There are many neurodegenerative diseases, with some common ones being Alzheimer’s disease, Parkinson’s diseases, and multiple sclerosis (MS). These are characterized by the irreversible deterioration of neurons in the central nervous system that can lead to a multitude of symptoms. Multiple sclerosis in particular is a chronic and unpredictable autoimmune disorder. This means it causes the body’s immune system to target and attack the myelin sheath of neurons, leading to a disruption of communication between the brain and the body. There is currently no cure for this disease, but there are many works of research that are in the progress of trying to find possible treatments for MS patients and possible prevention for MS development.
Inflammation was found to impair the ability of
oligodendrocyte precursor cells (OPC) to mature and remyelinate axons,
contributing to the possible causes of multiple sclerosis. However, it was
found that there was a way to protect oligodendrocytes and enhance myelination
in Yanan Chen’s research titled, “Insights into the mechanism of
oligodendrocyte protection and remyelination enhancement by the integrated
stress response.” In this study, she and her colleagues found that activating
the Integrated Stress Response (SR) with compounds like Sephin1 and
bazedoxifene (BZA) were able to accelerate remyelination even under
inflammation. These findings suggested that a combination therapy targeting
both the ISR pathway and OPC differentiation could possibly restore and enhance
neuronal functions in patients with multiple sclerosis. Essentially, a way to
overcome inflammatory damage was found but preparing these oligodendrocyte
precursor cells for myelination does not mean they have the necessary means for
the actual repairing process.
Certain resources are required for remyelination to
occur and a finding related to such is that cholesterol biosynthesis is one of
these critical requirements for remyelination to occur. Rhonda Voskuhl’s work
titled, “Gene expression in oligodendrocytes during remyelination reveals
cholesterol homeostasis as a therapeutic target in multiple sclerosis,” found
that oligodendrocytes upregulate cholesterol synthesis genes during
remyelination and that the activation of estrogen receptor-beta (ERβ) enhances remyelination
as well. This review presents another possible therapeutic strategy that could
be used as treatment for myelin repair in MS patients. If clinically proven to
be able to be done, targeting ERβ could boost remyelination, as it was found to
amplify the expression of the cholesterol synthesis genes that were being
upregulated during remyelination.
By utilizing both of these studies and doing further
research until it reaches clinical human trials, it is possible that treatment
for multiple sclerosis may be achieved if all goes well and side effects are
not too risky. Dr. Chen’s research allows for a way to protect OPCs so that
they are able to be prepared to be differentiated into myelinating
oligodendrocytes even under inflammation where they are getting damaged, by
targeting the ISR with Sephin1 and BZA. This serves almost as a template for
Dr. Voskuhl’s study of what resources are then needed to repair the myelin
sheaths after the damage once they are differentiated. Combining both of these
research studies suggest possible therapeutic processes that could be used to
help treat MS patients, showcasing that they must counteract or overcome
inflammation and support the metabolic demands regarding the resources needed
during remyelination. Both studies fundamentally highlight the importance of
directly supporting oligodendrocytes as a whole rather than focusing on
different aspects of it, such as only looking to enhance remyelination but not
looking to see if it has the resources to do so. Perhaps, future research could
combine these two in a way where they are investigated together to see how
everything would work out cohesively and how this could be applied to actual
patients, or to see what is missing from being able to develop treatment.
Ultimately, the ongoing research on multiple sclerosis and the possible
pathways that could be targeted in order to find a cure is going relatively
well with new findings that support and help these professionals get closer to
being able to treat this unpredictable and debilitating disease.
References
Chen, Y., Quan, S., Patil, V., Kunjamma, R.B., Tokars, H.M., Leisten, E.D., Chan, J., Wong, Y., & Popko, B. Insights into the mechanism of oligodendrocyte protection and remyelination by the integrated stress response. Glia, 71. https://doi.org/10.1101/2023.01.23.525156
Voskuhl, R.R., Itoh, N., Tassoni, A., & Itoh, Y.
Gene expression in oligodendrocytes during remyelination reveals cholesterol
homeostasis as a therapeutic target in multiple sclerosis. Proc. Natl. Acad.
Sci. U.S.A., 116. https://doi.org/10.1073/pnas.1821306116
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