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Viagra reduces the risk of developing Alzheimer’s by 18%, study suggests

Taking Viagra could cut the risk of developing Alzheimer’s by 18 per cent, a study of 300,000 men has revealed.

The finding has fuelled hopes that Viagra and other erectile dysfunction drugs could prove to be a cheap and effective way to protect people at risk of dementia.

Scientists said they have been greatly encouraged by the findings and now want to see a major trial designed to prove cause and effect.

They are also looking at whether the drug may help to protect women as well as men – something they say seems entirely likely.

Ruth Brauer, of University College London, which conducted the study, told i:”We have found an unexpected benefit of a widely used drug. This may be an excellent candidate for ‘re-purposing’ to prevent Alzheimer’s in people at high risk of the disease.

“These results are encouraging and warrant further research … to determine whether these findings would apply to women as well.”

She added: “Although we’re making progress with the new treatments for Alzheimer’s disease that work to clear amyloid plaques in the brain for people with early stages of the disease, we desperately need treatments that can prevent or delay the development of Alzheimer’s disease.”

The first of these new amyloid clearing drugs – known as lecanemab – is thought likely to be approved in the UK later this year after being approved in the US last year.

Despite the positive findings from the study, which involved 269,725 men with an average age of 59, scientists have stressed that more research is needed to confirm the effectiveness of erectile dysfunction drugs – and warned that men should not start taking them as a precautionary measure.

That’s because the study found an “association” between Viagra and Alzheimer’s risk – finding that people who took it were less likely to develop dementia – rather than proving for certain that the drug was responsible for the reduced risk.

The study followed men who were newly diagnosed with erectile dysfunction over an average of five years, during which time 1,119 people developed Alzheimer’s disease.

The group was split into two, with 55 per cent who had prescriptions for erectile dysfunction drugs and 45 per cent who did not. The participants did not have any memory or thinking problems at the start of the study.

Once researchers adjusted for other factors that could affect the rate of Alzheimer’s disease, such as age, smoking status and alcohol consumption, they found that people who took erectile dysfunction drugs were 18 per cent less likely to develop Alzheimer’s than people who did not take the drugs.

Independent scientists have welcomed the news but want more research into the benefits of Viagra in preventing the disease.

Dr Leah Mursaleen, head of research at Alzheimer’s Research UK, said: “While this is an encouraging finding, it doesn’t yet confirm whether these drugs are directly responsible for reducing Alzheimer’s risk, nor whether they can slow or stop the disease. Further research – including clinical trials – will be needed to confirm whether these drugs can indeed play a role in preventing or treating Alzheimer’s.

“Such studies should also uncover whether these drugs might have effects in other groups, such as women, and men without a diagnosis of erectile function.”

But she added: “Developing drugs for diseases like Alzheimer’s is a costly process and can take many years. Being able to repurpose drugs already licensed for other health conditions could help accelerate progress and open up new avenues to prevent or treat dementia-causing diseases.”

Ivan Koychev, consultant neuropsychiatrist at Oxford University Hospitals NHS Foundation Trust and a senior clinical researcher at Dementias Platform UK, a group of scientists and pharmaceutical companies funded by the Medical Research Council to further research into the area, said: “Overall, this is a significant development as re-purposing already existing drugs for the prevention of dementia is a promising strategy to stop dementia from developing in the first place using drugs with known safety profile.”

He said clinical trials should be conducted, where erectile dysfunction drugs are given against a dummy pill to people at risk, in order to come to a conclusion on their usefulness for dementia prevention.

Tara Spires-Jones, president of the British Neuroscience Association and a professor at the UK Dementia Research Institute at the University of Edinburgh, said that while the study does not conclusively prove that drugs like Viagra reduce Alzheimer’s risk, it does “provide good evidence that this type of drug is worth further study in future”.

How does this add to previous studies?

Those behind the new research hope it will go some way to settling the contradictory conclusions of two previous studies looking at Viagra and Alzheimer’s Disease.

The first, led by Cleveland Clinic and published in the Nature Aging journal in 2021, suggested a much greater effect for the drugs finding them to be associated with a 69 per cent risk reduction for Alzheimer’s.

But the second, led by Harvard Medical School and published in Brain Communications in 2022 found there to be no effect.

The researchers behind the new study say that, while not conclusive, their results are much more reliable because it involved more people using erectile dysfunction drugs, was less open to biases that could skew the results than the others and had a longer follow-up period. It is also the only one to use UK data.

Dr Brauer said: “Based on these conflicting results we decided to run an analysis using UK data which have several advantages compared to US data.

“For example, a benefit of the UK database we used made it possible to include additional key variables in our analysis, such as blood pressure, alcohol status, BMI and socioeconomic status, which are commonly unavailable in US insurance claims data. Furthermore, we restricted our cohort to men with Erectile Dysfunction (ED), therefore using a homogenous population.”

An editorial about the new study, published in the journal Neurology, noted the limitations in the two previous studies. Pointing to a number of limitations in the Nature Aging study, it said “all of which have been addressed in the [new] study”.

And on the Harvard Medical School study, the editorial – by Sevil Yasar and Lolita Nidadavolu, both of Johns Hopkins Medicine – pointed out that the differing results could, in part, be down to the shorter followup period, of five months, compared to five years for the new study.

“Five months may have been too short for the outcome of interest to occur,” they said.

How Viagra may protect against Alzheimer’s

Viagra works by dilating blood vessels to allow more blood to flow through and was first developed to treat high blood pressure. It is sometimes used to treat pulmonary hypertension – high blood pressure in the blood vessels that supply the lungs.

Erectile dysfunction drugs can also cross the blood-brain barrier where they are thought to affect brain cell activity by acting on a “signalling” chemicals in the brain that help cells communicate that are being researched separately for its links to memory. While the precise mechanism is little understood research in animals has found the drugs protect the nerve cells in the brain against damage.

Matthew Adesuyan of UCL, one of the study’s co-authors, said that evidence based largely on animal studies suggests two possible mechanisms for how these drugs may help lower the risk of Alzheimer’s disease.

“First, the relaxation of blood vessels has been shown in animal models to extend to the brain and result in increased cerebral blood flow – which can be neuroprotective.”

“And second, some studies have suggested these erectile dysfunction drugs help facilitate greater availability of a chemical in the brain (acetylcholine), which supports memory function and cognition”.

Dr Koychev adds: “[The effect] is more pronounced in people with heart disease risk factors – such as high blood pressure and diabetes – suggesting that the effect may be due to neuroprotection through vascular mechanisms”.

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