The Early Signs of Alzheimer's — and Everything They Get Mistaken For

The early signs of Alzheimer’s disease: what to look for

Alzheimer's usually begins with the memory for events, because it usually begins in the part of the brain that lays those memories down. The pattern is particular. It is losing the whole event, not the detail within it, not forgetting a name from the dinner party, but having no memory that the dinner happened at all. It is repeating a question or a story with no sense of having asked it, something families see long before the person does. It is fresh information slipping away while old memories stay vivid, which is precisely what fools everyone into thinking the memory is fine. It is losing the thread of a conversation or a book and reading the same page twice. It is the keys turning up somewhere strange, with no way to retrace the steps that put them there. It is fumbling a task that was second nature, a recipe cooked for years, a route driven for decades. It is getting lost where you have never been lost, or losing your grip on the date and the order of things. It is the word that will not come, well past the ordinary tip-of-the-tongue. And it is often, first of all, a quiet withdrawal from the things a person used to love.

Two honest qualifications. Alzheimer's does not always begin with memory, some forms start with vision and space, others with language or behaviour. And the whole picture is one of change over months and years. A bad fortnight is not this.

The five things it is mistaken for

Ordinary ageing. Change with age is real: recall slows, names take longer, lists become necessary. But it comes on gently, holds steady, and does not stop you doing what you have always done. The little word "just", as in "just getting older", does a great deal of quiet work, and it is the reason so many people wait two years before they ask.

Depression and low mood. This is the most consequential confusion of all, and it runs in both directions at once. Depression in later life often speaks in the language of memory rather than sadness (poor concentration, slowed thinking, a mind that will not hold things) and when the depression is treated, the memory frequently returns. That treatable picture used to be called pseudodementia, and to miss it is to treat someone as though they have an incurable disease when in fact they have a curable one. But the traffic runs the other way too. Depression is itself one of the modifiable risks for dementia, and a new low mood, a new anxiety, a new flatness in later life can be the first sign of a neurodegenerative process rather than a thing apart. Apathy in particular, the loss of drive without the weight of sadness, is read as depression, and read by families as laziness. Three possibilities, then, from a single presentation: depression causing the symptoms, depression signalling early disease, or both together. That is not a distinction a ten-minute appointment can safely make.

The menopause. Perimenopause routinely brings fog, lost words, poor concentration and slips of memory. They are real, they are driven by hormones, and they usually settle. The trouble is that they arrive in the same decade as the earliest changes of young-onset Alzheimer's, and from the outside they look alike. A woman coming forward at fifty with cognitive symptoms will usually, and often rightly, be told it is hormonal. The skill lies in knowing when that answer does not fit: when the symptoms march steadily on rather than ebb and flow, when they do not track the cycle, when function is genuinely slipping, when there is a strong family history behind them.

Stress and burnout. For anyone carrying real responsibility, chronic stress, thin sleep and a nervous system running hot will produce genuine forgetfulness and a scattered mind. The trap is that there is always a reason to be exhausted, always something to blame. The question worth asking is whether the symptoms lift when the pressure does, over a proper holiday, a quieter month. Recovery is reassuring. Symptoms that survive the break are not.

Lifelong neurodivergence. This one is badly under-recognised, and it grows more relevant every year, as the first generations of formally diagnosed ADHD and autistic adults reach later life. An adult with ADHD has always lost keys, always struggled to sequence, always leaned on external structure. When something changes, both patient and clinician reach for the ready explanation, this is just my ADHD, and the change goes unexamined. The question that matters is not whether the difficulties exist but whether they have shifted from that person's own long-standing baseline, and answering it means knowing what the baseline was. The mistake runs the other way as well: disorganisation and forgetfulness in someone with never-diagnosed ADHD are taken for early dementia, especially in older adults, in whom ADHD is missed almost as a rule. And there is emerging evidence that ADHD may itself carry a raised dementia risk, which makes getting the assessment right more important, not less. The same holds for autistic adults, whose lifelong differences in routine, memory and communication can either hide a new decline or be mistaken for one.

Alzheimer’s in women and men: why they are not the same story

Around two in three people living with Alzheimer's are women. Longer life explains part of that, but not all of it, and the differences matter at the bedside in three ways.

Women are diagnosed later, for a reason we can actually measure. Across the whole of life, women outperform men on tests of verbal memory, a real, repeatedly confirmed advantage. And because verbal memory tests sit at the heart of detecting early Alzheimer's, that advantage behaves like a form of reserve: a woman can carry more underlying disease before her score falls into the abnormal range. It is the same phenomenon as reserve in a high-performing professional, and it has the same consequence, a later diagnosis, and less time to act.

