Can Viagra (sildenafil) prevent Alzheimer’s disease?
Reviewed by Yael Cooperman, MD, Ro,
Written by Gina Allegretti, MD
Reviewed by Yael Cooperman, MD, Ro,
Written by Gina Allegretti, MD
last updated: Jan 25, 2022
3 min read
Here's what we'll cover
Here's what we'll cover
Viagra (sildenafil) made a name for itself as a medication for the treatment of erectile dysfunction, but its ability to improve erections was actually a side effect of the drug. Pfizer designed the drug as a blood pressure medication, and now more than two decades after the drug was launched, there seems to be another side effect grabbing headlines. It’s the pill that keeps giving.
New research suggests that people who use Viagra may have a lower risk of developing Alzheimer’s disease. Alzheimer’s disease is the most common type of dementia, causing progressive and debilitating cognitive decline and affecting almost six million Americans. Hallmarks of Alzheimer’s are memory loss, difficulty thinking and reasoning, mood changes, and impaired judgment, all of which get worse over time.
There is currently no cure for Alzheimer’s disease, so researchers are always searching for ways to prevent it. Sometimes new treatments may be found in already existing drugs. Enter Viagra.
Does Viagra (sildenafil) prevent Alzheimer’s disease?
It may, according to a new study analyzing insurance data. Researchers reviewed data from over 7 million insurance claims and analyzed the risk of Alzheimer’s disease in people taking certain medications. These included Viagra (generic name sildenafil), high blood pressure treatments (losartan and diltiazem), and type 2 diabetes drugs (metoprolol and glimepiride).
The study found that the chances of developing Alzheimer’s within six years was almost 70% less in participants taking Viagra compared to those not taking the drug. Researchers suggest that sildenafil may help nerve cells grow, which is important for brain health.
One of the hallmarks of Alzheimer’s disease (as well as other neurological diseases) is the accumulation of misfolded proteins in the brain, including amyloid and tau proteins, and something called neurofibriallary tangles. There’s some evidence that Viagra may interfere with the formation of these proteins, perhaps delaying or preventing Alzheimer’s disease (Fang, 2021).
The authors caution that it’s too early to tell whether it was Viagra specifically that reduced the risk of Alzheimer's disease. Still, the scientific evidence so far is a reason to explore further.
Viagra Important Safety Information: Read more about serious warnings and safety info.
How Viagra may help protect your brain
There haven’t been any clinical trials testing whether Viagra helps prevent Alzheimer’s disease, but there is plenty of recent laboratory research and animal studies suggesting it might be able to play a role in treatment.
Better blood flow
Some of the beneficial effects may be explained by the way Viagra works. It prevents the breakdown of a chemical called nitric oxide in the body, which is involved in opening up our blood vessels and increasing blood flow throughout the body; this is also what helps you get and keep an erection.
But Viagra doesn’t just affect blood flow to the penis—it also increases blood flow to the brain. More blood flow boosts metabolism and brings in more oxygen, which is especially helpful in the areas of the brain most affected by Alzheimer’s disease (Sheng, 2017).
Improved memory and reasoning
Alzheimer’s disease harms your ability to think, reason, and remember. Studies on rats suggest that Viagra may improve these cognitive functions in people with Alzheimer’s disease. It may even improve short-term memory in people with dementia (Venkat, 2019; Cuadrado-Tejedor, 2011).
Increased nitric oxide
Along with increased blood flow, nitric oxide helps brain cells grow, develop, and send signals to each other. In people with AD, nitric oxide levels in the brain are low, meaning communication between neurons doesn't work as well.
Increased nitric oxide levels from Viagra may improve these signals, therefore slowing the progression of Alzheimer’s symptoms. These increased brain signals can even be seen on an MRI (Samudra, 2019; Sanders, 2020).
Decreased inflammation
Inflammation and stress play a role in the development of AD. Animal studies suggest that Viagra may reduce inflammation in the brain, helping to alleviate stress (Ölmestig, 2017).
What’s the downside?
The idea that Viagra can work as an Alzheimer's treatment sounds exciting, but it’s important to remember that so far all studies on this topic have been done on animals or in a lab. Clinical trials are needed before we know for sure whether Viagra is an effective prevention tool for Alzheimer’s (Zuccarello, 2020).
Viagra is usually a well-tolerated drug, though it does have possible side effects including headaches, nausea, and flushing. It may also interact with other drugs you’re taking, such as nitrates, and those interactions can be dangerous or even deadly. ED medications like Viagra might not be the best option for everyone so you should speak with a healthcare provider about which options are best for you.
There’s no cure for Alzheimer’s disease, but as you can see researchers are working hard to tackle this challenging condition. Even though it’s still too early to know for sure, Viagra and other PDE5 inhibitors seem like a promising prospect that may be used in the future to help prevent Alzheimer’s disease.
DISCLAIMER
If you have any medical questions or concerns, please talk to your healthcare provider. The articles on Health Guide are underpinned by peer-reviewed research and information drawn from medical societies and governmental agencies. However, they are not a substitute for professional medical advice, diagnosis, or treatment.
