In the effort to understand Alzheimer’s disease, an intriguing idea has arisen suggesting that the plaque build-up in the brain, which causes the disease, is actually a result of the brain trying to protect itself.
The plaque is a gathering of protein called amyloid-beta, and a series of experiments with mice revealed that the protein binds to invading microbes in the brain.
First researchers noticed the animals that produce higher levels of amyloid-beta were more resistant to brain infection. The protein restricted the growth of bacteria, allowing the animals to survive longer. For example, when a disease-causing bacteria was introduced to a mouse brain, widespread amyloid-deposits occurred within 48 hours wherever there were bacteria. In contrast, no protein deposits were seen in uninfected mice.
The same was observed in a petri dish. Amyloid-beta stuck to a microbe’s surface while attracting other molecules, and extended into slender fibers. The growing fibers entrapped or clumped microbes and impeded their growth.
These results suggest amyloid-beta may play an antimicrobial protective role against brain infection. We actually see this concept of clumping and entrapping infecting bacteria elsewhere in the body. However, in the case of Alzheimer’s, what defends us may also lead to later problems. It’s possible that every time an infection occurs in the brain amyloid deposits are produced, but way before symptoms of Alzheimer’s are noticed. This could make the linkage between the two events harder to prove and even harder to control.
That said, researchers hope that this connection might help us eventually manage this heartbreaking disease.
For more information…
Amyloid-β peptide protects against microbial infection in mouse and worm models of Alzheimer’s disease
Deepak Kumar Vijaya Kumar, et al. Science Translational Medicine, May 25, 2016.
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