Scientists find a key contributor to Alzheimer’s disease and new treatment

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The protein known as sTREM2 is increasingly seen as important in understanding Alzheimer’s disease, though its exact role remains complex and not fully understood.

Research indicates that during the early stages of Alzheimer’s, the levels of sTREM2 in cerebrospinal fluid are lower compared to those in healthy individuals.

As the disease progresses, these levels rise significantly above normal. The reasons behind these fluctuations and their implications on the progression of the disease have not yet been clearly established.

In groundbreaking research published in the journal Molecular Neurodegeneration, Carlos Cruchaga, the Barbara Burton & Reuben Morriss III Professor of Psychiatry at the School of Medicine, along with his team, has shed new light on this phenomenon.

They identified four genomic regions that are linked to variations in the levels of sTREM2. Through detailed functional analyses, they pinpointed specific genes that are responsible for these associations.

To advance their findings, the researchers employed a technique known as Mendelian randomization.

This method allowed them to demonstrate that the relationship between sTREM2 and Alzheimer’s is not merely correlational but causal. This discovery suggests that sTREM2 plays a direct role in the development of Alzheimer’s disease.

Cruchaga emphasized the potential implications of these findings. Identifying the genes associated with sTREM2 levels opens up new possibilities for therapeutic strategies.

By targeting these genes, it may be possible to modulate the levels of sTREM2 and, consequently, influence the course of Alzheimer’s disease.

This research not only deepens the understanding of the biological mechanisms behind Alzheimer’s but also highlights potential pathways for future treatment options.

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For more information about brain health, please see recent studies about antioxidants that could help reduce dementia risk, and coconut oil could help improve cognitive function in Alzheimer’s.

The research findings can be found in Molecular Neurodegeneration.

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