The hormonal transition thickens the fog. Perimenopausal symptoms overlap with early disease, and the fall in oestrogen is itself an active question in Alzheimer's research; symptoms in the years around fifty are attributed to hormones almost by default. And the presentation differs. Men more often come in with behavioural change or a withdrawal that a partner has noticed; women more often report the symptoms themselves, and are more likely to have those reports set down to mood, anxiety or hormones. None of this means a woman's symptoms are more likely to be serious. It means the reasons for delay differ by sex, and an assessment should know that, rather than reach for a single template.

What prevention actually achieves

The reason to take these early signs seriously is that so much of the risk is not fixed. The Lancet Commission on dementia has shown that up to 40% of dementia is bound up with things we can change, hearing loss, high blood pressure, inactivity, diabetes, depression, isolation, too much alcohol, smoking, obesity, air pollution, head injury and a poor early education. Two things follow. Prevention does its best work in midlife (the forties, fifties and sixties) long before symptoms would appear. And it keeps mattering after a diagnosis: blood pressure, hearing, activity, mood all shape the road ahead as much as the risk of setting out on it. Prevention is not a promise that you will never develop dementia. No test and no plan can offer that. What it offers is the part of the risk that is genuinely within reach.

How Alzheimer’s disease is diagnosed — and why precision matters

Every confusion in this piece can be resolved, but only by an assessment built to resolve it. That means time, and a real history: what changed, when, and in what order, with someone who has known the person well, because the sequence of events is often the single most telling thing there is, and it cannot be gathered in ten minutes. It means testing pitched to the individual, a full neuropsychological assessment detailed enough to show a fall relative to a person's own expected level, which is essential where reserve, a verbal-memory advantage or a lifelong neurodivergent baseline would otherwise hide it. It means going looking, on purpose, for the mimics, depression and apathy, thyroid, B12, sleep, medication, alcohol, hearing and vision. It means biomarkers and imaging where the question demands them: a volumetric 3-Tesla MRI, advanced genetic testing where the family history calls for it, blood markers such as p-tau217 that can flag Alzheimer's pathology with an accuracy approaching a lumbar puncture, with the crucial caveat that a biomarker shows whether the pathology is present, not whether it is what is causing the symptoms, a judgement that stays clinical. And it means a team drawing all of it together before a diagnosis is spoken, so that the unusual and the mixed presentations are caught rather than forced into the nearest familiar box. Because "dementia" alone is not enough to treat safely: get Lewy body disease wrong, and a person can be harmed by the very antipsychotics used routinely in other dementias.

Six reasons patients choose Eton Brain Health

1. Depth in exactly this problem. Our consultants include Professor Dag Aarsland of King's College London, a world authority on Lewy body dementia; Dr Ash Venkataraman, an NIHR Academic Clinical Lecturer at King's; Dr Chris Kalafatis, who built the first virtual NHS Brain Health Clinic; and Dr Hossein Rostamipour, dual-trained in general adult and old age psychiatry. Recognising the earliest signal is an active research question for us, not only a clinical one, Professor Aarsland and Dr Rostamipour are among the authors of the PREDICTOM study, which is testing whether Alzheimer's risk can be identified in the community before symptoms declare themselves.
2. An assessment built to separate the mimics, depression, hormones, stress, neurodivergence and early disease examined as rival explanations rather than assumed.
3. Neurodevelopmental expertise in the same clinic, we assess ADHD and autism across the whole of life, so a patient whose baseline has always been unusual is seen by people who understand that baseline.
4. Advanced diagnostics, used with judgement, volumetric 3-Tesla MRI, amyloid and FDG PET, DAT scans, advanced genetic testing and p-tau217, where the question warrants them rather than as a default package. Our Comprehensive Brain Health Diagnostic Programme brings all of it into one consultant-led pathway, £14,000, in person in London or virtual, with fully transparent fees and no hidden costs.
5. A genuine team review, followed by a feedback appointment in which the diagnosis is explained properly.
6. Prevention taken as seriously as diagnosis, a specific, prioritised plan aimed at the risks that are actually yours to change.

Where this leaves you, either way

If we find Alzheimer's early, that knowledge is what opens the options: treatment where it exists, real work on the risks that shape the trajectory, time to plan while you hold full capacity, and access to trials. If we find something else (depression, thyroid disease, sleep apnoea, a medication, an unrecognised neurodevelopmental condition) that is not a wasted visit. It is very often the better outcome, and one only a thorough look would have found. And if we find nothing wrong, you have a baseline. Most people worrying at sixty have nothing to measure against; with a baseline, a future fear becomes a question you can answer.

