The Biggest Myths About Alzheimer’s – And What the Science Actually Shows

Alzheimer’s disease is one of the most feared diagnoses of modern life. And where there is fear, myths flourish.
Many of the biggest myths about Alzheimer’s have become widely accepted beliefs. We are told it is purely genetic, that it is an inevitable part of ageing, and that the main hope lies in new drugs targeting amyloid in the brain.

The science tells a far more complex and, importantly, far more hopeful story.

Myth #1 in the biggest myths about Alzheimer’s: ‘It’s all in your genes’

When Alzheimer’s runs in families, it is natural to assume destiny is fixed. Both your grandmothers had it, so you assume you will too.

Yet fewer than 1% of cases are caused by rare deterministic mutations in APP, PSEN1 or PSEN2 that lead to early-onset familial Alzheimer’s disease [1].

The vast majority of Alzheimer’s cases are late-onset and multifactorial. That means risk is shaped by multiple influences across a lifetime.

What about APOE4?

Celebrities like Liam Hemsworth have put the APOE4 gene on the map and into the public sphere and it is the strongest common genetic risk factor for late-onset Alzheimer’s. Having one copy increases risk; two copies increase it further [2]. But it does not determine outcome, as many APOE4 carriers never develop dementia. Many people with Alzheimer’s do not carry APOE4.

Genes influence vulnerability but they do not dictate your future.

APOE4 affects lipid transport, inflammatory signalling and neuronal repair. These processes are influenced by metabolic health, vascular function, nutrient status, sleep, stress physiology and lifestyle.

One of the most important things to remember is that gene expression is not static, as genes respond to the environment they are in.

The most important question is not necessarily ‘How do I check my genes?’ The question is ‘What environment are your genes operating in?’ Because you cannot change your genes but you can influence how they function and are expressed.

Myth #2 in the biggest myths about Alzheimer’s: ‘Amyloid causes Alzheimer’s‘

Amyloid plaques are a defining feature of Alzheimer’s disease. For more than 30 years, the dominant theory has been that amyloid buildup in the brain drives the disease. That theory has shaped billions in research funding and the development of new drugs designed to remove amyloid from the brain.

Recent anti-amyloid drugs such as lecanemab and donanemab have shown statistically significant slowing of cognitive decline in people with early symptomatic Alzheimer’s [3,4]. But it’s important to understand what that actually means.

All participants continued to worsen and this is an important distinction. A result can reach statistical significance and still fall short of changing the lived experience of patients and families in a substantial way.

Participants receiving these drugs declined slightly more slowly than those on placebo but no one’s memory improved and the disease was not reversed. The difference, while measurable, was modest. At the same time, these drugs carry recognised risks. In clinical trials, some participants experienced brain swelling and bleeding, known as ARIA. A proportion required hospital treatment, and rare fatal cases were reported [3,4].

So what does this tell us?

It tells us that amyloid may be part of the disease process. It does not tell us that Alzheimer’s is solely an amyloid disease.

If removing amyloid were the complete solution, the clinical effect would likely have been transformative. Instead, we see limited slowing in selected early-stage patients. More recently, scrutiny within the research community has highlighted how complex the biology truly is.

Amyloid is part of the picture but Alzheimer’s is not simply an amyloid problem.

Lowering amyloid slightly slows decline in some early cases. It does not address the upstream metabolic, vascular and inflammatory processes that develop over decades.

And that distinction matters.

Myth #3 in the biggest myths about Alzheimer’s: ‘Nothing can be done’

This is the most damaging myth of all.

The 2020 Lancet Commission concluded that around 40% of dementia cases worldwide are attributable to modifiable risk factors [5]. The 2024 update increased that estimate to approximately 45% [6].

Nearly half of cases.

And this is mainstream consensus. (Read more about the Alzheimer’s Expert Prevention Group’s APEG response to this recent Lancet report here.)

The identified risk factors include hypertension, diabetes, obesity, physical inactivity, smoking, depression, hearing loss and social isolation. Highlightly, Alzheimer’s risk is not fixed, it develops gradually over decades.

However, many researchers (ourselves included) believe even 45% may underestimate the true preventable proportion.

A large UK Biobank analysis published in Nature Human Behaviour modelled a broader range of modifiable factors and estimated that up to around 73% of dementia cases could be attributable to modifiable influences [10]. Professor David Smith of Oxford University, co-author of that study, member of our Scientific Advisory Board, and lead investigator of the VITACOG trial, has suggested this may still be conservative, as certain blood biomarkers were not included in the modelling.

Whether the true figure is closer to 45% or 73%, the direction of evidence is consistent

A large proportion of dementia and Alzheimer’s is preventable and you can modify your risk with simple changes.

Why biology supports prevention?

Alzheimer’s develops through interacting processes such as impaired glucose metabolism, vascular dysfunction, inflammation and elevated homocysteine.

Raised homocysteine, reflecting impaired methylation and B vitamin status, is associated with increased dementia risk and accelerated brain atrophy [7].

In the VITACOG trial, homocysteine-lowering B vitamins significantly slowed whole-brain atrophy in people with mild cognitive impairment [8]. The benefit was strongest in those with adequate omega-3 status [9].

That is structural brain change.

(When compared to anti-amyloid drug trials, which show modest slowing of decline in already symptomatic patients, VITACOG demonstrated slowing of brain shrinkage itself in an at-risk group.)

Once significant neuronal loss has occurred, reversal is unlikely, but years before diagnosis, measurable risk is accumulating and that is where prevention has its power.

Myth #4 in the biggest myths about Alzheimer’s: ‘It has a single cause‘

The reductionist model searches for one target and one solution.

Alzheimer’s reflects the interaction of multiple biological systems:

Glucose regulation
Vascular health
Lipid transport
Inflammation
Oxidative stress
Methylation
Sleep and stress regulation
Hormonal balance

People arrive at cognitive decline through different combinations of biological drivers. For some, insulin resistance may be central. For others, vascular stiffness and hypertension. In others, chronic inflammation and elevated homocysteine may play a key role. The destination may look similar, but the route is not.

This systems view explains why targeting one downstream marker, such as amyloid, yields modest slowing. Correcting multiple upstream drivers is biologically more plausible for meaningful long-term risk reduction.

Watch the video below to learn how Food for the Brain uses a systems-based approach.

Myth #5 in the biggest myths about Alzheimer’s: ‘It’s inevitable with ageing’

Age increases risk. However, that is only part of the story.

There are many individuals in their 80s and 90s with preserved cognition. The difference often lies in lifelong vascular, metabolic and lifestyle patterns, also known as patterns for prevention.

It is clear from what you have read so far that this is not an inevitable part of getting older. With the right knowledge and habits, it is something most people can avoid.

And that is why Food for the Brain exists, because not enough people know this and not enough people know what action they need to take to protect their brain.

A More Accurate Framework

Ageing is not the enemy. It is a privilege denied to many.

The goal is not to avoid growing older. It is to protect the brain as we do.

Alzheimer’s is not a single event. It reflects decades of interacting biological stress: metabolic strain, vascular change, inflammation and nutrient imbalance. These processes build slowly and often silently.

By the time symptoms appear, significant damage has already occurred.

This is why timing matters.

Late-stage drug therapies attempt to slow decline once pathology is established. Prevention strategies aim much earlier: identifying risk, strengthening resilience and reducing the biological pressures that drive degeneration in the first place.

The science is clear that a substantial proportion of dementia risk is modifiable [6,10]. That does not mean guarantees. It means opportunity.

You cannot change your genes and you cannot stop the passage of time.

Yet, you can influence how your brain responds to both.

And you can start today!

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