A genetic adaptation that helps animals like yaks and Tibetan antelopes survive in low-oxygen environments could open up a new pathway for repairing nerve damage in humans, according to a new study.
Researchers say the mutation may aid in restoring damaged nerve insulation, known as myelin, in conditions such as multiple sclerosis and cerebral paralysis. The findings, published in the journal Neuron, point to a natural biological process that could potentially be harnessed using molecules already present in the human body.
Lead researcher Liang Zhang from Songjiang Hospital, affiliated with Shanghai Jiao Tong University School of Medicine, said evolution offers valuable insights into how organisms adapt and survive in extreme conditions, and much remains to be learned from these natural genetic changes.
The study highlights the importance of myelin, a protective layer surrounding nerve fibres in the brain and spinal cord that ensures efficient transmission of electrical signals. Damage to this layer, particularly due to low oxygen levels during early brain development, can lead to cerebral paralysis in newborns.
In adults, myelin damage is a key feature of multiple sclerosis, a condition in which the immune system attacks nerve insulation. Reduced blood flow to the brain, often associated with ageing, can also harm myelin and contribute to disorders such as vascular dementia.
Previous research found that animals living in high-altitude regions like the Tibetan Plateau carry a mutation in a gene called Retsat, believed to support brain function in low-oxygen conditions.
To explore this, scientists exposed newborn mice to oxygen levels similar to those found at high altitudes. Mice with the Retsat mutation performed better in learning, memory and social behaviour tests compared to those without it. Their brains also showed higher levels of myelin.
Further experiments revealed that the mutation also supports faster and more complete repair of damaged myelin, similar to what is seen in multiple sclerosis. The affected areas contained more mature oligodendrocytes, the cells responsible for producing myelin.
The researchers also discovered that mice with the mutation had higher levels of ATDR, a compound derived from vitamin A, in their brains. This appears to enhance the conversion of vitamin A into active forms that promote the growth and development of oligodendrocytes, helping rebuild the myelin sheath.
When ATDR was given to mice with a condition similar to multiple sclerosis, the animals showed reduced disease severity and improved movement.
The findings suggest a potential new approach to treating myelin-related diseases. Unlike current therapies for multiple sclerosis, which mainly focus on suppressing the immune system, this method could use naturally occurring molecules to promote nerve repair.
The study received support from several Chinese national and regional research programmes, including major science and technology initiatives and talent development funds.
#From Science Daily