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Integrative Health

93% of Alzheimer’s Cases Could Be Tied to This One Gene

Author: Ava Durgin

April 06, 2026

Assistant Health Editor

By Ava Durgin

Assistant Health Editor

Ava Durgin is the former Assistant Health Editor at mindbodygreen. She holds a B.A. in Global Health and Psychology from Duke University.

Image by Kike Arnaiz / Stocksy

April 06, 2026

Many of us have been touched by Alzheimer’s in some way. Maybe a parent or grandparent. At some point, we tend to wonder whether we, too, will be affected down the line. And whether or not our vulnerability is already written within our genes.

It’s easy to think about genetics in extremes. Either you’re predisposed, and it’s out of your hands, or you’re not, and you’re in the clear. But the reality is more nuanced than that. And a new study1, published in NPJ Dementia, is offering interesting insight into the tension.

How one gene shapes Alzheimer’s risk

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How much of Alzheimer’s disease can actually be traced back to variation in a single gene? This was the question researchers set out to answer.

To get there, they pulled from four massive datasets, including UK Biobank and FinnGen, along with brain imaging data and neuropathology-confirmed cases. Altogether, the analysis covered hundreds of thousands of people and approached Alzheimer’s from multiple angles, from clinical diagnoses to what’s happening inside the brain itself.

The focus was a gene called APOE, which comes in three common versions: ε2, ε3, and ε4. Every person carries two copies. For decades, ε4 has been labeled the “high-risk” variant, while ε2 is thought to be protective. ε3, the most common version, has largely been treated as neutral.

This study took a more comprehensive approach than most. Instead of focusing only on the well-known high-risk ε4 variant, the researchers looked at the combined impact of both ε3 and ε4. They also compared these groups to people with the lowest-risk profile, which gave them a clearer baseline for what “low risk” actually looks like.

That shift matters. In many earlier studies, ε3 was treated as neutral, which likely understated how much risk is shared across the general population. By using a truly low-risk group as the reference point, this study offers a more accurate picture. It shows that what we’ve been calling “normal” risk may actually include a meaningful level of underlying vulnerability.

Up to 93% of Alzheimer’s cases may be linked to APOE variation

The headline finding is hard to ignore. Depending on how Alzheimer’s was measured, between 72% and 93% of cases could be attributed to the combined effects of the ε3 and ε4 variants.

That’s a much larger share than previous estimates, and it comes down to one key shift. When you stop treating ε3 as neutral and include it in the risk equation, the gene’s overall influence expands dramatically.

Most people carry some level of risk linked to the APOE gene, not just a small group with a so-called “high-risk” variant. In other words, this isn’t about rare genetic bad luck that only affects a few people. It’s something much more common and much more shared than we once thought. The majority of us have at least one version of this gene that can influence risk, which shifts how we think about Alzheimer’s. It’s less about a clear divide between “at risk” and “not at risk,” and more about a spectrum that most people fall somewhere on.

There’s another layer to this, too. When researchers looked at all types of dementia, not just Alzheimer’s, this same gene was linked to about 45% of cases. That’s still a significant portion, but noticeably lower than what they found for Alzheimer’s alone. It highlights an important point that not all cognitive decline is driven by the same biology. Alzheimer’s appears to be more tightly connected to APOE, while other forms of dementia likely involve different pathways and risk factors.

Why this changes how we think about prevention

It’s easy to hear something like this and think, well, if it’s in my genes, what’s the point? But that’s not what this research is saying.

Even people with higher-risk versions of this gene don’t always develop Alzheimer’s, meaning your genetics influence risk, but they don’t seal your fate.

Part of the reason comes down to how this gene actually works. The APOE gene influences how the brain handles things like amyloid buildup, inflammation, and energy use. Those processes don’t operate in isolation. They interact with cardiovascular health, metabolic function, sleep, and lifestyle exposures that accumulate over decades. So the same genetic risk can look very different from one person to another, depending on the environment it’s operating in.

Plus, if one gene contributes this much to disease risk, it becomes a clear target for intervention. Researchers are already exploring ways to modify ho