December 22, 2017
Scientists still aren’t sure what causes Alzheimer’s disease, though there are many theories—beta-amyloid, an accumulation of a type of protein in the brain, being the one most drugs are trying to target. However, the brain of an Alzheimer’s patient has many potential culprits, and isolating the main cause of dementia would help researchers develop a drug that could address how the disease spreads across the brain. A new study pinpoints inflammation as the main driver behind Alzheimer’s disease.
Researchers at the German Center for Neurodegenerative Diseases and the University of Bonn found that microglia, cells that are part of the body’s immune response and are responsible for cleaning up plaque that many point to as the cause of Alzheimer’s, are also responsible for sowing specks of a protein called ASC in the brain, especially when they become agitated.
Brains of Alzheimer’s patients are riddled with ASC. To see whether it causes Alzheimer’s, researchers did tests on mice that were genetically engineered to have Alzheimer’s disease. Some of the mice were also engineered to not produce ASC.
They found that the mice without the ASC protein produced less plaque and appeared to have less severe Alzheimer’s and performed better on memory tests. When scientists planted plaques from the Alzheimer’s mice into young mice, new plaques formed. But when they simultaneously injected an ASC antibody, the spread of new plaques was limited. If there was no ASC present, no plaques formed. This led scientists to conclude that ASC, produced by inflammation, is possibly the necessary ingredient for plaques to form.
This means that minor and major injuries to the brain—a concussion or a virus, for example—could set off a series of inflammatory responses that kills neurons and causes plaques to form.
“Additionally, analysis of human brain material indicates at several levels that inflammation and [beta-amyloid] pathology may interact in a similar fashion in humans. Together our findings suggest that brain inflammation is not just a bystander phenomenon, but a strong contributor to disease progression,” Heneka says. “Therefore, targeting this immune response will be a novel treatment modality for Alzheimer’s.”
Read the full write-up here.