Gut bacteria · Alzheimer's

LSU Health New Orleans Uncovers Key Piece to the Alzheimer’s Puzzle

Gloved hands place a slide under a lab microscope, as in research on gut bacteria and Alzheimer's disease

Gut bacteria may help drive Alzheimer’s disease. LSU Health New Orleans researchers found a neurotoxin (nerve poison) called BF-LPS. A common gut bacterium, Bacteroides fragilis, makes it. BF-LPS adds to Alzheimer’s. Enough dietary fiber may help block the process. The finding ties gut health straight to brain health.

Summary: LSU Health New Orleans researchers led a study on a neurotoxin called BF-LPS. It comes from the gut bacterium Bacteroides fragilis. The study found evidence that it adds to Alzheimer’s disease. It also found that eating enough dietary fiber may stop this process. So gut health may be linked to Alzheimer’s. That link may lead to new ways to find and treat the disease.

Why has a century of hard research failed to find a strong remedy for Alzheimer’s? The answer is simple. We still understand little about how the disease develops (its pathogenesis). We even understand little about what causes it (its etiology). Alzheimer’s seems to have many causes. In recent years, researchers have paid more attention to the gut-brain axis and gut microbiota (gut germs).

Infection, toxins and gut health may all help cause Alzheimer’s disease. Some studies suggest certain infections, like the herpes simplex virus, may raise the risk. Toxins like heavy metals and pesticides may also play a role. And more and more research suggests that gut health and the gut microbiome may add to Alzheimer’s.

The gut microbiome is the mix of tiny living things in your gut. They help with digestion, immune defense and other body work. When the gut microbiome falls out of balance, it is tied to several brain and nerve disorders, including Alzheimer’s. Still, we need more research to fully understand how these factors drive the disease.

Drs. Yuhai Zhao and Walter J. Lukiw led the study. They work at the LSU Health New Orleans Neuroscience Center and the Departments of Cell Biology and Anatomy, Neurology, and Ophthalmology. The bacterium Bacteroides fragilis lives in the human gastrointestinal (GI) tract. It is Gram-negative. It carries a strong toxin made by microbes, called lipopolysaccharide or LPS. From it comes a neurotoxin known as BF-LPS. BF-LPS is a pro-inflammatory toxin, meaning it drives swelling and irritation. It adds to Alzheimer’s disease. The study also found that adequate intake of dietary fiber can head off the process.

The study found that a neurotoxin from gut bacteria, called BF-LPS, can add to Alzheimer’s disease. BF-LPS travels from the gut to the brain. It inflames brain cells. It also damages a protein that helps keep brain cells healthy. Sadly, this damage ends with brain cells dying, just as in Alzheimer’s disease.

The study also found that the gut microbiome plays a big role in Alzheimer’s disease. That is the mix of tiny living things in your gut. Eating enough dietary fiber can control how many BF-LPS-making bacteria live there.

The study points to a link between the gut, the brain and Alzheimer’s. That link could lead to new ways to find and treat the disease. People in the US eat about 10-15 grams of fiber a day. The USDA says women up to age 50 should eat 25 grams a day and men 38 grams. After age 50, women should eat 21 grams a day and men 30 grams. Alzheimer’s disease is the most common cause of dementia. It is one of the leading causes of death in the US. About 5.8 million people over 65 in the US have Alzheimer’s disease. That number is expected to climb to 13.8 million by 2050.

This study shows how much gut health matters in Alzheimer’s disease. It suggests that dietary fiber may help prevent it. These findings may lead to new ways to find and treat Alzheimer’s disease and other diseases that wear down the brain. Still, more research is needed to fully understand how gut health, dietary fiber and Alzheimer’s disease fit together.

Frequently asked questions

Which gut bacteria is linked to Alzheimer’s disease?

Bacteroides fragilis. This common gut bacterium makes a strong neurotoxin called BF-LPS, a form of lipopolysaccharide. Drs. Yuhai Zhao and Walter J. Lukiw led a study at the LSU Health New Orleans Neuroscience Center. They found that BF-LPS is a pro-inflammatory toxin that adds to Alzheimer’s disease. The finding ties the health of your gut straight to how the disease begins.

How do gut bacteria affect the brain in Alzheimer’s?

BF-LPS does not stay in the gut. It travels to the brain and inflames brain cells. It damages a protein that helps keep those cells healthy. Over time that damage kills brain cells, the same loss seen in Alzheimer’s disease. The gut microbiome is the mix of tiny living things in your gut. It is part of the disease process, not a bystander.

Can eating more fiber help prevent Alzheimer’s?

The LSU study found that adequate dietary fiber can head off the process. Fiber controls how many BF-LPS-making bacteria live in your gut. Fewer of those bacteria means less toxin reaching the brain. That makes fiber one of the few Alzheimer’s levers you control yourself. You pull it every day, at every meal.

How much fiber should you eat a day?

The USDA says women up to age 50 should get 25 grams a day, and men 38 grams a day. After age 50, the targets drop to 21 grams for women and 30 grams for men. People in the US eat only 10 to 15 grams of fiber a day on average. That is far short of either target.

How many Americans have Alzheimer’s disease?

About 5.8 million people over age 65 in the US have Alzheimer’s disease. That number is expected to reach 13.8 million by 2050. Alzheimer’s is the most common cause of dementia. It is one of the leading causes of death in the country. That is why a cause that starts in the gut deserves attention.

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Medical Disclaimer: Keep in mind that the content provided is not direct medical advice for patient care, but is provided for thoughtful discussion.

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Sources

  • Zhao Y, Lukiw WJ. Bacteroidetes Neurotoxins and Inflammatory Neurodegeneration. Mol Neurobiol. 2018;55(12):9100-9107. PMID 29637444 · DOI 10.1007/s12035-018-1015-y.