Amyotrophic lateral sclerosis (ALS) is said to be a progressive and lethal disease caused by the deterioration of motor neurons which are the nerve cells in the central nervous system that apparently manage voluntary muscle movement.
A new research from the Instituto Clemente Estable and the University of the Republic in Montevideo, Uruguay, and at Oregon State University claims that new findings have been made as to how a higher level of lead, which is a neurotoxic heavy metal, could slow the development of ALS or Lou Gehrig’s disease.
The discoveries apparently astonished researchers, since lead is also claimed to be an identified risk factor for ALS. But scientists are of the opinion that this occurrence could result in potential different approaches to the gene therapies.
“We know that environmental exposure to lead is a risk factor for ALS. That’s why it’s so surprising that, according to studies done with laboratory animals, higher levels of lead appear to significantly reduce motor neuron loss and progression of ALS,” commented, Joseph Beckman, holder of the Ava Helen Pauling Chair in the Linus Pauling Institute and director of the Environmental Health Sciences Center at OSU.
Research may carry on exploring the essential methods that could be causing this. But the discoveries also raise instant queries about the chelation therapy in efforts to treat ALS. Several people have attempted in spite of no proof that it works. Chelation therapy apparently tries to get rid of heavy metals from the body, counting lead.
As per Beckman, a few of the results about the function of lead in this disease apparently resulted out of the joint research OSU is performing with universities in Uruguay, where considerable amount of children from impoverished families are said to be enduring lead poisoning caused by setting up camps over deserted lead factories close to Montevideo.
Lead seems to have some communication with astrocytes, which is a special kind of cell that is alleged to affect the spread of ALS. Astrocytes are believed to be a chief constituent of brain cells. In healthy systems, it apparently assists in supporting neurons, shielding them against infection and injury and eliminating neurons when they become impaired.
This procedure, nonetheless, might get interrupted in ALS, at which point astrocytes are thought to play a function in causing unsuitable motor neuron death.
Beckman mentioned, “These systems are very carefully balanced and many factors have to work together. The proper functioning of astrocytes is essential to life, but their dysfunction may lead to disease. We think that lead somehow is modulating the neuroinflammatory actions of astrocytes and, in the case of ALS, helping to shift their balance back to one of protection, rather than damage.”
When that happens, it seems that astrocytes could fuel the manufacturing of ‘vascular endothelial growth factor,’ which in turn could shield motor neurons. There appears to be a surge in this growth factor as a probable method to aid in treating ALS.
More research is apparently needed to find out whether the mechanisms by which lead has this defensive effect could assist in identifying pharmacological targets for the disease.