Nearly half of dementia cases may trace to risks you can still change, a Lund University study finds

A study from Lund University in Sweden reports that a large share of dementia cases may be tied to risk factors people can potentially change, such as smoking and high blood pressure. Using brain scans and spinal-fluid analysis, the researchers went a step further than most prior work by tracing exactly how those risk factors damage the brain over time. The results suggest that different modifiable factors harm the brain through different biological routes, a nuance with real consequences for prevention.

Following 494 adults with brain imaging

The researchers analyzed data from 494 adults with an average age of 65 who were not cognitively impaired when the study began and were followed for an average of four years. Rather than relying on cognitive tests alone, the team used magnetic resonance imaging and positron emission tomography scans together with analysis of cerebrospinal fluid to watch how the participants’ brains changed. That combination let them link specific risk factors to specific forms of damage as they accumulated, an approach summarized in coverage that noted nearly half of dementia cases may be linked to risks people can change.

Dementia is not a single disease but an umbrella term for a loss of memory and thinking severe enough to interfere with daily life. Alzheimer’s disease and vascular dementia are the two most common causes, and the Lund analysis focused on the physical signatures of both: the amyloid and tau proteins associated with Alzheimer’s, and the blood-vessel damage that underlies vascular dementia.

Different risks damage the brain in different ways

The central finding was that modifiable risk factors did not all act on the brain in the same way. Most of them, including smoking, cardiovascular disease, high blood lipids and high blood pressure, were linked to damage in the brain’s small blood vessels and to a faster buildup of so-called white matter changes. That vascular damage impairs how well blood vessels function and can ultimately lead to vascular dementia. The pattern points to blood-vessel health as a major, and modifiable, driver of cognitive decline.

Two factors stood apart. Diabetes was associated with an increased accumulation of amyloid beta, the protein fragment that clumps into the plaques characteristic of Alzheimer’s disease. And people with a lower body mass index showed a faster accumulation of tau, the second hallmark protein. The Lund University summary of the work described how these lifestyle-related factors map onto distinct brain changes, reinforcing the idea that a one-size-fits-all view of dementia prevention is too simple.

Why the biological pathways matter

Distinguishing the pathways is more than an academic exercise. If most modifiable risk factors damage the brain by harming its blood vessels, then interventions that protect vascular health, such as controlling blood pressure and cholesterol and not smoking, could plausibly reduce a substantial fraction of dementia by preventing that damage. If diabetes drives amyloid buildup through a different mechanism, then managing blood sugar might address a route to Alzheimer’s pathology that blood-pressure control alone would not reach.

The peer-reviewed report underpinning the coverage, published under the title describing associations of modifiable and non-modifiable risk factors with longitudinal white matter changes, amyloid and tau, laid out these distinct relationships in detail. The full study is available through the National Library of Medicine, and it frames the modifiable factors as targets whose effects can be traced through measurable changes in brain tissue over the four-year follow-up.

What “nearly half” does and does not mean

The estimate that nearly half of dementia cases may be connected to modifiable risks aligns with a broader body of research, including prior expert reviews that have put the share of potentially preventable dementia in a similar range. But the phrase requires care. It reflects population-level attributable risk, an estimate of how many cases might be avoided if those factors were eliminated across a whole population, not a promise that any individual can cut personal risk in half. It also depends on assumptions about how strongly each factor contributes.

The study was observational, so it identified associations between risk factors and brain changes rather than proving direct causation. Its strength lies in the longitudinal imaging and fluid data, which show risk factors preceding measurable damage rather than simply coexisting with it. That temporal sequence makes a causal interpretation more plausible, though controlled trials of specific interventions remain the standard for confirming that changing a risk factor changes outcomes.

A prevention message grounded in mechanism

The practical takeaway is consistent with existing public-health advice but adds a mechanistic reason to follow it. Not smoking, controlling blood pressure and cholesterol, and managing diabetes are already standard recommendations for heart health; the Lund findings suggest they also protect the brain, in part by preserving the small blood vessels whose failure contributes to vascular dementia. The observation that lower BMI tracked with faster tau accumulation is a reminder that the relationships are not always simple, and that unintended weight loss in older adults can itself be a warning sign rather than a goal.

By mapping which risk factors travel through which biological pathways, the study offers a more targeted picture of dementia prevention than the familiar list of dos and don’ts. It does not overturn that list. Instead, it explains why the items on it may work, and it points toward a future in which prevention could be tailored to the specific way a given risk factor threatens the brain.

This article was produced with the assistance of AI and reviewed by Morning Overview editors prior to publication.

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