Nearly half of all dementia cases worldwide may be linked to lifestyle and health factors that people can actively change, and new research from Lund University has now gone a step further by showing precisely which risk factors damage which parts of the brain.
Published in January 2026 in The Journal of Prevention of Alzheimer’s Disease, the study followed almost 500 cognitively healthy adults over four years and tracked real, measurable changes happening in the brain before any symptoms of dementia appeared.
The finding that stands out: smoking, high blood pressure, cardiovascular disease, and high blood lipids are each individually linked to faster damage to the brain’s blood vessels and accelerating changes in white matter, the inner wiring network of the brain that is most commonly affected in vascular dementia.
Separately, diabetes was linked to faster accumulation of amyloid beta, the sticky protein at the heart of Alzheimer’s disease.
These are not theoretical associations.
The researchers watched these changes unfold in real time, in real people who had no dementia symptoms at the start of the study.
And the window they observed, the years before symptoms appear, is increasingly seen as the most important period for prevention.
Why This Study Matters More Than Most
Dementia research is not short on studies linking lifestyle to risk.
What makes this Lund University study different is the level of precision it applies.
Most previous research on modifiable dementia risk has treated the condition as a single disease.
The truth is more complicated.
Dementia describes a group of symptoms caused by different underlying processes in the brain, and those processes respond to different risk factors in different ways.
By tracking specific biological markers in the brain, rather than simply asking whether participants later developed dementia, the researchers could see which lifestyle factors were feeding which underlying disease mechanisms.
This distinction carries real practical weight.
A person trying to protect their brain health needs to know whether addressing blood pressure will help with Alzheimer’s specifically, or with vascular damage, or both.
This study gives clearer answers to that question than most research has managed before.
The Two Types of Dementia at the Centre of This Research
To understand the findings, it helps to know what separates these two forms of dementia.
Alzheimer’s disease is the most common form globally.
It is characterised by the accumulation of two proteins in the brain: amyloid beta, which clumps into sticky plaques between nerve cells, and tau, which forms tangled fibres inside cells and disrupts their internal transport systems.
According to the National Institute on Aging, as beta-amyloid builds up to a tipping point, tau begins to spread rapidly throughout the brain, connections between neurons break down, and widespread cell death follows.
The result is the memory loss, confusion, and personality changes that most people associate with Alzheimer’s.
Vascular dementia works through a different mechanism entirely.
As Alzheimer’s Research UK explains, it develops when blood vessels in the brain become damaged, reducing the flow of oxygen and nutrients to nerve cells.
The area most often affected is the brain’s white matter, the network of insulated nerve fibres that connects different brain regions and allows them to communicate.
When the small blood vessels feeding white matter become narrowed or blocked, brain cells in those areas die and the connections are lost.
This can cause a different pattern of cognitive problems, often affecting speed of thinking, planning, and attention rather than memory initially.
Many people with dementia have damage from both processes simultaneously, which is why the Lund University researchers argue that managing vascular risk factors matters even for Alzheimer’s patients.
What the Study Actually Measured
The research team studied 491 participants with an average age of 65.
All were cognitively healthy at the start, meaning no existing dementia or cognitive decline.
Over four years, the researchers tracked three specific markers of brain change:
White matter hyperintensities are bright spots visible on brain MRI scans that indicate damage to the brain’s white matter from impaired blood supply.
Their volume and rate of accumulation were measured across the four years.
Amyloid beta levels in the brain were monitored as a marker of Alzheimer’s-related change.
Tau protein levels were also tracked as a secondary Alzheimer’s marker.
Participants’ modifiable risk factors, including smoking status, blood pressure, blood lipid levels, cardiovascular disease, diabetes, BMI, physical activity, alcohol consumption, and hearing loss, were documented.
Non-modifiable factors such as age, sex, and genetic profile were also recorded.
The goal was not simply to see who developed dementia over four years, but to identify which risk factors were accelerating the underlying biological changes associated with each type.
The Vascular Risk Factors: Smoking, Blood Pressure, and the White Matter Connection
The clearest finding from the study was that most of the common modifiable risk factors converged on the same target: the brain’s blood vessels and white matter.
Smoking, high blood pressure, cardiovascular disease, and high blood lipids were all independently associated with faster accumulation of white matter damage.
This makes biological sense.
According to the Cleveland Clinic, high blood pressure, elevated blood sugar, high cholesterol, and smoking can all increase the number of damaging lesions in the brain’s white matter by impairing blood flow or damaging blood vessel walls directly.
Smoking, in particular, harms blood vessels throughout the body.
It promotes inflammation, narrows arteries, and reduces the elasticity of vessel walls, all of which compromise the flow of blood and oxygen that brain tissue depends on.
High blood pressure compounds this by placing the small, fragile blood vessels of the brain under sustained physical stress.
Mayo Clinic notes that conditions like high blood pressure, high cholesterol, diabetes, and smoking are well-established risk factors for vascular dementia precisely because they damage these tiny vessels over time.
The Lund University study adds something important to this picture: it shows these changes beginning and accelerating in people who are cognitively normal, years before any symptoms would appear.
That gap between biological damage and clinical symptoms is the window for prevention.
Diabetes and Alzheimer’s Proteins: A More Complex Relationship
The study’s second major finding drew a different kind of line, connecting diabetes to faster accumulation of amyloid beta in the brain.
This connection has been suspected for some time, and the Lund University data adds prospective human evidence to support it.
The mechanism is not fully understood, but several pathways have been proposed.
Insulin resistance, the hallmark of type 2 diabetes, may impair the brain’s ability to clear amyloid beta before it builds up into plaques.
Chronically elevated blood sugar also promotes inflammation and oxidative stress throughout the body, including in the brain.
These conditions are known to accelerate the cellular damage associated with Alzheimer’s pathology.
