New Alzheimer’s Research Shows the Good and Bad of Beta-Amyloid Proteins

Scientists believe Alzheimer’s disease is caused by an accumulation of beta-amyloid plaques in the brain. Research has shown that certain individuals carry a genetic mutation that makes them more susceptible to beta-amyloid buildup, however, a large majority of Alzheimer’s patients have no such gene, and the propensity to develop beta-amyloid plaques in these cases remains unknown. New research sheds light on a possible cause.

Beta-Amyloid Proteins: the Good and the Bad 

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Beta-amyloid proteins are antimicrobial peptides that are activated as part of the immune response. Harvard researchers theorize that these proteins actually act as natural antibiotics that help defend your brain against infection.

Your brain is protected by a blood-brain barrier that keeps invaders, such as bacteria and viruses, out. If a pathogen makes it through the blood-brain barrier, then beta-amyloid proteins are sent to trap it in a viscous “cage” where the infectious agent eventually dies. This is a good thing. The danger lies in the cages that are left behind. They eventually form the beta-amyloid plaques that have been instigated as a primary cause of Alzheimer’s disease.

The theory makes sense. As we age, the impermeability of the blood-brain barrier weakens and more infectious viruses and bacteria are able to enter the brain. According to research from Dr. Berislav Zlokovic, the director of the Zilkha Neurogenetic Institute at the University of Southern California, the hippocampus is the most permeable part of the blood-brain barrier…and it’s also the region of the brain where beta-amyloid plaques usually accumulate!

To test this theory, Harvard researchers first infected brain cells in petri dishes with bacteria. Beta-amyloid plaques formed, as suspected. They then repeated the process with yeast, roundworms, fruit flies, and mice. Mice infected with salmonella developed beta-amyloid plaques in their hippocampus overnight! Rudolph E. Tanzi, Ph.D., of Harvard Medical School and Massachusetts General Hospital, explains: “each plaque had a single bacterium at its center.”

But some mice were more prone than others to beta-amyloid plaques. Those that didn’t form plaques may not have exhibited a risk for Alzheimer’s, but they were definitely at a greater risk of dying from the infection.

Researchers also note that there are many brain infections that never manifest symptoms, and that many people with Alzheimer’s may have previously had a brain infection without knowing it.