Researchers find molecular switch to make old brains young again
By Darren Quick
March 7, 2013
It’s no secret that juvenile brains are more malleable and able to learn new things faster than adult ones – just ask any adult who has tried to learn a new language. That malleability also enables younger brains to recover more quickly from trauma. Researchers at Yale University have now found a way to effectively turn back the clock and make an old brain young again.
As we enter adulthood, our brains become more stable and rigid when compared to that of an adolescent. This is partially due to the triggering of a single gene that slows the rapid change in synaptic connections between neurons, thereby suppressing the high levels of plasticity of an adolescent brain. By monitoring the synapses of living mice for a period of months, the Yale researchers were able to identify the Nogo Receptor 1 gene as the key genetic switch responsible for brain maturation.
They found that mice without this gene retained juvenile levels of brain plasticity throughout adulthood and by blocking the function of this gene in old mice, the researchers were able to reset the old brain to adolescent levels of plasticity. This allowed adult mice lacking the Nogo Receptor to recover from brain injury as quickly as adolescent mice, and also saw them master new, complex motor tasks faster than adult mice with the receptor.
“This raises the potential that manipulating Nogo Receptor in humans might accelerate and magnify rehabilitation after brain injuries like strokes,” said Feras Akbik, Yale doctoral student.
The researchers also showed that the Nogo Receptor slows the loss of memory, so that mice without the Nogo Receptor lost stressful memories more quickly than those with the receptor. The researchers say this suggests that manipulating the receptor could help treat those suffering post-traumatic stress disorder.
“We know a lot about the early development of the brain. But we know amazingly little about what happens in the brain during late adolescence, said Dr. Stephen Strittmatter, Vincent Coates Professor of Neurology, Professor of Neurobiology and senior author of the paper which appears in the journal Neuron.
Source: Yale University