The finding adds to a growing body of evidence that has led some researchers to describe type 3 diabetes as an informal term for the specific pattern of insulin signalling problems seen in Alzheimer’s brains.
The researchers also found that lower BMI was associated with faster tau accumulation, a finding they describe as requiring further investigation before conclusions are drawn.
This is an unexpected result, and it does not mean being underweight is protective or that weight loss increases risk.
It may reflect reverse causation, where changes already occurring in the brain affect body composition before symptoms appear.
It may also be specific to this older, metabolically compromised population.
Future research will need to unpack this finding more carefully.
The 45% Figure: What the Broader Science Is Saying
The Lund University study lands in the middle of a growing global consensus about dementia prevention.
The 2024 report of the Lancet Commission on Dementia Prevention, Intervention and Care, one of the most comprehensive analyses of dementia risk in the world, concluded that approximately 45% of dementia cases are potentially preventable by addressing 14 modifiable risk factors across the life course.
That figure represents an increase from the Commission’s 2020 estimate of 40%, reflecting new evidence that has accumulated in recent years.
The 2024 report also added two newly identified risk factors to its list: untreated vision loss and high LDL cholesterol, bringing the total number of modifiable risk factors identified to 14.
As Alzheimer’s Disease International reported, the Lancet Commission is clear that this 45% figure assumes those risks are genuinely causal and fully eliminable, a theoretical upper bound, but the message it sends is powerful.
Dementia is not an inevitable consequence of ageing.
Its trajectory can be shaped, and shaped significantly, by what happens in the decades before symptoms emerge.
The Earlier in Life, the Better
One of the most important insights from the current wave of dementia research is about timing.
Most modifiable risk factors do their most significant damage in midlife, roughly between the ages of 40 and 65, even though dementia symptoms typically appear decades later.
The Lund University study followed participants with an average age of 65.
That means the damage being observed was accumulating in a group that had likely been building risk factors for years or even decades prior.
This is not a reason for pessimism.
It is a reason to act early.
Research published in Neurology found that people who maintained four to five healthy lifestyle factors had a 60% lower risk of Alzheimer’s dementia compared to those who maintained fewer than two.
Even adopting healthier habits in midlife or early older age appears to have measurable protective effects.
The brain retains significant capacity for adaptation, and reducing the burden of vascular and metabolic risk can slow the accumulation of the biological changes that lead to dementia.
What This Means for Mixed Dementia
A point the Lund University researchers emphasise is particularly relevant for real-world clinical care.
Many people with dementia do not have a pure form of either Alzheimer’s disease or vascular dementia.
They have mixed dementia, where both vascular damage and Alzheimer’s-related protein accumulation are present simultaneously.
This is more common than often appreciated, particularly in older age groups.
The practical implication is significant.
Even someone who carries genetic risk factors for Alzheimer’s, or who already shows some amyloid accumulation in the brain, stands to benefit from addressing their cardiovascular and metabolic risk factors.
Reducing vascular burden reduces one of the contributing layers of damage, even if it cannot eliminate the Alzheimer’s pathology entirely.
As senior author Sebastian Palmqvist puts it: “Focusing on vascular and metabolic risk factors can still help reduce the combined effects of several brain changes that occur simultaneously.”
That is a message of genuine hope, grounded in careful science.
The Risk Factors Worth Addressing Right Now
Taken together, the Lund University study and the broader body of evidence from the Lancet Commission point to a clear set of priorities for anyone wanting to protect their long-term brain health.
Blood pressure management sits at the top of the list.
Hypertension is one of the most prevalent modifiable risk factors globally and one of the most consistently linked to both vascular brain damage and accelerated cognitive decline.
According to the US government’s Alzheimer’s information resource, keeping blood pressure in a healthy range is one of the primary strategies for preventing vascular dementia.
Stopping smoking removes one of the most potent sources of vascular inflammation and oxidative stress affecting both the heart and the brain.
Managing cholesterol and cardiovascular health reduces the risk of the blood vessel damage that feeds white matter deterioration.
Controlling blood sugar and preventing or managing diabetes may reduce the rate at which amyloid beta accumulates in the brain, targeting the Alzheimer’s pathway specifically.
Physical activity appears repeatedly in dementia prevention literature as one of the most broadly protective habits, improving vascular health, reducing inflammation, and supporting the brain’s ability to clear damaging proteins.
Hearing loss, included among the Lancet Commission’s modifiable risk factors and also examined in the Lund University study, is worth addressing promptly because untreated hearing loss has been linked to social withdrawal, cognitive underuse, and accelerated decline.
The same applies to vision loss, newly added to the Lancet Commission’s list in 2024.
A Prevention Opportunity the World Cannot Afford to Ignore
The global numbers behind this research are stark.
Approximately 55 million people worldwide are currently living with dementia, with a new case diagnosed every three seconds.
That number is projected to nearly triple by 2050 as populations age.
There are currently no treatments that stop or reverse the disease.
Which is exactly why prevention has become the most urgent frontier in dementia research.
The Lund University study adds something specific and valuable to that conversation: it shows which lifestyle factors are damaging which biological systems in the brain, years before any symptoms emerge, in people who look and feel cognitively normal.
It is a reminder that the brain changes associated with dementia begin long before the disease becomes visible.
And it is a reminder that the choices being made today in kitchens, clinics, and living rooms around the world are shaping the cognitive health of populations decades from now.
Half of dementia cases may be preventable.
That is not a small margin for hope.
That is an extraordinary opportunity, and one that belongs to all of us.
Sources: The Journal of Prevention of Alzheimer’s Disease (study) | Lund University | The Lancet Commission 2024 | Alzheimer’s Disease International | National Institute on Aging | Mayo Clinic | Alzheimer’s Research UK