Centers for Disease Control and Prevention (CDC). (2020). Alzheimer's Disease and Related Dementias. Retrieved on Dec. 14, 2021 from https://www.cdc.gov/aging/aginginfo/alzheimers.htm
Cuadrado-Tejedor, M., Hervias, I., Ricobaraza, A., Puerta, E., Pérez-Roldán, J. M., García-Barroso, C., et al. (2011). Sildenafil restores cognitive function without affecting β-amyloid burden in a mouse model of Alzheimer's disease. British Journal of Pharmacology , 164 (8), 2029–2041. doi:10.1111/j.1476-5381.2011.01517.x. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3246665/
Fang, J., Zhang, P., Zhou, Y., Chiang, C., Tan, J., Hou, Y., et al. (2021). Endophenotype-based in silico network medicine discovery combined with insurance record data mining identifies sildenafil as a candidate drug for Alzheimer’s disease. Nature Aging, 1, 1175-1188. doi:10.1038/s43587-021-00138-z. Retrieved from https://www.nature.com/articles/s43587-021-00138-z
Gutsaeva, D. R., Carraway, M. S., Suliman, H. B., Demchenko, I. T., Shitara, H., Yonekawa, H., et al. (2008). Transient hypoxia stimulates mitochondrial biogenesis in brain subcortex by a neuronal nitric oxide synthase-dependent mechanism. The Journal of Neuroscience , 28 (9), 2015–2024. doi:10.1523/JNEUROSCI.5654-07.2008. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6671843/
Ibrahim, M. A., Haleem, M., AbdelWahab, S. A., & Abdel-Aziz, A. M. (2021). Sildenafil ameliorates Alzheimer disease via the modulation of vascular endothelial growth factor and vascular cell adhesion molecule-1 in rats. Human & Experimental Toxicology , 40 (4), 596–607. doi:10.1177/0960327120960775. Retrieved from https://pubmed.ncbi.nlm.nih.gov/32959702/
Nabavi, S. M., Talarek, S., Listos, J., Nabavi, S. F., Devi, K. P., Roberto de Oliveira, M., et al. (2019). Phosphodiesterase inhibitors say NO to Alzheimer's disease. Food and Chemical Toxicology, 134,
doi:10.1016/j.fct.2019.110822. Retrieved from https://pubmed.ncbi.nlm.nih.gov/28648945/
Ölmestig, J., Marlet, I. R., Hainsworth, A. H., & Kruuse, C. (2017). Phosphodiesterase 5 inhibition as a therapeutic target for ischemic stroke: A systematic review of preclinical studies. Cellular Signalling, 38, 39–48. doi:10.1016/j.cellsig.2017.06.015. Retrieved from https://pubmed.ncbi.nlm.nih.gov/28648945/
Samudra, N., Motes, M., Lu, H., Sheng, M., Diaz-Arrastia, R., Devous, M., et al. (2019). A Pilot Study of Changes in Medial Temporal Lobe Fractional Amplitude of Low Frequency Fluctuations after Sildenafil Administration in Patients with Alzheimer's Disease. Journal of Alzheimer's Disease , 70 (1), 163–170. doi:10.3233/JAD-190128. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6743329/
Sanders, O. (2020-a). Sildenafil for the Treatment of Alzheimer's Disease: A Systematic Review. Journal of Alzheimer's Disease Reports , 4 (1), 91–106. doi:10.3233/ADR-200166. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7242821/
Sanders, O. & Rajagopal, L. (2020-b). Phosphodiesterase Inhibitors for Alzheimer's Disease: A Systematic Review of Clinical Trials and Epidemiology with a Mechanistic Rationale. Journal of Alzheimer's Disease Reports , 4 (1), 185–215. doi:10.3233/ADR-200191. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7369141/
Sheng, M., Lu, H., Liu, P., Li, Y., Ravi, H., Peng, S. L., et al. (2017). Sildenafil Improves Vascular and Metabolic Function in Patients with Alzheimer's Disease. Journal of Alzheimer's Disease , 60 (4), 1351–1364. doi:10.3233/JAD-161006. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5805465/
U.S. Food and Drug Administration (FDA). (2010). Viagra (sildenafil citrate). Retrieved on Dec. 15, 2021 from https://www.accessdata.fda.gov/drugsatfda_docs/label/2010/020895s033lbl.pdf
Venkat, P., Chopp, M., Zacharek, A., Cui, C., Landschoot-Ward, J., Qian, Y., et al. (2019). Sildenafil treatment of vascular dementia in aged rats. Neurochemistry International , 127, 103–112. doi:10.1016/j.neuint.2018.12.015. Retrieved from https://www.sciencedirect.com/science/article/pii/S019701861830559X?casa_token=FTaoFrP0odUAAAAA:dih5VqCcFQjpvgCcmWbdnL4khyP45XX3qaEDVXO0iI-cOoM9oqKVOyXlIrAeg3tjOihYiVf8HQ
Zuccarello, E., Acquarone, E., Calcagno, E., Argyrousi, E. K., Deng, S. X., Landry, D. W., et al. (2020). Development of novel phosphodiesterase 5 inhibitors for the therapy of Alzheimer's disease. Biochemical Pharmacology, 176, 113818. doi:10.1016/j.bcp.2020.113818. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7263960/