In a new study, researchers at the University of California, Irvine discovered that a protein known as TOM-1 plays a role in inflammation associated with Alzheimer’s disease.
“Scientists have known for a long time that inflammation is a driver of Alzheimer’s disease, but inflammation is complex and involves many factors. That’s why we decided to look at TOM-1.”
– Frank LaFerla, Dean of the School of Biological Sciences at the University of California
Details of the study
In the study, the researchers zeroed in on TOM-1’s link to inflammation in the brain.
“We were interested in TOM-1 because its levels are low in the Alzheimer’s brain and in the brains of Alzheimer’s rodent models. However, its specific role in the disease has largely been unexplored. Reducing TOM1 worsens inflammation, impairs microglial phagocytosis, and significantly exacerbates amyloid deposition. Conversely, restoration of TOM1 reverses these effects and reduces amyloid-beta pathology. These results highlight the importance of endosomal adaptors and their interaction with inflammatory receptors in the pathogenesis of Alzheimer’s disease.”
– Alessandra Martini, postdoctoral researcher and first author of the study
The study found that when TOM-1 levels were decreased in rodents, the animals experienced a rise in Alzheimer’s pathology—such as an increase in beta-amyloid build-up, inflammation, and cognitive impairment—while boosting TOM-1 levels reversed these negative effects.
What next?
The researchers of the latest study believe that TOM-1 may hold some answers to stopping inflammation as they continue to search for new therapeutic routes.
“You can think of TOM-1 as being like the brakes of a car and the brakes aren’t working for people with Alzheimer’s. This research shows that fixing the brakes at the molecular level could provide an entirely new therapeutic avenue. With millions of people affected by Alzheimer’s and the numbers growing, we must research a diverse portfolio of approaches so we can one day vanquish this terrible disease.”
– Frank LaFerla
Sources:
https://www.eurekalert.org/pub_releases/2019-10/uoc–abp093019.php
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