Mayo Clinic Discovers Molecular Switch for Central Nervous System Repair

Researchers Find ‘Molecular Switch’ for Repair of Central Nervous System

Table of Contents

1 Researchers Find ‘Molecular Switch’ for Repair of Central Nervous System
2 Nerve protection and myelin regeneration
3 Repairing the central nervous system
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Researchers at Mayo Clinic have made a discovery that might help correct neural damage in cases of Alzheimer’s disease and other neurological disorders.

Neuron

The scientists reported that they have found a “molecular switch” with the potential of fixing neurological damage in a new study that appeared in the Journal of Neuroscience.

The treatment of people with Alzheimer’s diseases and other neurological conditions is difficult mainly because damage to neurons is deemed permanent in many cases.

But the story may be about to change for the better with the latest discovery by the Mayo Clinic researchers.

In this study, scientists found that the body produces a substance known as myelin when Protease Activated Receptor 1 (PAR1) is genetically turned off. A repair of neurological damage can take place when this fresh production occurs.

“Myelin regeneration holds tremendous potential to improve function,” said lead researcher Dr. Isobel Scarisbrick. “We showed when we block the PAR1 receptor, neurological healing is much better and happens more quickly.”

The senior author said that the findings could play a part in the development of treatments for fighting central nervous system disorders.

Nerve protection and myelin regeneration

Myelin is a fatty substance that surrounds and protects nerves. It serves a somewhat similar function as a wire insulator, shielding electrical signals that are being sent across the nervous system.

An injury to the myelin, or demyelination, causes electrical signals to move slowly between cells in the brain. Loss of sensory and motor function results from this. Damage could be permanent in some cases.

Researchers have found demyelination to be a factor in Alzheimer’s, multiple sclerosis (MS), and some other neurological disorder.

Thrombin, which promotes healing, is believed to inhibit the production of myelin. This effect can result when the amount of the protein gets too high, thereby turning on the PAR1 receptor.

This receptor is also known as the thrombin receptor.

According to the researchers, oligodendrocyte progenitor cells (OPCs) are typically present at demyelination sites. These cells help to promote myelin regeneration.

“These oligodendroglia fail to differentiate into mature myelin regenerating cells for reasons that remain poorly understood,” Scarisbrick said. “Our research identifies PAR1 as a molecular switch of myelin regeneration.”

She explained that blocking the PAR1 receptor turns on myelin regeneration.

Repairing the central nervous system

To arrive at their conclusion, the scientists studied two different experimental mouse models of “demyelinating disease.” One model reflected an acute myelin injury, while the second was that of chronic demyelination.

The models showed signs of myelin loss typical of MS, Alzheimer’s, and other neurological conditions.

The researchers found that a molecular switch turned on myelin regeneration with the switching off of PAR1. This helped to inhibit the undesirable effects of high thrombin levels.

What’s more? The team also discovered a link between PAR1 and brain-derived neurotrophic factor (BDNF) that was not known before.

A highly potent growth system, BDNF is crucial for the health and function of brain cells. Researchers likened it to a fertilizer for these cells.

Another interesting finding was that a drug already approved by the Food and Drug Administration (FDA) has the potential to boost myelin regeneration, going by evidence from laboratory study. The substance blocks the thrombin receptor to achieve this effect.

However, the scientists said they are not advising the use of the drug yet for the treatment of neurological disorders. There is a need for further research to confirm the study results.