top of page

WHAT SCIENCE NOW KNOWS ABOUT MEMORY LOSS AND DEMENTIA


A clinically grounded guide to mild cognitive impairment, the four major dementia types, and the landmark advances of 2023–2024 that are reshaping how we diagnose and treat these conditions.


Every three to four seconds, somewhere in the world, a person develops dementia. That is roughly ten million new diagnoses each year. The figure can feel abstract until it lands in your consulting room, your family, or your own life. What has changed, and what it means for anyone living with or alongside memory difficulties, is worth understanding clearly.


This post draws on the most significant evidence published in 2023 and 2024, a period that has produced more actionable advances in dementia medicine than any comparable two-year window in the past three decades.



MEMORY LOSS IS NOT ONE THING


Perhaps the most important thing a clinician can communicate to a worried patient is this: not all memory difficulties are dementia, and not all dementia begins with memory loss.


Forgetting where you left your keys, losing a name that comes back to you an hour later, taking longer to process a complex task — these are the hallmarks of normal ageing. Fluid cognitive abilities, including processing speed and the ease of encoding new information, decline modestly from midlife. Wisdom, vocabulary, and accumulated knowledge remain stable or improve. A formally tested, normally ageing brain performs within age-corrected norms, even when subjective experience suggests otherwise.


Between normal ageing and dementia sits mild cognitive impairment (MCI), a state in which measurable cognitive decline exceeds what age alone would predict, but daily functioning remains substantially preserved. It is not a diagnosis of dementia. A meaningful proportion of people with MCI remain stable or revert to normal cognition, particularly those without underlying biological evidence of neurodegeneration.


Dementia itself is defined by impairment in two or more core cognitive domains, severe enough to interfere with everyday life. It is caused by pathological processes in the brain, and it is not a normal part of ageing.



THE GLOBAL PICTURE


The World Health Organisation's most recent estimates place the number of people living with dementia at 55 million worldwide, projected to reach 78 million by 2030 and 139 million by 2050. Over 60 percent of those affected live in low- and middle-income countries, where diagnostic and care infrastructure remain chronically under-resourced.


The societal economic cost was estimated at USD 1.3 trillion in 2019. Dementia is now the seventh leading cause of death globally and fourth in high-income countries.


There is, however, a note of cautious optimism. Age-specific incidence appears to be declining in several high-income settings, most credibly explained by improved cardiovascular risk management and rising educational attainment over past decades. Absolute case numbers continue to rise because populations are ageing faster than incidence is falling, but the trajectory demonstrates that dementia is not inevitable.



THE FOUR MAJOR DEMENTIA TYPES


Most dementia falls into one of four subtypes, collectively termed Alzheimer's Disease and Related Dementias (ADRD). Each has a distinct biological signature, clinical presentation, and treatment implication.



Alzheimer's Disease


The most common form, accounting for 60 to 70 percent of all cases. Alzheimer's disease is caused by accumulation of two abnormal proteins in the brain: amyloid-beta, which forms plaques, and phosphorylated tau, which forms neurofibrillary tangles inside neurons. These changes begin silently, potentially two decades before symptoms appear.


Early symptoms are characteristically episodic memory failures: difficulty encoding new information rather than retrieving old memories. The person cannot recall what they had for breakfast; they can usually still recall their wedding day. Management of finances and other complex daily tasks are typically affected early; basic self-care is preserved until moderate-to-severe stages.



Vascular Dementia


The second most common type, caused by cerebrovascular disease disrupting blood supply to the brain. The cognitive profile often differs from Alzheimer's disease: retrieval of information is more impaired than encoding, and executive dysfunction, gait disturbance, and mood changes can dominate the early picture.


Vascular dementia is also the most preventable form. Hypertension is present in approximately 50 percent of cases, and early treatment meaningfully reduces both incidence and rate of progression. Managing cardiovascular risk is the primary therapeutic intervention.



Lewy Body Dementia


An umbrella term for two closely related conditions: dementia with Lewy bodies (DLB) and Parkinson's disease dementia (PDD). Together they account for up to 30 percent of dementia cases, yet they remain substantially underdiagnosed.


IMPORTANT SAFETY NOTE: Antipsychotic medications can precipitate severe and potentially fatal reactions in Lewy body dementia. Any person with dementia and prominent visual hallucinations, Parkinsonian features, or pronounced fluctuations in alertness should be assessed by a specialist before antipsychotics are initiated.


Key features of DLB include recurrent well-formed visual hallucinations (in up to 80 percent of cases), Parkinsonism, fluctuating cognition and alertness, and REM sleep behaviour disorder, where the person physically acts out vivid dreams. This last feature can precede the dementia diagnosis by years to decades and is now recognised as a prodromal marker of neurodegeneration.



Frontotemporal Degeneration


The second most common cause of early-onset dementia (onset before 65). Frontotemporal degeneration targets the frontal and temporal lobes, responsible for behaviour, personality, social conduct, and language. Memory networks are typically spared in early disease, which is why it is frequently misdiagnosed as a psychiatric disorder for months or years.


The behavioural variant presents with progressive personality change, disinhibition, loss of empathy, apathy, and compulsive or impulsive behaviours. Between 15 and 40 percent of cases have a family history, and 10 to 30 percent show autosomal dominant inheritance.



WHAT HAS CHANGED IN 2023–2024


The past two years have produced advances that will directly affect clinical practice and patient outcomes. Three deserve particular attention.



