Study on TREM2 Gene and Alzheimer’s Disease

Research Overview

A recent investigation published in *Nature Neuroscience* explored the significance of the TREM2 gene in relation to Alzheimer’s disease and its potential implications for treatment development. Alzheimer’s disease is the most prevalent form of dementia, impacting around 70% of individuals diagnosed with dementia. This progressive and chronic condition leads to brain damage, affecting memory, cognitive functions, and behavior.

Link Between TREM2 Gene and Alzheimer’s Disease

The study identified a mutation within the TREM2 gene that correlates with an elevated risk of developing Alzheimer’s disease. Researchers from the German Center for Neurodegenerative Diseases and Ludwig Maximilians-University Munich conducted this study to understand the essential role of TREM2 in maintaining healthy brain function. Their findings were published in *Nature Neuroscience*.

TREM2 as a Target for Therapeutic Development

TREM2 plays a crucial role in activating microglial cells, a type of specialized immune cell in the brain responsible for clearing harmful substances. These substances, often known as plaques, accumulate in the brains of Alzheimer’s patients. The researchers proposed that TREM2 could serve as a vital target for innovative therapeutic strategies against Alzheimer’s disease.

To investigate this hypothesis, the team studied the progression of the disease in mice with and without the TREM2 gene. Their results indicated that mice with a functional TREM2 gene produced microglial cells capable of encasing small plaques, preventing their enlargement and proliferation. Conversely, mice lacking the TREM2 gene generated microglial cells that failed to manage these small plaques effectively. Consequently, the researchers emphasized that therapies aimed at activating TREM2 during the early stages of the disease might help prevent the accumulation of toxic amyloid-beta protein aggregates.

Need for Further Research on TREM2

An important finding from this study warrants attention as research progresses: while TREM2 appears to inhibit plaque formation in the early stages of Alzheimer’s disease, it may have an adverse effect in the later stages. In advanced Alzheimer’s, TREM2 may stimulate the production of ApoE, which could lead to increased plaque formation.

Further exploration of TREM2 is essential, as it holds promise for a novel therapy that could inhibit plaque development. However, this research must be approached cautiously to avoid the potential risk of accelerating plaque growth in the later stages of the disease.

References

Parhizkar, S et al. 2019. Loss of TREM2 function increases amyloid seeding but reduces plaque-associated ApoE. [Online]. [13 February 2019]. Available from: https://www.nature.com/articles/s41593-018-0296-9

Eurekalert. 2019. Defective immune cells in the brain cause Alzheimer’s disease. [Online]. [13 February 2019]. Available from: https://www.eurekalert.org/pub_releases/2019-01/d-gc-dic010819.php

Dementia Australia. 2019. Alzheimer’s disease. [Online]. [13 February 2019]. Available from: https://www.dementia.org.au/about-dementia/types-of-dementia/alzheimers-disease