Infections might cause Alzheimer’s disease
In findings published in Science Translational Medicine, have rekindled the role of beta amyloid in Alzheimer’s, and raised questions about whether finding a drug to clear it from the brain should be the holy grail for researchers.The root cause of Alzheimer’s is still not completely understood. Researchers know that hallmarks of the disease are tiny balls of plaque that accumulate in Alzheimer’s patients’ brains. But how and why they form was still pretty much a mystery. “Historically beta amyloid has been thought of as junk something we don’t want,” said Dr Gawain McColl, an expert in the biology of ageing from the Florey Institute of Neuroscience and Mental Health and a co-author of the study.”So the focus hasn’t been on finding out whether it has a normal function, and if so, what it is.”The new study builds on previous research by senior author Dr Rob Moir from Harvard University that found the structure of beta amyloid had similarities to antimicrobial peptides that are part of the body’s immune system.Now Dr Moir and colleagues, including Dr McColl, have tested whether in fact beta amyloid can protect against infection.They genetically engineered mice and round worms to produce excessive amounts of human beta amyloid, and then tried to infect the animals with bacteria.
Compared to controls, the transgenic animals did not get sick from the infection.Upon closer examination, the researchers found that in these animals, beta amyloid aggregated in the area where the bacteria were, and entrapped the microbes.”The inference is that beta amyloid is part of our normal innate immune response,” said Dr McColl.Dr McColl said it was possible that an inappropriate immune response could lead to accumulation of beta amyloid, which is exactly the process that is implicated in loss of neurones and Alzheimer’s disease.”If that is the case, it may change the focus of where to intervene for potential therapeutics.”To date most research has focused on clearing amyloid from the brain, but these efforts have so far shown little success.Dr McColl said this could be because by the time you see amyloid in the brain, too much damage has been done.He said the new research could help identify what triggers the accumulation of beta amyloid in the first place, leading to earlier diagnosis and more effective treatment.The new research could pave the way to more precise research on how to stop or prevent the disease.When infections enter our bodies, our immune systems kick into gear and generate proteins called beta amyloids that encircle the virus or bacterium, killing it and stopping the infection from spreading. Afterwards, the beta amyloid shells that trapped the infection are left and create little balls of plaque.
Researchers think it’s this process, of fighting off common infections, that could be causing Alzheimer’s.However, if everyone is constantly bombarded by infections, why do only some people develop Alzheimer’s? Researchers think that some people over produce beta amyloid proteins, making them more likely to develop these plaques. Similarly, some people’s immune systems are better at getting rid of those balls of plaques than others.These differences may have to do with having different versions of certain genes already identified in Alzheimer’s, like ApoE4.The next step, according to the study the brains of people with and without the disease, to look for microbes found in plaque. Once researchers better understand how and why the plaque is remaining in the brain, they might be able to find ways to prevent it.In my view, the paper will create a lot of interest and add some new ideas to the Alzheimer’s disease field.The evidence that beta amyloid was the “bad guy” in Alzheimer’s disease was much stronger than the idea that its antimicrobial function might be helpful. Future studies that identify bacterial infection in post-mortem Alzheimer’s disease brains would add support to the idea that bacteria may trigger increased beta amyloid production.The cause of Alzheimer’s disease remain controversial and more research on amyloid’s normal function was needed to help target treatment research.Overall, from my understanding of the disease, I think it’s potentially risky to be removing amyloid without considering the importance of its normal function.