New Research Uncovers A Possible Cause Of Alzheimer's Disease That Is Both Surprising And Promising

May 26, 2016

A team of researchers from Harvard has presented evidence that suggests a mechanism for fighting infections in the brain may be a contributing factor to the development of Alzheimer’s disease. The research, reported in Science Translational Medicine, opens up a new and surprising window into the possible causes of Alzheimer’s.

According to the new research, the process that results in Alzheimer’s goes something like this. The blood-brain barrier keeps many bacterial pathogens that are present in the bloodstream out of the brain. As people age, the blood-brain barrier weakens and viruses, bacteria and fungi that were previously contained within the bloodstream begin to enter the brain.

The new research indicates that the brain defends against these invading pathogens by isolating them within cages built from proteins called beta amyloids. Once it is caged, the pathogen dies and the beta amyloid cage is left behind. Over time, the cage can gather a collection of defective tau proteins that normally play a role in the maintenance of cell structure and function. The defective tau proteins kill surrounding nerve cells. If this process goes too far, inflammation that kills more nerve cells around the cage can occur. The loss of these nerve cells is the root cause of Alzheimer’s disease.

In previous research the investigators reported that beta amyloids cage microbial pathogens in vitro (in a preparation outside a living organism). In the new research they confirmed this finding with in vivo (inside a living organism) preparations using roundworms and mice. As yet, the finding has not been demonstrated with humans although there are no compelling reasons to think that beta amyloids function differently in people.


Previously, beta amyloids were thought to be nothing more than leftover junk proteins called plaque that accumulated in the brain over time. No one realized that these plaque deposits were empty cages that had played an important role in fighting bacterial infections in the brain.

How do the new findings hook up with what we know about Alzheimer’s disease? The hippocampus is a brain structure that plays a central role in memory, learning and spatial orientation. It also is one of the first areas of the brain to be damaged by Alzheimer’s. This damageaccounts for the disorientation and loss of memory that are symptomatic of the disease. It has long been recognized that the damage in question is the destruction of nerve tissue surrounding the beta amyloid deposits that were previously thought to be nothing more than plaque.

The hippocampus has another part to play in linking Alzheimer’s with the role beta amyloids play in fighting bacterial infections. Remember that this hypothetical process begins with the weakening of the blood-brain barrier that results in pathogens entering the brain. Independent research has shown that Alzheimer’s patients typically show weakening of the blood-brain barrier and that age-related weakening of the blood-brain barrier begins in the hippocampus.

The new findings are very exciting but it is important to recognize that it is early days yet. The role played by beta amyloids in fighting bacterial infection has yet to be demonstrated in humans. However, if these findings hold up, it suggests at least two ways of attacking Alzheimer’s that had not been considered before. First, research can be carried out to find ways to kill the bacterial infections that trigger the beta amyloid response before the cages are constructed. Second, ways can be sought to strengthen the aging blood-brain barrier so that the pathogens don’t get into the brain in the first place. This has the potential to be a game changer.

Kevin Murnane covers science & tech for Forbes. You can find more of his writing about these and other topics at The Info Monkey and Tuned In To Cycling. Follow on Twitter@TheInfoMonkey.



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