Analysis of brain tissue from donors reveals new potential breakthroughs in the fight against Alzheimer’s disease, according to American scientists.
Research led by the University of Washington, published in the journal Nature Aging, has discovered significant differences in the functioning of microglia cells in the brains of Alzheimer’s patients compared to healthy brains.
Microglia are immune cells that help keep our brains healthy by removing waste and maintaining normal brain function.
From left to right: Healthy brain cells, Alzheimer’s-affected cells, and cells “drowned” by microglia – (Image: SCIENCE PHOTO LIBRARY).
In response to infection or to eliminate dead cells, microglia can “transform” to become more agile and capable of engulfing harmful substances in the brain.
They also “prune” synapses during development, helping to create smoother and more efficient brain circuits.
To delve deeper into the role of microglia in Alzheimer’s disease, neuroscientists analyzed brain tissue from donors, including 12 individuals with Alzheimer’s and 10 healthy controls.
They employed snRNA-seq, a gene expression analysis method, to identify 10 distinct microglia clusters in the brain tissue based on their unique gene expression profiles, which guide the behavior of these cells.
Three of these clusters had never been seen before, with one being more prevalent in Alzheimer’s patients. This type of microglia exhibited activated genes associated with inflammation and cell death.
Overall, researchers found that these types of microglia clusters in the brains of individuals with Alzheimer’s are likely in a pro-inflammatory state.
This means they are more likely to produce inflammatory molecules in an “overzealous” manner, which could potentially harm brain cells and contribute to the progression of Alzheimer’s disease instead of protecting the body.
Additionally, the microglia in the brains of Alzheimer’s patients were found to operate less efficiently than those in healthy individuals. This inefficient cleanup process diminishes the chances of maintaining a healthy aging brain.
Currently, the authors cannot definitively state that these microglia are a direct cause of Alzheimer’s or how they are altered by the disease. However, it is clear that the two issues are closely related.
Therefore, monitoring changes in microglia over time may help us understand their contribution to the onset of Alzheimer’s disease.
According to the World Health Organization (WHO), Alzheimer’s and other dementia-related diseases rank seventh among the leading causes of early death and are rapidly increasing worldwide.
As reported by Science Alert, this research is still in its early stages, but it enhances our understanding of the role of these cells in Alzheimer’s disease and indicates that certain microglia clusters may be targets for new treatment strategies.
