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Home » Study shows that Viagra may reduce risk of Alzheimer’s disease

Study shows that Viagra may reduce risk of Alzheimer’s disease


A year ago, I wrote about an observational study that Viagra (sildenafil citrate) might reduce the risk of developing Alzheimer’s disease. I didn’t take that research too seriously, since a few issues concerned me, such as confounding data.

However, this new research was broadened to more medical databases which provides us with more solid information that sildenafil can reduce the risk of Alzheimer’s disease. The researchers also provided a biological mechanism for how Viagra works in the brain.

As I usually do, I’ll discuss and critique this research to determine if there’s something there.

All about sildenafil

Sildenafil was developed by Pfizer (yes, the same company that makes one of the mRNA vaccines for COVID-19) in the late 1980s to be used as a drug for hypertension, or high blood pressure.

Sildenafil is still prescribed for a particular disease called pulmonary hypertension, a serious cardiovascular disease. Sildenafil is sold under the brand name Revatio for this indication. It also has some other off-label uses, including for altitude sickness — climbers preparing to ascend Mt. Everest used to take the drug to help them survive in the thin air on the ascent.

Sildenafil acts by blocking phosphodiesterase 5, an enzyme that promotes the breakdown of cGMP, which regulates blood flow in the penis. It requires sexual arousal, however, to work. It also results in the dilation of the blood vessels in the lungs, which is why it is effective in treating pulmonary hypertension.

All about Alzheimer’s disease

Before proceeding, it’s important to describe what we know about Alzheimer’s disease (AD). It is a chronic neurodegenerative disease that usually starts slowly and worsens over time. It accounts for 60-70% of dementia cases, even though the terms are sometimes used interchangeably. Alzheimer’s disease is a form of dementia. The other forms of dementia include Lewy body dementia, frontotemporal disorders, vascular dementia, and mixed dementia, which is a combination of two or more of the different forms of dementia.

Amyloid plaques (caused by amyloid beta, or Aβ), phosphorylated tau tangles (pTau), and neurofibrillary tangles are generally easily visible pathologies that can be observed by microscopic analysis of brain tissue from autopsies of those potentially afflicted by AD. These plaques and tangles seem to affect nerve functioning. Despite these observations, the precise pathophysiology, or development, of the disease is not known.

Since amyloid plaques are often identified in patients with Alzheimer’s disease, a large amount of research is focused on attacking those plaques as a way to reverse the effect on nerves which leads to AD.

The causes of AD are unknown (notice how much we do not know about this disease). However, it is speculated that it is mostly genetically related, with a large number of genes that underlie this relationship.

And since we have no clear understanding of the etiology and pathophysiology of AD, there are no effective treatments available today for the disease, although there are some drugs that target the amyloid plaques but have not been shown to change the course or outcomes of AD.

There are a couple of medications that help manage some of the symptoms of the disease, but they are certainly not cures. There are several drugs at the very earliest stages of development that may hold out hope to treat the underlying disease.

One more thing that needs to be made clear. There are no biological tests for Alzheimer’s disease — usually, you can only find the amyloid plaques and other pathologies in post-mortem autopsies. Unfortunately. in the absence of an autopsy, clinical diagnoses of AD are “possible” or “probable”, based on other findings, such as memory tests and other methods.

In the United States, about 10.7% of seniors (≥65 years) currently have Alzheimer’s dementia, and the incidence of dementia and Alzheimer’s disease is expected to rise substantially in the coming decades due to population aging, making it imperative to identify modifiable risk factors that may help mitigate its impact. The economic burden of AD is expected to surpass $2.8 trillion by 2030.

couple elderly man old
Photo by Pixabay on Pexels.com

Viagra and Alzheimer’s disease paper

In a paper published on 1 March 2024 in the Journal of Alzheimer’s Disease, Feixiong Cheng, Ph.D., director of the Cleveland Clinic Genome Center, and colleagues performed a large real-world analysis of patient data from two databases to examine the prevalence of Alzheimer’s disease among patients who took sildenafil (Viagra) than those who did not, after adjusting for potential confounding factors.

The study utilized data from the MarketScan Medicare Supplemental data (years: 2012– 2017) and the Clinformatics data (years: 2007– 2020).

Here are the key results:

  • Sildenafil use was associated with a 54% reduced incidence of AD in the MarketScan data.
  • It was associated with a 30% reduced prevalence in the Clinformatics data.
  • The investigators also found that sildenafil reduces certain tau proteins that are associated with AD.
  • Through RNA-sequencing data analysis, the researchers also demonstrated that sildenafil specifically targets AD-related genes and pathobiological pathways, mechanistically supporting the beneficial effect of sildenafil in AD.

The researchers concluded that:

These real-world patient data validation and mechanistic observations from patient iPSC-derived neurons further suggested that sildenafil is a potential repurposable drug for AD.

Summary

This adds to the research that Viagra seems to have a strong effect on reducing the risk of developing Alzheimer’s disease. However, there are a few issues:

  1. This study did not include women. We don’t know if sildenafil will affect women similar to men.
  2. There is no data as to whether sexual activity of men who take Viagra may affect the incidence of AD.
  3. We still need a large clinical trial to confirm these findings. At this time, I found no clinical trials registered to examine the effect of sildenafil on Alzheimer’s disease.

I still do not know what I think about this line of research. It seems to provide good data that Viagra reduces the risk of Alzheimer’s disease, and it provides a biologically plausible mechanism for how the drug may protect the brain from AD.

For now, I am intrigued by this study. It seems to provide even more evidence of a link between sildenafil and Alzheimer’s disease. But before anyone decides to get a prescription for it just to stop Alzheimer’s, we need more data before I’m convinced that it works.

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Michael Simpson

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