Viagra is linked to a nearly 70% lower risk of Alzheimer’s disease, according to a new study.

According to new research, using the drug sildenafil – more often known as the brand-name drug Viagra – is linked to a much lower risk of Alzheimer’s disease.

According to a study done by Cleveland Clinic experts, using sildenafil reduces the risk of Alzheimer’s disease by over 70% when compared to non-users.

This is based on a review of over 7.2 million people’s health insurance claim data, which revealed that claimants who took the prescription were considerably less likely to develop Alzheimer’s disease over the next six years than matched control patients who didn’t take sildenafil.

It’s vital to remember that observing relationships like these – especially on such a large scale – isn’t the same as proving a causal effect.

It’s possible, for example, that the people in the sildenafil cohort have something else to credit for their reduced risk of Alzheimer’s disease.

Nonetheless, the researchers claim that the correlation shown here, along with other indicators in the study, is sufficient to identify sildenafil as a promising candidate drug for Alzheimer’s disease, whose viability can be investigated in future randomized clinical trials to see if causality exists.

“Notably, we found that sildenafil use reduced the risk of Alzheimer’s disease in people with coronary artery disease, hypertension, and type 2 diabetes, all of which are comorbidities significantly associated with disease risk, as well as in people without,” says Feixiong Cheng, a computational biologist and senior author of the study.

It’s not the first time sildenafil has been connected to improved health results; the medicine has already shown promise in a variety of scientific contexts, including cancer and malaria research, to name a few.

Cheng’s team started by creating over a dozen endophenotype modules, then used computational tools to pinpoint genetic elements that could potentially influence Alzheimer’s disease manifestation.

After obtaining 13 of these modules, the researchers investigated which FDA-approved medications would be useful in combating the observed phenotypes.

Sildenafil was one of the most promising prospects among the nearly 1,600 such drugs currently approved by the FDA.

That may seem strange, given that the drug is primarily used to treat erectile dysfunction and pulmonary hypertension. However, given its interactions with the amyloid and tau proteins implicated in Alzheimer’s pathology, there were already signs in the research community that the sildenafil compound might have other health benefits.

“Recent studies demonstrate that the interaction between amyloid and tau causes Alzheimer’s disease more than either of them alone,” Cheng explains.

“We expected that medications targeting the molecular network junction of amyloid and tau endophenotypes would have the best chance of success… Sildenafil, which has been demonstrated to improve cognition and memory in preclinical models, appeared to be the best pharmacological candidate.”

The hypothesis appears to be supported by the health insurance data, with the team discovering that sildenafil users had a 69 percent lower risk of Alzheimer’s disease than non-users – a reduction that was significantly greater than other types of medications studied in the study, such as losartan, metformin, diltiazem, and glimepiride.

Of course, the researchers stress that none of this proves causation, but there may be more potential possibilities in this area.

In independent studies of human brain cells in vitro to see if sildenafil could help guard against Alzheimer’s disease, the researchers discovered that neurons treated with the drug grew faster and had less tau accumulation.

It’s still early, but such impacts could play a role in the insurance cohort’s lower risk of getting Alzheimer’s disease. As a result, the team believes it is critical to pursue these leads further.

“To prove causation and validate sildenafil’s therapeutic benefits for Alzheimer’s patients, we’re now preparing a mechanistic trial and a phase II randomized clinical trial,” Cheng explains.

“We expect to apply our technique to additional neurodegenerative disorders, such as Parkinson’s disease and amyotrophic lateral sclerosis, in order to speed up the drug discovery process.”