Dr Nathalie Helm
What the Lancet Commission, the FINGER study, and a new randomized trial tell us about the aging brain, and what we can do today.
Alzheimer’s disease and other forms of dementia have long been associated with old age and with little opportunity to change their course. But the picture is changing. A growing body of research shows that brain health is shaped by the same factors that affect the rest of the body, and that many of them can be influenced. That does not mean all dementia can be prevented. But we probably have more ability to influence how the brain ages than we used to think.
Blood pressure, blood lipids, blood sugar, physical activity, sleep, smoking, hearing, and social relationships are some examples of factors that affect not only the heart and blood vessels but also the brain. In this insight we review three lines of research that together give a clearer picture of what we can do, and where the limits of today’s knowledge lie.
Nearly half of dementia cases are linked to modifiable factors
In 2024 the Lancet Commission on dementia prevention published its latest major review of the research.1 The researchers identified 14 risk factors for dementia that can be at least partly modified. They are spread across the whole of life:
- Early life: less education.
- Midlife: hearing loss, high LDL cholesterol, depression, traumatic brain injury, physical inactivity, diabetes, smoking, high blood pressure, obesity, and excessive alcohol consumption.
- Later life: social isolation, air pollution, and untreated vision loss.
The Commission estimates that around 45 percent of dementia cases at the population level are linked to these factors.
That does not mean an individual can cut their dementia risk by 45 percent by living “perfectly.” The figure applies to the population as a whole, and age and genetics still play a large role. But the message is clear:
The future health of the brain is shaped by what happens in the body across much of our lives.
FINGER showed that several factors can be addressed at once
An important step came with the Finnish FINGER study, published in 2015.2 Just over 1,200 people aged 60 to 77 with an increased risk of cognitive decline took part for two years.
Half received regular health advice. The other half received a structured program with four components:
- a healthy diet
- physical exercise
- cognitive training
- monitoring of blood pressure, blood lipids, and other metabolic risk factors
After two years, the group on the structured program showed better development of overall cognitive ability, roughly 25 percent better than the control group, with the largest difference in executive function and processing speed.
FINGER supported a central idea: when it comes to the aging brain, perhaps we should not be looking for a single solution. Several smaller measures can together make a difference. The model is now being tested further within the World Wide FINGERS network, which brings together research teams in more than 70 countries.
Now researchers have gone a step further
A randomized trial in the United States, led by Dale Bredesen and published as a preprint in 2026, examined whether the same basic principle can be applied to people who have already begun to experience cognitive problems.3
Seventy-three people with mild cognitive impairment or early Alzheimer’s disease took part. Fifty were randomized to a comprehensive, individually tailored program and 23 to standard care. The trial ran for nine months.
Instead of giving everyone the same treatment, the researchers tried to identify the factors in each individual that might be contributing to their cognitive decline. They assessed, among other things, blood sugar and insulin resistance, blood lipids, inflammation, nutritional status, hormones, sleep and sleep apnea, and genetic factors.
Based on this, an individual program was put together. It could include dietary changes, aerobic and strength training, better sleep, treatment of sleep apnea, stress management, and cognitive training. The program also included dietary supplements, in some cases hormone therapy, measures targeting infections and toxins, and for some participants photobiomodulation (treatment with red and near-infrared light) and hyperbaric oxygen therapy.
1. What happened?
After nine months, participants in the individualized program had developed better than the standard-care group. The difference was statistically significant for:
- overall cognitive ability
- memory
- executive function
- processing speed
- participants’ own rating of their cognitive symptoms
- partners’ rating of the participants’ cognitive symptoms
Results on the MoCA, a short test often used to detect cognitive impairment, pointed in the same direction but were not statistically significant.
Several metabolic markers also improved in the treatment group, for example HbA1c (long-term blood sugar), insulin resistance, blood lipids, blood pressure, and weight.
On the other hand, the researchers saw no clear difference in brain volume between the groups, and blood markers of Alzheimer’s disease such as amyloid and p-tau217 changed only marginally.
These are interesting results. But there are important caveats.
2. Does this mean Alzheimer’s disease can be reversed?
No, we cannot say that based on this study.
