In studies in roundworms, mice, fruit flies, and cultures of mammalian cells, investigators have found that beta-amyloid, a key culprit in the brains of people with Alzheimer’s, is also involved with our innate immune system, the body system that protects against pathogens before antibodies are formed.
They hypothesized that when the brain is infected by a virus, fungus, or bacterium (an invasion that becomes more likely as people age and the blood-brain barrier becomes leaky), the beta-amyloid peptide moves into the brain to stem the infection and, when its work is done, leaves debris, namely the beta-amyloid plaque that is the hallmark of Alzheimer’s.
In their latest studies in mice, these investigators confirmed that pathogens injected into the brains do indeed incite beta-amyloid production. Further, they demonstrated that beta-amyloid’s presence was associated with increased survival of the animal. The results were published in the May 2016 issue of Science Translational Medicine.
Beta-amyloid appears to provide these protective effects by reducing microbes’ ability to adhere to cells or to clump together and by entrapping the pathogens with its filaments.
If the researchers’ hypothesis holds up in human studies, their findings may shift the emphasis in preventing Alzheimer’s disease to strategies that deal with these infectious agents. Since their findings raise the possibility that beta-amyloid is beneficial as well as harmful, their results also raise the possibility that Alzheimer’s treatments should lower but not totally remove beta-amyloid.
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