Clues to repairing human brain found

Toronto, Dec 19 (IANS) New Canadian research holds out hope for repairing and rejuvenating the human brain.

Researchers at Vancouver-based University of British Columbia have found the reasons why the brain loses its capacity to repair itself.

They have identified a protein which represses another protein responsible for the growth of neurons or nerve cells which are the livewire of the brain. These neurons are interconnected - through a mechanism called neural elasticity - to transmit information through the brain and spinal cord.

Led by Ana Mingorance-Le Meur and Timothy O'Connor, the researchers have found that the protein calpain suppresses the protein cortactin, blocking the sprouting of new neurons or nerve cells through neural plasticity.

They said while growing neurons are relatively plastic and can sprout new connections, their plasticity levels drop as they mature and become integrated into neuron networks.

Though this mechanism is used by the brain to regulate these networks from uncontrolled growth, its negative consequence is that the central nervous system is unable to reorganise itself to react quickly to injury or disease.

'This discovery is exciting because we now know that neurons have not lost their capacity to re-grow connections, but instead are under constant repression by the protein calpain,' a university release quoted Ana Mingorance-Le Meur as saying. The study has been published in the European Molecular Biology Organisation (EMBO) Journal.

'If we can target therapies that block this mechanism, then neurons should be able to sprout new connections, therefore stimulating the brain's ability to repair its wiring network.'

In their experiments on animal models, the researchers reduced calpain activity to unlock the sprouting potential of neurons. They found that when calpain activity is reduced, neural plasticity is enhanced.

'The maintenance of neuronal connections is an active process that requires constant repression of the formation of nerve sprouts by the protein calpain to avoid uncontrolled growth,' said Mingorance-Le Meur.

'But a consequence of this role is that calpain limits neural plasticity and the brain's ability to repair itself. The next step is to find a way to enhance neural plasticity without interfering with the good connections that are already in place,' she added.

According to her, drugs that could promote neural plasticity could potentially treat a wide range of neurological disorders, as well as boost the effects of other treatments under investigation.