Alzheimer's Disease Build Up May Stem From Body's Immune Response To Infection

A new Harvard University study could change our understanding of Alzheimer's disease. This is due to the revelation that the building up of amyloid plaques in the brain, which are thought to cause Alzheimer's disease, may be due to the body's immunity to bacterial infection.

A study by Harvard University scientists shows that the plaques are not just "brain waste," as believed earlier, but may help in treatment and prevention of the disease.

At present, Alzheimer's diagnosis is tough and conclusive verification can happen only when a deceased patient's brain is examined. Even as amyloid-beta plaques collect in the brain, they could lead to the formation of tau proteins, severing nerve cell connections and leading to memory loss as well as cognitive defects.

"Our findings raise the intriguing possibility that Alzheimer's pathology may arise when the brain perceives itself to be under attack from invading pathogens, although further study will be required to determine whether or not a bona fide infection is involved," said Robert Moir of the Massachusetts General Hospital and senior author of the study. "It does appear likely that the inflammatory pathways of the innate immune system could be potential treatment targets."

As earlier research indicated that amyloid-beta limits pathogen growth, Moir and his team introduced salmonella into the brains of two groups of mice. While one group had the capacity to express amyloid-beta, the other group did not have the ability to express it.

The study showed that the group without the ability to produce the protein got killed by salmonella infections, while the other group that could express the proteins lived for a longer time. The results were replicated in roundworms as well as cultured human brain cells.

Amyloid plaques in patients with the disease might be due to earlier immune system battles. Pathogens that could enter the brain through the blood-brain barrier getting weaker with age can create an immune response leading to the collection of plaques after fighting these pathogens.

However, further research is needed to comprehend the link between the immune system, amyloid-beta build-up, and Alzheimer's disease.

"While our data all involve experimental models, the important next step is to search for microbes in the brains of Alzheimer's patients that may have triggered amyloid deposition as a protective response, later leading to nerve cell death and dementia," said Rudolph Tonzi, also of the Massachusetts General Hospital and co-author of the study. "If we can identify the culprits - be they bacteria, viruses, or yeast - we may be able to therapeutically target them for primary prevention of the disease."

The findings were published in the May 25,2016, issue of the journal Science Translational Medicine.