Neural stem cells mature into different types of brain cells, with different functions.
There are some words that just don’t mean what they sound like they should mean. “Senescence” is one such word. While it evokes a mashup of ethereal pleasure and a hair conditioner brand, it is a biological term for the process of deterioration due to aging.
Cellular senescence occurs naturally as we grow older, but it may also contribute to some neurodegenerative diseases, possibly including progressive forms of multiple sclerosis (MS).
That’s what Stephen Crocker, PhD, associate professor of neuroscience at the University of Connecticut School of Medicine in Farmington, found when he and fellow researchers studied neural progenitor cells (NPCs) within the brain matter of people with progressive MS.
They published their results in March 2019 in the journal Proceedings of the National Academy of Sciences.
In PPMS, Brain Stem Cells Age More Quickly
NPCs are sort of like stem cells that are predetermined and targeted to become specific types of brain cells.
Oligodendrocyte progenitor cells become oligodendrocytes, and oligodendrocytes produce myelin, the protective nerve coating that gets damaged in MS — or at least, they’re supposed to produce myelin.
Dr. Crocker’s team found that NPCs in the brain tissue around lesions of deceased patients with progressive MS showed chemical signs of unnatural “aging.”
By “aging,” the researchers were referring to telltale protein activity (or inactivity) in cells that inhibits the NPC from attaining their final stage of development, or properly producing myelin once they do mature.
It appears that oligodendrocytes, which are supposed to fix natural damage to the myelin sheath around nerves, as well as MS-related damage are, in MS patients, not acting their age. They’re acting like much older cells.
The research paper reports that compared with like-aged control patients without MS, those with primary-progressive MS expressed cellular senescence markers.
In a press release, Crocker is quoted as saying, “We know MS is not a disease of the aged, but it may be a disease of aging.”
Treatment With Rapamycin Helped
This is, obviously, an important breakthrough in understanding the mechanism of MS progression. Often these breakthrough discoveries give us hope, but we have to wonder what will come of the practical applications of the research. In this case, however, there is already evidence that something might be done about the cellular senescence.
The researchers report that they were able to reverse the expression of cellular senescence in NPCs of PPMS progenitor cells by treating the cells with the drug Rapamune (rapamycin), also known as sirolimus, an immunosuppressive drug used to prevent rejection of transplanted organs.
There are also a small number of drugs that are being explored as anti-aging medication that may also prove useful in this flank of MS research.
And it’s possible this research into progressive MS may lead to benefit for relapsing forms of the disease, too. Only time will tell. We can only hope that our “aging” neural progenitor cells will stay “young” enough for us to see the outcomes of further research.
