Infections connected to Alzheimer's disease

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Elizabeth Newman
Elizabeth Newman

Alzheimer's disease and a long-term care magazine is analogous to nursing home administrators and the Centers for Medicare & Medicaid Services: No matter what you do, you're not breaking them apart.

Over the past decade, McKnight's has written about everything from how weight loss is a precursor to Alzheimer's disease (2006) to how a nutrient cocktail helps improve brain function in those with early-stage Alzheimer's (2010) to how discontinuing donepezil impacts nursing home placement (2016). That's why my eyes tend to glaze over when there's a new study released, especially when the title is “Amyloid-β peptide protects against microbial infection in mouse and worm models of Alzheimer's disease.” A shirtless nurse headline it is not.

But kudos to New York Times reporter Gina Kolata, who did not ignore that study in Science Translational Medicine. That's because the research could have a more colloquial title, which is “Everything we think we know about Alzheimer's disease may be wrong.”

The researchers' hypothesis is that infections could trigger plaques in the brains of those with the disease. In dementia research, that's the equivalent of yelling “Fire!” in a movie theater. While naked.

The Harvard researchers posit that a virus goes on a journey to hit the blood-brain barrier, which becomes weaker with age. As explained by Kolata, “The brain's' defense system rushes in to stop the invader by making a sticky cage out of proteins, called beta amyloid. The microbe, like a fly in a spider web, becomes trapped in the cage and dies. What is left behind is the cage — a plaque that is the hallmark of Alzheimer's.”

Robert D. Moir, Ph.D., an associate professor at Harvard Medical School and Massachusetts General Hospital, was the one to notice that amyloid proteins resembled proteins in the innate immune system. The fact that he noticed this makes you think that Harvard and Mass General may know what they're doing in terms of who they hire.

The research, to be honest, is a little gross. In one study, the researchers put salmonella into the brains of young mice without plaques. Mice without amyloid proteins succumbed to infections the amyloid would have stopped.

But those mice contributed to science. The news provides illumination to weird discoveries previous researchers found, such as that Alzheimer's patients have higher levels of antibodies to herpes. As much as parents, teachers or a nun may have told you that promiscuous sex will kill you, no one really thought herpes was causing a degenerative brain disease. But the new research indicates how there's a link. That's also potentially true of gum disease.

The latest study also ties into the research around genes. Those with the mutated or “Alzheimer's” gene overproduce beta amyloid. Those with a gene called ApoE2 have brains that clear out beta amyloids after it kills microbes, according to the NYT.

The reduction in dementia rates is believed to be tied to better control of blood pressure and cholesterol, which are critical issues to monitor in long-term care residents. To me, the study fleshes out the ways we think about Alzheimer's. Absolutely, we should continue to be physically active and challenge our brains. If I can remain sharp as I age, I suspect I'll credit walking and reading. But what if those actions are part of a more holistic picture in how our bodies fight off infection? Additionally, since there's no way to ward off germs and infections completely, what if we can develop treatments addressing how these microbes impact the brain? If that's where research is heading, it's an exciting time for long-term care residents, employees and the people who write about them.

Follow Elizabeth Newman @TigerELN.


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Daily Editors' Notes

McKnight's Daily Editors' Notes features commentary on the latest in long-term care news and issues. Entries are written by Editorial Director John O'Connor, Editor James M. Berklan, Senior Editor Elizabeth Newman and Staff Writer Marty Stempniak.