In a new study, researchers found that a protein that wreaks havoc in the nerves and heart when it clumps together can prevent the formation of toxic protein clumps linked to Alzheimer’s disease.
The findings could lead to new treatments for this brain-ravaging condition, which currently has no truly effective therapies and no cure.
The research was conducted by a team at UT Southwestern.
Researchers have long known that sticky plaques of a protein known as amyloid-beta are a hallmark of Alzheimer’s and are toxic to brain cells.
As early as the mid-1990s, other proteins were discovered in these plaques as well.
One of these, a protein known as transthyretin (TTR), seemed to play a protective role.
In healthy people and animals, TTR helps transport thyroid hormone and the vitamin A derivative retinol to where they’re needed in the body.
However, when it separates into molecules called monomers, these individual pieces can act like amyloid-beta, forming sticky fibrils that join together into toxic clumps in the heart and nerves to cause the rare disease amyloidosis.
In this condition, the amyloid protein builds up in organs and interferes with their function.
In the study, the team found there might be a connection between TTR’s separate roles in both preventing and causing amyloid-related diseases.
They mixed TTR variants with amyloid-beta and placed them on neuronal cells, and found stark differences in how toxic the amyloid-beta remained.
The researchers are currently testing whether modified TTR peptides can prevent or slow the progression of Alzheimer’s in mouse models.
If they’re successful, she says, this protein could form the basis of a new treatment for this recalcitrant condition.
One author of the study is Lorena Saelices, Ph.D., an assistant professor of biophysics.
The study is published in the Journal of Biological Chemistry.
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