Recent research suggests that drugs commonly used to treat erectile dysfunction (ED) may also help reduce the risk of developing Alzheimer’s disease. This revelation comes from a large study conducted at University College London in the UK, which tracked the health records of around 270,000 men over several years.
The primary focus of this study was on phosphodiesterase type 5 (PDE5) inhibitors, a class of drugs that includes sildenafil (Viagra), tadalafil (Cialis), vardenafil (Levitra), and avanafil (Stendra). These drugs are known for their ability to treat DM by boosting blood flow, but they also have potential benefits for cardiovascular and cognitive health.
The current study included 269,725 men newly diagnosed with erectile dysfunction between 2000 and 2017. Those with a previous history of cognitive decline or dementia were excluded to ensure a more accurate estimate of Alzheimer’s risk. The mean age of the participants at the start of the study was 58.5 years and the median follow-up period was 5.1 years. During this period, 1,119 men were newly diagnosed with Alzheimer’s disease.
A total of 749 men who used PDE5 inhibitors developed Alzheimer’s, which translates to an incidence rate of 8.1 per 10,000 person-years at risk. In contrast, 370 men who did not use these drugs were diagnosed with Alzheimer’s, an incidence rate of 9.7 per 10,000 person-years.
During the median follow-up period, men who started using PDE5 inhibitors showed a significant reduction in the likelihood of an Alzheimer’s diagnosis compared to those who did not use these drugs. Specifically, the researchers found that men taking PDE5 inhibitors had an 18% lower risk of Alzheimer’s disease, indicating a hazard ratio of 0.82.
In medical research, a “hazard ratio” (HR) is a measure used to compare the risk of a particular event occurring at any given time between two groups. Therefore, in the context of this study, an HR of 0.82 means that the group taking PDE5 inhibitors had an 18% lower risk of developing Alzheimer’s compared to the group not taking the drugs. An HR less than 1 indicates a reduced risk, while an HR greater than 1 indicates an increased risk.
Interestingly, the protective effect of PDE5 inhibitors appeared to be dose-dependent. Men who had more than 20 prescriptions for these drugs showed even greater reductions in Alzheimer’s risk. People with 21 to 50 prescriptions of these drugs had a hazard ratio of 0.56, and those with more than 50 prescriptions had a hazard ratio of 0.65.
The potential cognitive benefits of PDE5 inhibitors are also supported by animal studies, where sildenafil has been shown to improve memory and cognition, enhance synaptic plasticity (i.e. the adaptability of connections between neurons in the brain), and reduce amyloid plaques. which are linked to Alzheimer’s. Tadalafil has also shown similar results in animal tests. However, translating these findings to humans remains a challenge, and more research is needed to confirm these benefits in clinical settings.
One of the limitations noted in the study is the reliance on electronic health records and insurance claims data, which may reflect underdiagnosis or misdiagnosis of dementia. While the findings are promising, the data must be interpreted with caution due to potential biases in diagnosis and classification.
Given these limitations, there is a need for additional studies to investigate the underlying mechanisms of PDE5 inhibitors in reducing Alzheimer’s risk. The authors of this study emphasized that a well-designed randomized controlled trial is necessary to establish a causal relationship and to consider PDE5 inhibitors as a potential preventive measure for Alzheimer’s disease.
Bibliographical references:
Adesuyan, M., Jani, YH, Alsugeir, D., Howard, R., Ju, C., Wei, L., & Brauer, R. (2024). Phosphodiesterase type 5 inhibitors in men with erectile dysfunction and risk of Alzheimer’s disease: A cohort study. Neurology, 102(4).
Brauer, R., et al. (2024). Erectile dysfunction drugs linked to lower risk of Alzheimer’s. Neurology. Retrieved from MedPage Today.
