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The study, which was spearheaded by the Washington University School of Medicine in St. Louis, gives us concrete details about the structure of the protein involved in Alzheimer’s.
The protein is called, TREM2. Researchers discovered that mutations related to another brain disorder alter the protein’s interior. These tend to change the TREM2’s role in cleaning cellular waste through the process called phagocytosis.
Study Details Molecular Roots Of Alzheimer’s
A new study at Washington University School of Medicine in St. Louis details the structure of TREM2, a protein involved in Alzheimer’s disease and other neurodegenerative disorders. Read more…
WUSTL.edu says that it’s a good thing the researchers were able to implicate the molecule related to the disease. Simply knowing the shape of this molecule gives us a chance. It can help us understand how other neurodegenerative diseases develop. We can take a look at potential preventive measures and treatment.
The idea that this protein is somehow responsible for cognitive decline has long been supported. Previous studies show that mutations which affect the structure of TREM2 puts an individual at a higher risk for developing late-onset Alzheimer’s.
Cellular ‘Housekeeping’ Molecule’s Structure Linked To Neurodegeneration
Knowing the shape of the molecule — and how that shape may be disrupted by certain genetic mutations — can help in understanding how Alzheimer’s and other neurodegenerative diseases develop and how to prevent and treat them. Read more…
Senior author Thomas J. Brett, PhD, an assistant professor of medicine, says that they’re not sure what TREM2 contributes to neurodegeneration but inflammation is common among these conditions.
The study takes a closer look at the mutations. They also tackled what it does to the structure and how it can affect the function. If they understand it, they might be able to find ways how to correct it.
Study Details Molecular Roots Of Alzheimer’s
Other TREM2 mutations are linked to Nasu-Hakola disease, a rare inherited condition that causes progressive dementia and death in most patients by age 50. Read more…
The chance of correcting the mutation presents a lot of possibilities when it comes to treatment. The researchers remain hopeful that they’ll be able to understand the mechanism behind the molecular roots of the disease.
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