UofL researching potential Alzheimer's breakthrough

LOUISVILLE, KY (WAVE) - There is new hope for Alzheimer's patients.

A researcher at the University of Louisville is exploring a link between Alzheimer's disease and bacteria our intestines. It might be the most significant breakthrough in Alzheimer's treatment so far.

The impact of Alzheimer's disease is staggering. It is the sixth leading cause of death in the United States. Five-million Americans are living with the disease, and 15 million people are taking care of them. The thought was that there was nothing to be done to prevent or reverse the symptoms of Alzheimer's, but now, that's changing.

You may have heard reports recently about a Stanford University study published in the Journal of Clinical Investigation in which scientists reportedly found a cure for the disease. In fact, that was not the case. When contacted, the researcher sent this response via Margarita Gallardo with Stanford University's Public Relations Department.

"Dr. Katrin Andreasson's recent study, as the title of our news release (posted online Dec. 8) noted, was a mouse study, not a clinical trial. Dr. Andreasson and her team did not use a drug that blocked the deleterious EP2 signaling on microglial cells. They used genetic-engineering methods of blocking that receptor that can't be used in humans.

Alzheimer's is a devastating disease, and this research is very promising. But no cure is in sight yet, despite what you may have read in the tabloid headlines or social media posts. It will first be necessary not only to develop drugs that safely block EP2 (or that block the inappropriate inflammatory process triggered by EP2 signaling) in animal models, but also to ensure via costly and lengthy clinical trials that such a drug, once found, is both safe and effective in humans. Substantially more testing in animals will be required before clinical trials can be envisioned.

Every journey begins with the first step. We are proud of the basic research performed in this institution's laboratories and fervently hope that, with proper financial support and investigator follow-up, our work and others' will someday yield the treatments that so many desperately seek. But picking a winner at this early stage of the game is like picking a needle out of a haystack. "

We may be closer to finding that needle because of work at the University of Louisville. Scientists there are conducting research on manipulating proteins in another more promising way involving human patients.

"We are sampling bacterial content from the nose, and also the gut," said Dr. Robert Friedland, Chief of the Laboratory of Neurogeriatrics at the University of Louisville. "We are working with collaborators in Ireland to do a complex genomic analysis. So my talk next Thursday, I gave it the title, "Can we do gene therapy in the kitchen?"

In other words, can we change the proteins that cause degenerative diseases like Alzheimer's and Parkinson's by changing what we eat?

"Humans have 27-to-28,000 genes that we're born with," Friedland continued, "but we have 10 times more genes in our bacteria -- the majority in our nose, mouth and gut. These my be the genes that cause certain proteins to fold, causing Alzheimer's and Parkinson's disease."

"Preliminary results indicate that there may be proteins made by certain groups of bacteria, which lead to more misfolding of proteins in the brain and neurons in the wall of the intestines," said Friedland.

Because the bacteria in the intestines eat what we eat, Friedland believes we can change them by what we eat.

The beneficial bacteria are best fed a diet low in fat and high in fiber, fish, vegetables, fruits and antioxidants.

For Alzheimer's that means, "It could possibly be a way to prevent or reverse or slow down" the disease, said Friedland.

His work is slated to be published in the Journal of Alzheimer's Disease.

We will continue to follow this work and bring you any new developments. In the meantime, click here for a link to a story about the aforementioned Stanford University study.

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