The immune response in mice affects the severity of late-stage brain diseases in mice through immune memory. The innate immune system can retain the "memory" of infection for several months, after which the immune response will change. There are two forms of immune memory. The first is training, which enhances the immune response to reinfection. The other is resistant, and continuous exposure will suppress the immune response.
It is well known that inflammation in the body triggers an immune response in the brain, but it is not clear whether immune memory occurs in the microglia of the brain’s innate immune cells. The potential to modulate the response of microglia has attracted widespread interest because these cells are involved in diseases such as Alzheimer's disease and stroke.
Moreover, they have a long lifespan, even if they are not permanent, they can be permanently modified. German Jonaseher and colleagues from the German Center for Neurodegenerative Diseases found that when lipopolysaccharides were injected into Alzheimer's disease model mice, β-amyloid protein in the brains of the mice increased significantly. Beta-amyloid plaques are thought to activate microglia, absorb and process beta-amyloid. After injection of lipopolysaccharide, microglia appeared to respond to training. After six months, the injected mice accumulated more β-amyloid than the uninjected mice.
However, after 4 injections, immune tolerance increased and β-amyloid protein decreased. Similarly, the authors found that immune tolerance can reduce nerve damage after stroke. By studying these processes, new ways to reduce neurological diseases can be found.