A Reactivation

It's commonly believed that brain cells stop multiplying when our bodies become fully grown. Researchers from the German Centre for Neurodegenerative Diseases (DZNE) theorized that our bodies have a sort of "molecular break", that signals the neurons to stop growing when adulthood is reached. Reawakening neurons past this "break" could be key to treating diseases that cause damage to the neural network.

The scientists searched for the gene causing the molecular break through mice and cell cultures. “That was like looking for the proverbial needle in the haystack. There are hundreds of active genes in every nerve cell, depending on its stage of development," said neurobiologist Frank Bradke, leader of the study.

They found a suspect gene using a data-analysing approach called bioinformatics. "This gene, known as Cacna2d2, plays an important role in synapse formation and function, in other words in bridging the final gap between nerve cells," discussed Bradke.

A Linking Gene

Cacna2d2 controls the structures within a molecular complex that regulate calcium levels. This is essential to communication between neurons. The researchers aimed to reactivate Cacna2d2 using Pregabalin (PGB), a drug used to bind calcium channels within the complex. PGB was adminstered to mice with spinal cord injuries. The researchers observed that new nerve connections grew in the mice.

Credit: DZNE/A. Tedeschi

“Our study shows that synapse formation acts as a powerful switch that restrains axonal growth. A clinically-relevant drug can manipulate this effect,” says Bradke. PGB is presently used to treat lesions of the spinal cord. “PGB might have a regenerative effect in patients, if it is given soon enough. In the long term this could lead to a new treatment approach. However, we don’t know yet.”

The study could lead to a feasible treatment for paralysis together with other neurodegenerative diseases. While the research is far from human testing, the discovery and reactivation of the molecular break is indeed valuable.

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