Researchers from Charité – Universitätsmedizin Berlin and the Max Delbrück Center have identified a precise mechanism by which the inflammatory signaling molecule IL-12 contributes to the development of Alzheimer’s disease. According to their study, published in Nature Aging, IL-12 damages two key brain cell types: mature oligodendrocytes and interneurons.
In healthy brains, these cells play crucial roles in cognition and memory. However, when IL-12 binds to interneurons, it causes them to die. This triggers a vicious circle where more microglia produce IL-12, leading to further damage to brain cells and an accumulation of Alzheimer’s plaques.
The researchers developed a new method for analyzing single-cell data using artificial intelligence and machine learning. They sequenced RNA from over 80,000 cell nuclei and reconstructed communication between cells. Their findings show that IL-12 can be measured in blood or cerebrospinal fluid, making it a potential target for combination therapy.
Blocking IL-12 has already shown promising results in mouse models and cell cultures. The study’s authors hope that clinicians will build on their findings and initiate clinical trials. They also explored a new hypothesis that microplastic in the brain could drive microglia to produce IL-12, which may reveal a link between environmental factors and widespread diseases.
The study provides a detailed picture of how IL-12 contributes to Alzheimer’s disease progression and highlights the importance of understanding inflammation as a key factor driving the disease. With its potential for combination therapy and implications for early intervention, this research has significant implications for the treatment and management of Alzheimer’s.
Source: https://scitechdaily.com/alzheimers-puzzle-piece-found-the-inflammatory-trigger-that-may-accelerate-dementia