1. Forty-Five Percent of Dementia Cases Are Potentially Preventable

[2024 LANCET COMMISSION UPDATE]


The 2024 Lancet Commission on Dementia Prevention, Intervention, and Care identified 14 modifiable risk factors that together account for approximately 45 percent of global dementia cases. This is up from 12 factors and 40 percent in the 2020 report. The two additions are untreated vision loss and elevated LDL cholesterol.


The full list of 14 risk factors:

1. Low educational attainment

2. Hearing loss

3. Hypertension

4. Smoking

5. Obesity

6. Depression

7. Physical inactivity

8. Diabetes

9. Excessive alcohol consumption

10. Traumatic brain injury

11. Air pollution

12. Social isolation

13. Untreated vision loss

14. High LDL cholesterol


This does not mean that addressing these factors guarantees prevention. But it does mean that population-level investment in cardiovascular health, education, hearing care, and mental health has the potential to forestall nearly half of all future dementia cases. That is an extraordinary public health opportunity.



2. Alzheimer's Disease Can Now Be Defined — and Diagnosed — Biologically

[2024 NIA-AA REVISED CRITERIA]


In June 2024, the Alzheimer's Association Workgroup published revised criteria that redefine Alzheimer's disease as a biological process, not a clinical syndrome. Biomarker evidence of AD neuropathological change is now equivalent to a diagnosis of the disease, even in the absence of symptoms.


Crucially, the 2024 criteria formally incorporate blood-based biomarkers alongside cerebrospinal fluid and PET imaging. Plasma assays measuring phosphorylated tau (pTau181, pTau217) and glial fibrillary acidic protein (GFAP) can now, in the appropriate clinical context, support a biological diagnosis of Alzheimer's disease. These tests are entering clinical practice and will progressively democratise access to early diagnosis beyond specialist centres.


This shift matters practically. The gateway to the new disease-modifying therapies is biomarker confirmation. Memory services and neurology departments need to build biomarker-informed diagnostic pathways now, not at some point in the future.



3. The First Disease-Modifying Treatments Are Here


[FDA APPROVALS: LECANEMAB 2023 & DONANEMAB 2024]


Two anti-amyloid monoclonal antibodies have received full FDA approval:


- Lecanemab (Leqembi): full FDA approval July 2023; EMA approval late 2024

- Donanemab (Kisunla): FDA approval July 2024; EMA marketing authorisation July 2025


Both drugs target and clear amyloid plaques from the brain and demonstrated statistically significant slowing of cognitive and functional decline in Phase 3 clinical trials. They are indicated for early symptomatic Alzheimer's disease, specifically MCI due to AD or mild AD dementia, with confirmed amyloid burden.


These are not cures. The effect is approximately 27 to 35 percent slowing of decline relative to placebo over 18 months. Both drugs carry a risk of amyloid-related imaging abnormalities (ARIA), including cerebral oedema and microhaemorrhage. Pre-treatment MRI and APOE genotyping are mandatory. These therapies are not yet routinely available through NHS England; the evidence review process is ongoing.



WHAT THIS MEANS IF YOU ARE WORRIED ABOUT YOUR MEMORY


If you are reading this because you are concerned about your own memory, or that of someone you care for, a few things are worth holding on to.


First, seeking an assessment is always the right step. Most people who present to memory services with subjective memory complaints do not have dementia. Many have treatable conditions — depression, sleep disorders, thyroid dysfunction, medication effects — that can be addressed. Clarity, even when the news is difficult, is almost universally preferable to uncertainty.


Second, the things that reduce your risk of dementia are the same things that reduce your risk of heart disease, stroke, and diabetes. Staying physically active, maintaining social connections, managing blood pressure and cholesterol, not smoking, protecting your hearing, getting adequate sleep, and staying cognitively engaged are evidence-based strategies. None of them requires a prescription.


Third, if you or a family member receives a diagnosis of MCI or early dementia, the landscape has changed. There are now more diagnostic tools, more specialist services, and, for the first time, treatments that modify the course of Alzheimer's disease biology.



A NOTE ON TIMELY DIAGNOSIS


In the borough of Hammersmith and Fulham, where I lead the Memory Service, the dementia diagnosis rate sits above the national average at around 66 percent. That means approximately one in three people living with dementia in this borough remains undiagnosed. Nationally, the gap is larger. Undiagnosed dementia means missed opportunities for treatment, planning, legal and financial preparation, carer support, and access to disease-modifying therapy.


If you have a concern, ask your GP for a referral to your local memory service. If the concern relates to language, behaviour, or personality change rather than memory, ask specifically for neurology review. You are entitled to a diagnosis.


REFERENCES

Livingston G et al. Dementia prevention, intervention, and care: 2024 report of the Lancet standing Commission. Lancet. 2024.

Jack CR Jr et al. Revised criteria for diagnosis and staging of Alzheimer's disease: Alzheimer's Association Workgroup. Alzheimers Dement. 2024;20(8):5143–5169.

van Dyck CH et al. Lecanemab in early Alzheimer's disease. N Engl J Med. 2023;388:9–21.

Sims JR et al. Donanemab in early symptomatic Alzheimer's disease. JAMA. 2023;330(6):512–527.

WHO Fact Sheet: Dementia. Updated 2023.


This post is written for informational purposes and does not constitute individual clinical advice. If you have concerns about your memory or cognition, please speak with your GP or healthcare provider.

Comments


bottom of page