Older blood pressure drug may reduce Alzheimer's risk, study finds

A commonly used diuretic drug may reduce Alzheimer's disease risk, a new study suggests. Photo by Gundula Vogel/Pixabay
A commonly used diuretic drug may reduce Alzheimer's disease risk, a new study suggests. Photo by Gundula Vogel/Pixabay

Oct. 11 (UPI) -- A diuretic commonly used to treat high blood pressure may help prevent the onset of Alzheimer's disease in people who have a high genetic risk, a study published Monday by Nature Aging found.

The drug, bumetanide, has been used to treat high blood pressure, as well as fluid retention caused by heart failure, liver failure or kidney problems, since the early 1970s.


There was a lower prevalence of Alzheimer's disease among study participants who took the diuretic, a drug that promotes the production of urine to, in effect, flush out the kidneys, than in those not given the drug, the data showed.

"We know that Alzheimer's disease will likely require specific types of treatments, perhaps multiple therapies," Dr. Jean Yuan, program director for translational bioinformatics and drug development at the National Institute on Aging, said in a press release.

"The data in this paper make a good case to conduct a proof-of-concept trial of bumetanide in people with genetic risk," Yuan said.

Alzheimer's disease affects about 6 million people in the United States, making it the most common form of dementia, the Alzheimer's Association estimates.


Although drugs can be used to slow progression of its symptoms, there is no cure, according to the association.

People who have a form of the apolipoprotein E gene, called APOE4 are at increased risk for late-onset Alzheimer's disease, research suggests.

For this study, researchers at the University of California-San Francisco and elsewhere analyzed data derived from 213 brain tissue samples and identified Alzheimer's gene expression signatures.

This refers the levels at which genes are turned on or off, specific to APOE4 carriers, they said.

Then they compared the APOE4-specific Alzheimer's signatures against those of more than 1,300 known FDA-approved drugs.

They identified five drugs with gene expression signatures that might help neutralize the disease, with bumetanide being the strongest candidate.

The researchers tested bumetanide in mice, as well as stem cell-derived human neurons, and found that treating mice that expressed the human APOE4 gene with the drug reduced learning and memory loss.

The neutralizing effects also were confirmed in the human cell-based models, which led to the hypothesis that people already taking bumetanide should have lower rates of Alzheimer's, they said.

To confirm that, the team pared down electronic health record data sets from more than 5 million people to two groups: adults over 65 who took bumetanide and a matching group who did not take the drug.


People who had the APOE4 gene and took bumetanide had a 35% to 75% lower prevalence of Alzheimer's disease compared to those not taking the drug, the data showed.

"This research underscores the value of big data-driven tactics combined with more traditional scientific approaches to identify existing FDA-approved drugs as candidates for drug repurposing to treat Alzheimer's disease," NIA Director Dr. Richard J. Hodes said in a press release.

However, "further tests and clinical trials are needed" to confirm these findings, he said.

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