Dr. Robert Friedland has been working with Alzheimer’s and Parkinson’s patients for more than 30 years. And he still doesn’t know how they developed the diseases.
Less than 1 percent of patients have a gene that can lead to either disease. For the rest, it’s a big unknown.
But Friedland’s latest research shows that it might be because of gut bacteria.
According to a new study published in the journal Science Reports, Friedland and a team of researchers have found a link between gut bacteria and Alzheimer’s Disease.
“We all have up to 2 kilograms of bacteria in the intestines, and these make proteins that could potentially trigger the clubbing of brain proteins.,” said Friedland, who heads up the neurogeriatric lab at the University of Louisville School of Medicine and led the study. “A kilogram is 2.2 pounds. It’s a lot of bacteria.”
Scientists working on Alzheimer’s already knew that these folding proteins formed hard plaques in the brain. These are called amyloid proteins. They form chains that eventually stretch and kill memory cells from one end of the brain to the other.
There was a groundbreaking discovery by Matthew Chapman at the University of Michigan in 2007: Bacteria make these folding proteins.
“The bacteriologists have made significant advances on how and why bacteria make this, but the scientists working on Alzheimer’s had little awareness about this protein made in the body,” Friedland said. “So it was our idea to investigate whether the amyloid made by bacteria, if that could be the trigger for the similar amyloid proteins in neurons in the brain, and that could be why they become misformed.”
Researchers exposed old but healthy rats and tiny worms to two types of bacterial strains: one that could produce the folding protein, and another that couldn’t.
“We found that rats exposed to amyloid protein had more aggregation of neurons in the gut wall and the brain, and regions that were affected in Alzheimer’s and Parkinson’s. And they had more inflammation, which is an important part of Alzheimer’s.”
And the rats that weren’t exposed to the folding-protein bacteria?
“They had lower levels of the protein, and they didn’t show aggregation of the main protein associated with Parkinson’s,” he said.
Friedland plans to conduct the same study on mice. Much of the research that ends up with an approved drug starts with the animal because their systems model ours. Beyond that, there will be have to be research on the specific bacteria that produce the folding proteins.
“We don’t know precisely what amyloid proteins are involved, or how many there are,” he said.
The road that led to this discovery is a personal one: Friedland’s grandfather likely had Alzheimer’s.
“He threatened my mother with a knife when he was trying to jump out of a window because he believed falsely that the building was on fire,” he said. “And he ended up in a mental hospital in New York. I was only a little boy. It’s likely at those age with those symptoms, it was actually Alzheimer’s.”
Researchers at the Brown Cancer Center, Case Western University in Cleveland and the University of California San Diego were also part of the study.
The funding for the study came from the Michael J. Fox Foundation for Parkinson’s Research. Friedland was turned down by the National Institutes of Health because they don’t generally fund experimental research due to fierce competition for money. He hopes NIH will now see his evidence and consider future funding.