Oxidative stress (OS) as a biomarker for multiple sclerosis (MS) and disease progression is the subject of studies being conducted around the world.
These studies are showing success at stopping and reversing the damage done by the demyelination caused by OS.
Known for years as an instigator of inflammation, OS is also considered to be neurodegenerative. Recent observations confirm the fact that OS is also an important factor associated with demyelination in MS.
OS is caused by an imbalance in free radicals that damage the nucleic acids, proteins, and lipids in the body. This is what creates inflammation. The byproduct of this action creates markers for OS.
The role of stress in MS
OS markers can be used to determine the progression of MS.
These markers are also showing success as predictors of high disability in MS, helping direct the course of treatments recommended by medical professionals.
Chronic inflammation causes damage to the central nervous system and is attributed to MS. By calming this activity, researchers believe they have the ability to slow down disease progression.
Understanding the role of OS in MS appears to be vital.
Multiple sclerosis is generally divided into three types: Relapsing-remitting (RRMS), secondary progressive (SPMS), and primary progressive (PPMS).
The recent studies are showing that inflammation is the key instigator for relapses in RRMS, while permanent nerve damage is the root of PPMS and SPMS.
Activating a pathway
This nerve damage was thought to be permanent, but studies are now showing that OS can be halted by activating the Nrf2 pathway in the human body.
The Nrf2 pathway is a powerful protein found in every cell throughout the body. It regulates the antioxidant stress defense.
By activating it, researchers say that remyelination can occur. When remyelination occurs, the progression and disability from MS can be slowed down or even reversed.
Looking at OS at each stage of MS is a key element in understanding how the disease progresses.
OS markers can predict high disability in MS and are associated with different aspects of disease progression.
New disease modifying drugs designed to treat MS target OS pathways.
Researchers say that activating one’s own self-defense mechanisms such as the Nrf2 pathway, the body can fight free radicals and slow down the damage caused by MS.
When Nrf2 is activated, it produces antioxidant enzymes such as catalase, glutathione, and superoxide dismutase (SOD). These antioxidant enzymes are powerful enough to neutralize many free radicals. Studies show that activated Nrf2 successfully slowed down the rate of demyelination.
The role of antioxidants
Antioxidants such as vitamin C, vitamin E, berries, and juices have typically been used to neutralize free radicals and prevent the damage they cause.
One molecule of antioxidants from these sources neutralizes one free radical. However, there is a tipping point where the antioxidants are inadequate to take care of the damage, and additional help is needed.
Myricetin is an antioxidant shown to mitigate demyelination. Plants such as Barleria lupulina are showing benefits to the Nrf2 pathway and warrant further research on their effects on MS and other neurodegenerative diseases.
It was also reported that melatonin —10 milligrams daily for 30 days — caused a statistically significant increase in antioxidative enzymes, benefitting the Nrf2 pathways.
While research shows therapeutic potential lies in antioxidants, using OS markers as biomarkers of MS severity or relapse could be a helpful diagnostic tool.
And due to their ability to reduce OS, adding antioxidants to immunotherapy may be beneficial for people with MS.
Continued research on OS, antioxidants, and the Nrf2 pathway could provide more solutions for people with MS.