The study was small and lasted only nine months. Participants and clinicians knew which treatment was being given, and the intervention group had considerably more contact with physicians, coaches, nutritionists, and trainers. The diagnosis was not confirmed with amyloid PET or spinal fluid testing either, and the participants were motivated people who had sought out the study themselves.
Nor do we know what produced the effect. Was it the exercise? The diet? Better sleep? Treatment of sleep apnea? Improved metabolic health? The cognitive training? Or the combination?
It is also important to distinguish between the parts of the program that have relatively strong scientific support and the more experimental elements. Treating high blood pressure, diabetes, high blood lipids, and sleep apnea, and promoting physical activity, rest on an entirely different evidence base than extensive testing and treatments aimed at toxins, certain infections, or various supplements.
What can we take with us today?
The Lancet Commission, FINGER, and the new study examine different things, and their results should not be conflated. But they point to a shared principle:
Brain health is shaped by far more than the brain alone.
Vascular health, blood pressure, blood sugar, physical activity, sleep, hearing, and vision probably affect our cognitive reserve and how well the brain copes with aging.
That is why the prevention of cognitive decline does not need to start when memory begins to fail. It can start much earlier.
The HELM perspective
The biological changes behind Alzheimer’s disease can begin many years, sometimes decades, before the first clear symptoms appear. That gives us an important window of time.
We cannot change our age or our genes, and we can never guarantee that a person will not develop dementia. But we can influence a great deal else:
- Treat high blood pressure and elevated blood lipids, especially LDL cholesterol.
- Prevent and treat diabetes and improve blood sugar control.
- Stay physically active and preserve fitness and muscle mass, with both endurance and strength training.
- Prioritize sleep, ideally at least seven hours a night, and investigate suspected sleep apnea.
- Reduce chronic stress and make room for recovery.
- Address hearing and vision, for example with a hearing aid for hearing loss.
- Avoid smoking and heavy drinking.
- Maintain social relationships and keep challenging the brain.
- Get the shingles vaccine as recommended. Several studies suggest that vaccination may be linked to a lower risk of dementia.4–7
There are also factors where the research is promising but not yet conclusive, for example hormone therapy around menopause. Here we make an individual assessment together with each patient rather than giving general advice.
This may sound less exciting than finding a single substance that can “rejuvenate the brain.” But that is exactly where one of the most valuable insights from today’s research lies.
The dementia prevention of the future is likely to be less about a miracle treatment and more about identifying and influencing risk factors early, individually, and over a long time.
It is a clear example of why preventive medicine needs to start long before we fall ill.
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- Why do we age, and what can we actually influence?Twelve biological processes behind aging, and the everyday factors that influence them.
The content on this page is general information and does not replace individual medical advice. If you have symptoms or questions about your own health, consult a physician.
- Livingston G, Huntley J, Liu KY, et al. Dementia prevention, intervention, and care: 2024 report of the Lancet standing Commission. Lancet. 2024;404(10452):572–628. PubMed
- Ngandu T, Lehtisalo J, Solomon A, et al. A 2 year multidomain intervention of diet, exercise, cognitive training, and vascular risk monitoring versus control to prevent cognitive decline in at-risk elderly people (FINGER): a randomised controlled trial. Lancet. 2015;385(9984):2255–2263. PubMed
- Toups K, Tanio CP, Hathaway A, et al., Bredesen DE. Precision Medicine Treatment of Alzheimer’s Disease: Successful Randomized Controlled Trial. Preprints.org. 2026, version 3. Not peer reviewed. Preprints.org
- Eyting M, Xie M, Michalik F, et al. A natural experiment on the effect of herpes zoster vaccination on dementia. Nature. 2025;641(8062):438–446. PubMed
- Taquet M, Dercon Q, Todd JA, Harrison PJ. The recombinant shingles vaccine is associated with lower risk of dementia. Nat Med. 2024;30(10):2777–2781. PubMed
- Xie M, Eyting M, Bommer C, et al. The effect of shingles vaccination at different stages of the dementia disease course. Cell. 2025;188(25):7049–7064.e20. PubMed
- Yin Y, Deng J, Liu J. The association between herpes zoster vaccination and the decreased risk of dementia: A systematic review and meta-analysis of cohort studies. J Alzheimers Dis. 2025;106(4):1232–1241. PubMed