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Arthur T Knackerbracket [soylentnews.org] writes:

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Arthur T Knackerbracket has processed the following story [gizmodo.com]:

One of the world’s most famous drug classes may have another trick up its sleeve. In a new study, scientists in the UK have found that erectile dysfunction drugs like sildenafil (more widely known as Viagra) are linked to a lowered risk of Alzheimer’s disease, the most common form of dementia. The findings don’t prove a cause-and-effect connection, the team says, but do merit clinical trials that could confirm a genuine benefit.

Sildenafil and similar drugs are called phosphodiesterase type 5 inhibitors, or PDE5Is. By inhibiting PDE5, these drugs can open up blood vessels in certain parts of the body, particularly the penis. That’s why, although sildenafil was originally developed to treat hypertension and chest pain, it was found to be especially effective at alleviating erectile dysfunction. And thus the little blue pill was born.

While these drugs are synonymous with ED, they are taken for other indications as well. Several are approved to treat pulmonary hypertension, or high blood pressure in the arteries of the lung. And scientists have been studying them for other medical uses, in both humans [gizmodo.com] and animals [gizmodo.com].

The most intriguing possibility for these drugs might be in their potential against Alzheimer’s, though. In 2021, a NIH-funded study found [nih.gov] evidence in the lab and from the real world that sildenafil could noticeably prevent or delay the onset of Alzheimer’s in older people—perhaps reducing people’s relative risk by as much as 69% compared to not taking the drug, based on insurance claims data. However, less than a year later, an October 2022 study from a separate team (also NIH-funded) that looked at Medicare data failed to find [nih.gov] any link between reduced Alzheimer’s risk and sildenafil.

The conflicting findings were enough to draw the attention of Ruth Brauer, an epidemiologist at the University of College London, and her team. So they decided to investigate for themselves, using medical record data collected through the UK’s National Health Service—data that gave them an advantage compared to past studies, according to Brauer.

“UK healthcare data can often be followed up for a very long time, and longer than U.S. insurance data. That’s because most of our data are collected by general practitioners or primary care physicians, and they often have patients under their care for decades,” she explained. “The second thing that is unique about UK healthcare data is that we have a lot of lifestyle variables in our data set, which can affect the risk of Alzheimer’s disease. So things like smoking or BMI, but also information on socioeconomic status.”

Brauer’s team analyzed data from 269,725 older male residents (average age 59) who were newly diagnosed with erectile dysfunction and either given a prescription for a PDE5I or not. They then tracked the outcomes of these two groups for five years on average.

By the end of the study period, 1,119 people overall had been diagnosed with Alzheimer’s disease. But those taking a PDE5I were significantly less likely to have Alzheimer’s than those who didn’t—about 18% less likely after adjusting for other potentially important factors. This reduced risk was only clearly seen with sildenafil and not other PDE5Is, but the discrepancy might be due to there being fewer users of these drugs and not any biological difference, Brauer said.

The team’s findings, published [neurology.org] Wednesday in the journal Neurology, suggest a more modest boon from these drugs than the 2021 study. But Brauer’s team was somewhat surprised they found any buffer at all, given that they used a similar method as the 2022 study. The different results might be explained by the longer follow-up data her team had on hand, she said, and she certainly thinks that the research could point to something real.

“It’s exciting to find this protective effect, and in a study that tried to rigorously control for all the variables that might influence your risk of Alzheimer’s disease,” she said.

There are still important questions left to be answered about this link, including exactly how these drugs might work to prevent or delay Alzheimer’s. Since they’re known to relax blood vessels, they could be improving blood flow in the brain enough to have a neuroprotective effect, Brauer said. Based on animal data, they might also be indirectly boosting levels of acetylcholine, a neurotransmitter important to cognition that steadily becomes depleted in those with Alzheimer’s (many Alzheimer’s drugs help manage symptoms by slowing this decline, but they can’t stop it).

Importantly, neither Brauer’s study nor any other to date provides conclusive evidence that PDE5Is can stop Alzheimer’s. But given the urgent need for medicines that can prevent or even just slow down the devastating condition, the authors say these drugs deserve a closer and extensive look from other researchers.

“The best thing, of course, would be to investigate this association with a randomized control trial,” she said. Ideally, this trial would study both men and women diagnosed with mild cognitive impairment, she adds. It would randomize them to either receive a PDE5I in conjunction with standard Alzheimer’s treatment or the standard treatment plus a placebo, then track their cognitive outcomes over time.

“We believe such a trial would provide a comprehensive understanding of the potential therapeutic benefits of these PDE5Is,” she said.

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