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Viagra could reduce likelihood of developing Alzheimer's, study says

According to researchers, sildenafil users were 69-percent less likely to develop Alzheimer’s disease than non-sildenafil users.

CLEVELAND — Editors Note: Video in the player above is from an unrelated story previously published.

According to a new study from Cleveland Clinic, there might be a way to prevent- or significantly reduce- the likelihood of developing Alzheimer’s disease.

A study published in Nature Aging from Cleveland Clinic’s Genomic Medicine Institute found that after an analysis of over seven million users of sildenafil were 69 percent less likely to develop Alzheimer’s than non-sildenafil users after six years of follow-up.

Sildenafil, the generic name for Viagra and Revatio, is an FDA-approved therapy mainly associated with erectile dysfunction or pulmonary hypertension.

Now, there is a need for follow-up clinical trial testing using sildenafil for patients that suffer from Alzheimer’s disease.

In the United States, Alzheimer’s disease is currently on track to affect 13.8 million Americans by 2050 unless a new effective treatment is found.

By turning to drug repurposing, the Cleveland Clinic hopes to find the use of an existing drug for new therapeutic purposes to offer a remedy to the increasing Alzheimer’s disease.

“This paper is an example of a growing area of research in precision medicine where big data is key to connecting the dots between existing drugs and a complex disease like Alzheimer’s,” said Jean Yuan, M.D., Ph.D., program director of Translational Bioinformatics and Drug Development at the National Institute on Aging (NIA), part of the National Institutes of Health (NIH), which funded this research. “This is one of many efforts we are supporting to find existing drugs or available safe compounds for other conditions that would be good candidates for Alzheimer’s disease clinical trials.”

According to a Cleveland Clinic news release, Dr. Feixiong Cheng, Ph.D. and his team from the Cleveland Clinic’s Genomic Medicine Institute have found via research that understanding the subtypes (endophenotypes) of neurodegenerative diseases like Alzheimer’s might help to find the common underlying conditions that can lead to actionable targets for drug repurposing.

“Notably, we found that sildenafil use reduced the likelihood of Alzheimer’s in individuals with coronary artery disease, hypertension and type 2 diabetes, all of which are comorbidities significantly associated with risk of the disease, as well as in those without,” added Dr. Cheng.

Currently, no FDA-approved, anti-amyloid, or anti-tau small molecule Alzheimer’s treatment exists. In the past decade, many clinical trials for treatments for Alzheimer’s disease have failed.

“Recent studies show that the interplay between amyloid and tau is a greater contributor to Alzheimer’s than either by itself,” said Dr. Cheng. “Therefore, we hypothesized that drugs targeting the molecular network intersection of amyloid and tau endophenotypes should have the greatest potential for success.”

Many researchers used genetic and biologic databases to determine which drug out of 1,600 FDA-approved drugs could effectively treat Alzheimer’s disease. The results showed that drugs targeting amyloid and tau have a better chance of preventing the disease.

“Sildenafil, which has been shown to significantly improve cognition and memory in preclinical models, presented as the best drug candidate,” said Dr. Cheng.

At this time, Dr. Cheng and his team are developing another phase of testing.

“Because our findings only establish an association between sildenafil use and reduced incidence of Alzheimer’s disease, we are now planning a mechanistic trial and a phase II randomized clinical trial to test causality and confirm sildenafil’s clinical benefits for Alzheimer’s patients,” said Dr. Cheng. “We also foresee our approach being applied to other neurodegenerative diseases, including Parkinson’s disease and amyotrophic lateral sclerosis, to accelerate the drug discovery process.”

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Editor's note: The video in the player above is from a previously published, unrelated story.

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