People with genetic variants that naturally lower cholesterol were found to have up to 80 per cent lower dementia risk in a study of more than one million participants.

The research analysed data from Denmark, England and Finland to assess how genes that mimic the effects of cholesterol-lowering drugs such as statins and ezetimibe influence dementia risk.

Scientists found that reducing blood cholesterol by one millimole per litre was linked to as much as an 80 per cent reduction in dementia risk for certain drug targets, suggesting possible benefits from cholesterol-lowering treatment.

The researchers used a method known as Mendelian randomisation, which allows scientists to study the effects of lowering cholesterol while avoiding confounding factors such as diet, weight and other lifestyle habits.

Dr Liv Tybjærg Nordestgaard led the research while at Bristol and now works at Copenhagen University Hospital–Bispebjerg and Frederiksberg hospital.

Dr Nordestgaard said: “What our study indicates is that if you have these variants that lower your cholesterol, it looks like you have a significantly lower risk of developing dementia.”

Some people are born with genetic variants that naturally affect the same proteins targeted by cholesterol-lowering drugs such as statins and ezetimibe.

By comparing these individuals with those without such variants, the researchers were able to measure differences in dementia risk.

Mendelian randomisation uses genetic variation as a natural experiment.

Because genes are inherited randomly at conception, this method can mimic randomised clinical trials and offer stronger evidence for cause-and-effect relationships than traditional observational research.

The findings suggest that having low cholesterol, whether due to genetics or medical treatment, could help reduce the risk of developing dementia. However, the study does not provide definitive evidence about the effects of the medicines themselves.

One of the main challenges in dementia research is that symptoms typically appear later in life, requiring decades of follow-up to detect meaningful changes. This makes long-term clinical trials difficult to conduct.

The biological link between high cholesterol and dementia is not yet fully understood. Dr Nordestgaard suggested that atherosclerosis — the build-up of cholesterol in blood vessels — may play a key role.

Dr Nordestgaard said: “Atherosclerosis is a result of the accumulation of cholesterol in your blood vessels.

“It can be in both the body and the brain and increases the risk of forming small blood clots—one of the causes of dementia.”

Blood clots can block small vessels in the brain, leading to vascular dementia — the second most common form of the condition after Alzheimer’s disease.

Even small clots can damage brain tissue over time and contribute to cognitive decline.

The study used data from large genetic research projects including the UK Biobank, the Copenhagen General Population Study, the Copenhagen City Heart Study, the FinnGen study and the Global Lipids Genetics Consortium.

These resources provide genetic and health information from diverse populations, improving the reliability of the findings across different ethnic and geographical groups.

The UK Biobank includes data from around 500,000 participants aged 40–69, while the Copenhagen studies have tracked Danish populations for several decades, providing detailed health records for long-term analysis.

“It would be a really good next step to carry out randomised clinical trials over 10 or 30 years, for example, where you give the participants cholesterol-lowering medication and then look at the risk of developing dementia,” Dr Nordestgaard added.

Such trials would provide direct evidence about whether cholesterol-lowering drugs can prevent dementia, rather than relying on genetic data.

However, their length and cost make them difficult to conduct.

Nimacimab significantly enhanced weight loss when combined with GLP-1 therapy without adding side effects, according to mid-stage clinical trial results involving 136 adults.

The experimental drug targets the body’s endocannabinoid system differently from existing weight-loss medications, offering a potential new approach to treating obesity when used alongside drugs such as semaglutide.

Participants given both drugs lost an average of 13.2 per cent of their body weight over 26 weeks, compared with 10.25 per cent for those on semaglutide alone — a statistically significant difference of nearly 3 per cent.

Skye Bioscience’s CBeyond study tested the first-in-class monoclonal antibody, which blocks CB1 receptors involved in appetite regulation and fat storage. The CB1 receptor is part of the endocannabinoid system, which helps control hunger, metabolism and fat accumulation. When these receptors become overactive, they can promote weight gain.

“This is the first clinical study to show that the combination of a CB1 inhibitor and a GLP-1 therapeutic can drive clinically meaningful additional weight loss beyond a GLP-1 drug alone,” said Louis Aronne, past president of The Obesity Society and clinical adviser to Skye Bioscience, the drug’s developers.

“Equally important, although the sample size is small, nimacimab achieved this without neuropsychiatric or additive gastrointestinal adverse events. I believe these results warrant further evaluation of the therapeutic potential of this novel CB1 inhibitor.”

Previous CB1-blocking drugs were abandoned because of psychiatric side effects such as anxiety and depression. Nimacimab has been engineered to stay outside the brain, potentially avoiding the problems that affected earlier drugs targeting this pathway.

In the 26-week trial, adults with overweight or obesity were randomly assigned weekly injections of nimacimab, semaglutide (the active ingredient in Wegovy), both drugs together, or placebo.

When used alone, nimacimab produced modest results — participants lost 1.5 per cent of their body weight compared with 0.26 per cent for placebo, a difference that was not statistically significant. Researchers said exposure to the 200 mg dose was lower than expected, suggesting higher doses may prove more effective.

“The 200 mg monotherapy arm provided important pharmacokinetic insight, showing that lower-than-expected drug exposure may have limited the observed effect and informing the dose-ranging strategy we are developing,” said Puneet Arora, the company’s chief medical officer.

Pharmacokinetic data describe how the body absorbs, distributes, metabolises and eliminates a drug, helping determine optimal dosing.

“At the same time, the combination of nimacimab with semaglutide produced a clinically meaningful additional weight loss that exceeded semaglutide alone, with a favourable tolerability profile even in patients who achieved the highest exposure levels.”

The most striking results came from the combination therapy. All participants receiving both drugs lost more than 5 per cent of their body weight, compared with 85 per cent of those on semaglutide alone. Two-thirds of the combination group lost more than 10 per cent, versus 50 per cent with semaglutide alone.