Why trust Eton Brain Health

Eton Brain Health is a consultant-led memory and brain health service in London, seeing people in person and online. Our consultants are GMC-registered and members of the Royal College of Psychiatrists, hold academic posts at King's College London, and have built NHS brain health services. We take self-referrals, and with your permission we write to your GP.

Our consultants publish on exactly this problem. Professor Dag Aarsland's 2026 study in Nature measured Alzheimer's biomarkers in 11,486 people and found the pathology present in 23.5% of cognitively unimpaired over-70s, which is why we are careful to separate what a test shows from what a person actually has. His work on mixed Alzheimer's and Lewy body pathology, and on the cognitive profiles that distinguish dementia with Lewy bodies from Alzheimer's disease, speaks directly to the mistaken-identity problem this article describes.

Conclusion

The early signs of Alzheimer's are not hard to see. They are hard to read, because stress, low mood, the menopause, ordinary ageing and a lifelong neurodivergent mind all produce something that looks the same from across the room. The point of a proper assessment is not to confirm a fear. It is to tell these possibilities apart, at the stage when telling them apart still changes what happens next.

If something has changed, and the explanations you have been offered do not quite fit, we would be glad to look at it properly with you.

Where to go next

• Memory assessment and our diagnostic programme: https://etonpsychiatrists.co.uk/services/memory-service
• Preventative assessment for people without symptoms: https://etonpsychiatrists.co.uk/services/memory-service
• Dementia prevention and risk: https://etonpsychiatrists.co.uk/services/memory-service
• ADHD and autism in older adults: https://etonpsychiatrists.co.uk/services/adhd-adult
• When should I worry about memory problems?: https://etonpsychiatrists.co.uk/blog/when-should-i-worry-about-memory-problems

Sources

• Aarsland, D., Creese, B., Politis, M. et al. Cognitive decline in Parkinson disease. Nature Reviews Neurology 13(4), 217–231 (2017). https://doi.org/10.1038/nrneurol.2017.27
• Aarsland, D., Sunde, A.L., Tovar-Rios, D.A. et al. Prevalence of Alzheimer's disease pathology in the community. Nature 650(8100), 182–186 (2026). https://doi.org/10.1038/s41586-025-09841-y
• Brem, A.-K., Khan, Z., Radermacher, J. et al. (including Rostamipour, H. and Aarsland, D.), PREDICTOM Consortium. Screening for Alzheimer's disease in the community using an AI-driven screening platform: design of the PREDICTOM study. The Journal of Prevention of Alzheimer's Disease 13(5), 100545 (2026). https://doi.org/10.1016/j.tjpad.2026.100545
• Gibson, L.L., Grinberg, L.T., Paes, V.R. et al. (including Aarsland, D.). Co-pathology in Alzheimer's disease and Lewy body disease and its association with neuropsychiatric symptoms. Alzheimer's & Dementia 21(9), e70693 (2025). https://doi.org/10.1002/alz.70693
• Livingston, G., Huntley, J., Sommerlad, A. et al. Dementia prevention, intervention, and care: 2020 report of the Lancet Commission. The Lancet 396(10248), 413–446 (2020). https://doi.org/10.1016/S0140-6736(20)30367-6
• Ma, X., Zhang, M., Zheng, Y. et al. (including Aarsland, D.). Distinct cognitive profiles differentiate dementia with Lewy bodies from Alzheimer's disease. International Psychogeriatrics 100203 (2026). https://doi.org/10.1016/j.inpsyc.2026.100203
• Sundermann, E.E., Biegon, A., Rubin, L.H. et al. Better verbal memory in women than men in MCI despite similar levels of hippocampal atrophy. Neurology 86(15), 1368–1376 (2016). https://doi.org/10.1212/WNL.0000000000002570
• Venkataraman, A.V., Kandangwa, P., Lemmen, R. et al. (including Kalafatis, C. and Aarsland, D.). The SLaM Brain Health Clinic: remote biomarker enhanced memory clinic for people with mild cognitive impairment within a National Health Service mental health trust. BJPsych Open 11(1), e8 (2024). https://doi.org/10.1192/bjo.2024.829
• Xue, L., Bocharova, M., Young, A.H. & Aarsland, D. Late-onset depression predicts cognitive impairment and subsequent dementia among older adults with major depressive disorder. BJPsych Open 12(2), e88 (2026). https://doi.org/10.1192/bjo.2026.10995

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