Scientists have long used animal models to further their understanding of the human body. But now, researchers from Oregon Health & Science University have used animal models to accomplish something truly extraordinary. Science Daily reports that the researchers successfully used a synthetic thyroid hormone to regulate a gene implicated in neurodegenerative diseases – diseases like Alzheimer’s, Parkinson’s, and multiple sclerosis. Read on to find out more about the implications of this groundbreaking study.
Using Animal Models to Regulate a Crucial Gene
In a brief shared with Science Daily, researchers at Oregon Health & Science University explained the key to better understanding neurodegenerative diseases: animal models created from tests in cells and mice. This research marks the first time that researchers have used a synthetic thyroid hormone to regulate a gene implicated in these debilitating diseases – the TREM2 gene, specifically. Per Science Daily, the research explained below could “raise the possibility of development of new medication to treat debilitating diseases.”
The Importance of the TREM2 Pathway
First, what is the TREM2 gene? Medline Plus explains that this gene “provides instructions for making a protein which serves as a ‘triggering receptor’ expressed on myeloid cells.” Myeloid cells are produced in bone marrow, and they form myelin, a protective sheath that covers certain nerve fibers. Myelin is damaged in disorders like multiple sclerosis. In order to reduce the effects of diseases like multiple sclerosis, scientists would need to reduce damage to myelin – but how? It all comes back to the TREM2 gene. The Oregon Health & Science researchers discovered that they could “increase the expression of TREM2.” But what, exactly, does that mean?
Animal Models and TREM2: Why Do They Matter?
TREM2 plays a role in multiple sclerosis, but that’s not all. Science Daily cites previous research indicating a link between genetic variants of TREM2 and Alzheimer’s disease. In other words, TREM2 plays a role in a variety of neurodegenerative conditions. Before now, scientists didn’t understand how to control TREM2 expression; now, the Oregon Health & Science team has cracked the code. The researchers started with a compound that was originally developed to lower cholesterol. Eventually, they created an analog of that compound – an analog meant to penetrate the central nervous system of mice. The researchers soon discovered that the compound increased the expression of TREM2 in the mice, thus reducing ongoing myelin damage.
Implications of the Study
Ultimately, the compound analog used in this study may pave the way for groundbreaking treatments for neurodegenerative diseases like Alzheimer’s, Parkinson’s, and multiple sclerosis. “TREM2 is a receptor,” one researcher explained to Science Daily. “It senses damaged cellular debris from disease and responds in a healing, productive way. The thought is, if you can simply turn up its expression, then that’s going to lead to a therapeutic effect in most neurodegenerative diseases.” In other words, TREM2 could become a “target” for disease treatment, which could revolutionize the therapeutic approach to similar diseases.
This study’s promising results will, hopefully, contribute to life-changing new drugs for individuals with Alzheimer’s, Parkinson’s, and other neurodegenerative diseases. Fortunately, those drugs may be much closer than one might think. “The possibility of doing clinical trials is not millions of miles away,” one researcher said. “It would be an achievable thing.”
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