Importantly, the combination produced a healthier lean-to-fat mass ratio, indicating weight loss came primarily from fat reduction rather than muscle loss — addressing a concern that some GLP-1 drugs may cause skeletal muscle wastage.

Weight loss was still ongoing at the end of the 26-week study, suggesting further reductions could occur with longer treatment.

Safety findings were encouraging across all treatment groups. No neuropsychiatric side effects — such as anxiety, depression or insomnia — were reported with nimacimab, either alone or combined with semaglutide.

Gastrointestinal side effects, a leading cause of discontinuation with GLP-1 therapies, did not increase when nimacimab was added to semaglutide. These typically include nausea, vomiting, diarrhoea and constipation.

The overall discontinuation rate was 27 per cent, with only 3.7 per cent of participants dropping out due to adverse events — most of them in the placebo group.

“Gastrointestinal side effects remain a leading cause of discontinuation with obesity therapies,” said Sean Wharton, director of the Wharton Medical Clinic and a clinical adviser to Skye Bioscience.

“It was notable that nimacimab did not increase GI adverse events while adding clinically meaningful weight loss in combination with semaglutide. In my view, a next study with higher nimacimab dosing is the logical step to fully define its role in clinical practice.”

“With our preclinical data, toxicology safety margin, and PK modelling, we believe we have a path to support higher dosing, and we are evaluating the next stage of development to optimise dosing in potential future clinical trials,” Arora said.

Participants from the Phase 2a study are continuing in a 26-week extension trial, with results expected in early 2026. This will provide data on the longer-term efficacy and safety of the combination approach.

GLP-1 drugs such as semaglutide mimic a hormone that regulates appetite and blood sugar. While highly effective for weight loss, some studies have raised concerns about side effects including kidney injury, skeletal muscle loss and gastrointestinal issues.

A combination therapy that enhances weight loss without compounding side effects could address a major unmet need in obesity treatment, where many patients struggle with the tolerability of current medications.

Ultra-fast MRI scans taking under seven minutes could double NHS dementia testing capacity and help boost diagnosis rates across the UK, experts have said.

Scientists have developed a way to cut MRI scan times from 20–30 minutes to less than seven minutes, tackling a key bottleneck in dementia diagnosis, where one in three people never receive one at all.

The technique uses advanced physics to gather more information simultaneously during the scan, reducing total time by almost two thirds. When set-up times are included, the method could at least double capacity across NHS hospitals.

The research was developed by UCL’s Functional Imaging Laboratory and part-funded by Alzheimer’s Society.

Professor Nick Fox, a neurology expert who led the team, said the approach could transform access to vital diagnostic tools.

“This is really exciting. It means that we can make MRI scans — that people deserve to have — much, much more available,” he said.

“One in three people don’t get a dementia diagnosis at all, we estimate. And for those people who do, there are long delays and the recommendation that everybody should have a scan doesn’t happen.

“This could at the very least double the number of MRI scans we can do. There’s no reason why this approach can’t be used across nearly all scanners across hospitals in the UK.”

Current guidelines recommend brain imaging to rule out other causes of cognitive decline or identify the specific type of dementia.

Many patients, however, never receive a scan, and those who do are often given computerised tomography (CT) scans, which provide less detailed images than MRI.

Magnetic resonance imaging (MRI) uses a strong magnet to align protons in the body before knocking them out of position with radio waves.

As the protons return to alignment, sensors detect the released energy to map tissue types and create detailed brain images.

Lying still in the scanner can be particularly difficult for patients with memory problems or claustrophobia. Any movement can blur images, sometimes making them unusable and requiring a repeat scan.

The team tested the faster method on 92 volunteers.

Three neuroradiologists reviewed anonymised scans without knowing which were fast or standard and found the shorter scans were equally reliable for diagnosis.

“What we found was that, when we didn’t tell them which scans were fast or standard, experienced neuroradiologists couldn’t tell the difference,” Prof Fox said.

“The diagnostic ability was just as good, and in some cases slightly better because there was less blurring from people moving. It made much more difference which radiologist looked at your scan, or which day of the week it was.”

Latest NHS data for August showed 66 per cent of people living with dementia were thought to have a diagnosis, meaning one third remain undiagnosed.

Prof Fox said the NHS and government should be more ambitious about not only detecting dementia but identifying the specific cause.

“Saying ‘it’s dementia’ is like saying ‘it’s a rash’. If you went to see your GP, you wouldn’t accept them just saying ‘yes, it’s a rash’. You’d want to know if it’s cancer, eczema, something else,” he said.

“Dementia just means brain failure, it’s not working in the way it should anymore. But the underlying cause could be Alzheimer’s disease, strokes, lots of different things.

“We can only make progress if we give people an accurate diagnosis and a much more timely, rapid one.”

Scans are used alongside cognitive tests to identify the type of dementia. A scan might show past strokes or shrinkage in brain areas linked to memory, such as those affected in Alzheimer’s disease.

Labour’s recent 10-Year Health Plan for England said the UK is “far behind other countries in the levels of CT, MRI and positron emission tomography (PET) scanners for its population”.

The UK has 8.6 MRI scanners per million people — the lowest among comparable nations.

The 2023/24 National Audit of Dementia found that 44 per cent of patients attending specialist memory assessment services had a brain scan, with rates varying from 0–90 per cent depending on the service. In 2021, only 31.8 per cent of scans for suspected dementia were MRI.

MRI scanners cost around £1m. Prof Fox said many hospitals could use the faster method and boost capacity with little or no extra cost, although some may need a software update.

The researchers now plan to work with hospitals to trial the technique, which could also be adapted for other types of body imaging.