Medical

Protein shown to slow progress of Alzheimer’s and multiple sclerosis

Protein shown to slow progress of Alzheimer’s and multiple sclerosis
Brain plaques (seen in blue) and other debris are normally swept away by cells called microglia (seen in green). But this process is impacted when the microglia is missing a protein called TREM2, as in the image above (Image: Yaming Wang, Bernd Zinselmeyer/Washington University in St Louis)
Brain plaques (seen in blue) and other debris are normally swept away by cells called microglia (seen in green). But this process is impacted when the microglia is missing a protein called TREM2, as in the image above (Image: Yaming Wang, Bernd Zinselmeyer/Washington University in St Louis)
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Brain plaques (seen in blue) and other debris are normally swept away by cells called microglia (seen in green). But this process is impacted when the microglia is missing a protein called TREM2, as in the image above (Image: Yaming Wang, Bernd Zinselmeyer/Washington University in St Louis)
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Brain plaques (seen in blue) and other debris are normally swept away by cells called microglia (seen in green). But this process is impacted when the microglia is missing a protein called TREM2, as in the image above (Image: Yaming Wang, Bernd Zinselmeyer/Washington University in St Louis)

Researchers have identified a promising new target in the battle against certain neurological diseases. A protein known as TREM2 has been proven effective in clearing away unwanted debris in the brain, the unchecked buildup of which can lead to both Alzheimer's disease and multiple sclerosis (MS).

Earlier research has suggested that variants of the TREM2 protein are related to neurological diseases, such as dementia, Alzheimer's disease, Parkinson's disease and amyotrophic lateral sclerosis. Located in brain cells called microglia, the protein carries out the task of maintaining and repairing the body' central nervous system, leading researchers to think it could function as a trigger in treating such conditions.

Scientists at the Washington University School of Medicine in St Louis undertook two independent studies exploring the ability of the TREM2 protein to keep the brain free of debris.

The first investigated its ability to treat Alzheimer's. One of the contributing factors to the onset of this condition is the buildup of brain plaques, which are made up of proteins known as amyloid beta. These proteins are meant to be cleared away naturally, but when they are able to accumulate they can cause damage to the synapses and result in symptoms like memory loss.

The research team bred mice without the TREM2 gene with mice that were engineered to have an Alzheimer's-like condition. They then tracked the buildup of the amyloid beta proteins in the offspring and observed that the absence of the TREM2 gene greatly increased the rate of accumulation.

"We found that microglia cluster around amyloid plaques when TREM2 is present, presumably because the cells are getting ready to absorb the plaques and break them down," says Marco Colonna, a Professor of Pathology at Washington University. "When TREM2 is absent, this clustering does not occur."

The second study was to explore the role of TREM2 in the onset of MS. A factor in the development of this disease is thought to be attacks by immune cells, mistakenly aimed at a protective layer on the nerve cells called myelin. This process sees fragments of myelin remain lodged in the brain tissue, compounding the effects of condition and impairing the ability of the brain to repair itself.

Working with mice who were missing the TREM2 gene, the scientists treated the rodents with cuprizone, a compound that mimics MS by creating a loss of myelin.

"When we give normal mice this chemical, they can clear most of the myelin fragments from the brain," says Laura Piccio, PhD assistant professor of neurology and senior author of one of the studies. "But when we gave cuprizone to mice that did not have the gene and looked at their brains four, six and 12 weeks later, we could still see evidence of damaged myelin."

The scientists are hopeful that the TREM2 protein might be manipulated in a way that halts the development of neurological disorders in humans.

"We’ve been very interested in identifying ways to control naturally occurring mechanisms that help clean and repair the brain, and these new studies provide clear evidence that TREM2 could be just such a target," says Piccio, MD.

The first study was published in the journal Cell, while the second relating to MS was published in Acta Neuropathologica.

Source: Washington University in St Louis

2 comments
2 comments
Kevin Ritchey
I would appreciate knowing how soon such technology will be available in real-time to the public at large as many individuals are willing to try anything to improve their odds of surviving, or at least stalling, the advancement of such diseases. It's certainly interesting to note the ability of proteins being able to be minimalized or eliminated in this process but there must become a "practical" methodology implemented so that this process can become effectual for use in people now as there are many willing to forgo the standard morality clauses and become test subjects as they are left with little or no choice in the matter of their own treatment. Time is running out for many and little can be done to slow the progression of these fast acting disease conditions. Lab rat studies are all fine and good but there is a vast pool of test subjects willing to take a chance as they have no other objective means of halting the end results quickly approaching. Side effects can't be worse than the current status quo, right?
bhbldon
I agree whole-heartedly with Kevin Ritchey's comments. There are desperate souls that need a lifeline with this and many other maladies.