THEY say that you can’t teach an old dog new tricks. And scientists have discovered why.
Researchers at Harvard Medical School believe that they have found the biological mechanism that makes people become set in their ways as they get older. They have identified a protein that stops new neural connections forming in adult brains.
The link between ageing and intransigence is commonly put down to a combination of world-weariness, experience and impatience. The scientists say that a mechanism involving the protein, called PirB, may explain the change in attitude.
They found that it settled the highly adaptable brains of children into a more stable, less flexible state by adulthood.
The findings could offer hope for victims of brain injury and strokes, after which the stability of the brain limits its ability for self-repair.
Normally, the connections in the brain that form and rewire during childhood become more fixed later in life. This is why human beings are so versatile and receptive to learning earlier in life and become less flexible with age.
Keeping connections fixed in the same place is normally an advantage, but after brain injury it would be helpful to have more flexibility. Being able to form new pathways might also allow adults to learn a new language, for example, with the facility of a child.
The results of the study, which are published in the journal Science Express, indicated that the brains of adult mice that lacked PirB retained the same rewiring ability of much younger brains. Without PirB to hold them back, the old mice were, in effect, able to learn new tricks.
Josh Syken, the lead researcher, said that the discovery could mean a quicker, fuller recovery for people who suffer strokes or brain trauma.
“In brain injury and strokes, pathways in the brain are broken,” he said. “In a normal adult brain, these connections are lost forever. By inhibiting the proteins that stop new connections growing, it may be possible for stroke victims to recover those missing links.”
The research could have implications for sufferers of epilepsy. This is caused by too many connections forming in the brain, which can lead to seizures. Increasing the presence of the protein could help to prevent inappropriate connections forming.
Dr Syken said that his team expected the same to be true in the human brain and the next step was to replicate the findings in people. The goal would be to design drugs that would target the protein in order to promote or inhibit the brain’s rewiring potential.
Previous research by the same scientists pinpointed the genes that encourage brain flexibility in early development.
Immediately after birth the brain is bombarded with sensory information. These genes instruct nerve cells to connect to form appropriate pathways, for instance between the eye and the “visual” area of brain.
Dr Syken said that this genetic research was more difficult to translate into therapy. “There are maybe 30 different versions of this gene, so it is hard to target with drugs,” he said.
“The great thing about the new protein we have found is that it is the same for everyone. If you could make a drug to target this, it would be like a skeleton key which could be used on anyone.”
GREY MATTER
