Amyloid plaques in the brain form due to infections, a new Alzheimer's disease (AD) study has found.
Researchers from Harvard University have found that amyloid-beta brain plaques, which cause Alzheimer's disease, are secondary to the body's immune response to an invading pathogen.
Their finding is important in understanding disease prevention, progression and treatment.
The progressive neurodegenerative disease is a challenge to diagnose, as verification of is only through an autopsy of the brain. Alzheimer's disease occurs as the brain accumulates amyloid-beta plaques and tau proteins tangle. As a result, nerve cell connections are lost, which eventually kills them and leads to loss of memory and decline of cognitive function.
Massachusetts General Hospital Genetic and Aging Research Unit researcher Robert Moir said that what they have found in their study suggests that Alzheimer's disease is a result of the brain interpreting that it is being attacked by pathogens. He clarified, however, that further studies must be carried out to identify if an infection indeed exists.
"It does appear likely that the inflammatory pathways of the innate immune system could be potential treatment targets," said Moir, who is also an assistant professor of Neurology at Harvard Medical School.
Early Study vs. Present Study
In Moir's past study, he and Massachusetts General Hospital Genetic and Aging Research Unit Director Rudolph Tanzi, have found that the pathogen growth is somewhat inhibited by amyloid-beta, which led them to think that the plaques in Alzheimer's could be fragments of an immune response.
For their present study, the researchers presented salmonella to mice brains that can and cannot extract the amyloid-beta. They noted that mice that did not express the amyloid-beta died from the infection, while the ones that produced the substance lived longer. Researchers have conducted the same experiment on roundworms and human brain cells in culture and arrived at the same results.
The scientists believe that the bacteria cross the blood-brain barrier, which deteriorate as one ages, and goes to the hippocampal region where the disease begins.
While many of the past and current studies focused on the inhibition of amyloid-beta buildup, the proponents of the study suggest that future Alzheimer's studies should look at the brain's immune response and the ways to mitigate it, which they believe is a more effective treatment of AD.
"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 Tanzi, who is also a Kennedy Professor of Neurology at Harvard. "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."
An earlier study suggested loss of Y chromosome testing can help diagnose and prevent disease progression of Alzheimer's in males.
The study is published in Science Translational Medicine on May 25.
Photo: National Institute on Aging/National Institutes of Health | Flickr
