Viral and bacterial infections may trigger a series of changes in the body that pave the way for the eventual development of Alzheimer’s disease, according to a new study. The research builds upon previous evidence linking this type of dementia with inflammation, finding that such neuroinflammation can result when the immune system is triggered by the invading pathogens. Key to the findings is a link between this inflammation and the depositing of amyloid plaques in the brain.
The new study comes from the Memorial Sloan Kettering Cancer Center, where researchers found that viral and bacterial infections, the immune system, neuroinflammation, and the build-up of plaques leading to Alzheimer’s disease may all be linked. According to the institute, this study represents a ‘direct link’ between the build-up of these plaques and the body’s immune response to such infections.
This study has linked the IFITM3 protein, which is triggered by the activation of the immune system in response to infections, to the accumulation of beta-amyloid plaques in the brain. These plaques have been strongly linked with Alzheimer’s disease in past research, though work is still underway to fully understand them, what triggers the accumulation, and the overall role they play in this type of dementia.
This most recent study involved mice, which were found to have increasing levels of the IFITM3 protein and inflammation markers as they got older. Likewise, a particular subset of patients suffering from late-onset Alzheimer’s disease was found to have increased levels of IFITM3, indicating that this may be a biomarker for the condition. In mice, the study found that removing IFITM3 decreased the activity of an enzyme and ultimately decreased the build-up on Alzheimer’s-linked plaques in the brain.
Sloan Kettering Institute chemical biologist Yue-Ming Li said:
We’ve known that the immune system plays a role in Alzheimer’s disease — for example, it helps to clean up beta-amyloid plaques in the brain. But this is the first direct evidence that immune response contributes to the production of beta-amyloid plaques — the defining feature of Alzheimer’s disease.