign of repair. It was also recorded, that the unaltered mice produced new cells that were capable of repopulating injured areas of the brain. Conversely, mice without the HCAR1 gene showed few signs of cell regeneration after brain damage.
The next step for researchers is to find out how the same effects can be achieved in humans. Rinholm’s data identified that the HCAR1 gene is an important factor in the repair of hypoxic-ischemic injury, which commonly occurs in human babies. The current treatment used, involves cooling the newborns down and Rinholm has emphasised that “drugs are needed that can protect the brain and help to generate new brain cells”. Under current treatment, many babies suffer from long-term brain damage.
Effects of lactate on brain damage
The scientists were also keen to research HCAR1 due to its relationship with lactic acid. Lactic acid, and its less acidic form, lactate, is produced when muscles are forced to perform strenuous exercise. However, lactic acid can also be produced in the brain. Previous experiments on mice have indicated that extra injections of lactate into the brain could improve brain damage rehabilitation. Until Rinholm’s research, the reason for this had been unclear.
Lactate works similarly to sugar, providing cells with metabolic energy. The research revealed that lactate could also function as a signalling molecule that helps to transmit information to surrounding cells. According to their findings, this happens when lactate binds to the HCAR1 receptor.