About This Page
This is a clinician-written, evidence-based summary aligned to the 2026 MLA Content Map. It is intended for medical students and junior doctors preparing for the UKMLA. Always cross-reference with NICE guidance, local protocols, and clinical judgement.
The Bottom Line
- Alzheimer's disease is the most common cause of dementia (~60–70%), followed by vascular dementia, Lewy body dementia, and frontotemporal dementia
- Insidious onset of progressive memory loss (especially episodic/short-term memory) with preserved procedural memory early on
- Diagnosis: clinical assessment + cognitive testing (ACE-III or MMSE) + MRI brain (medial temporal lobe atrophy)
- First-line treatment (mild-moderate): acetylcholinesterase inhibitor — donepezil 5–10 mg OD (or rivastigmine, galantamine)
- Moderate-severe: add or switch to memantine (NMDA receptor antagonist)
Overview
Dementia is a clinical syndrome of progressive cognitive decline sufficient to interfere with daily functioning. Alzheimer's disease (AD) is the most common cause, accounting for approximately 60–70% of cases. It is characterised pathologically by extracellular amyloid-beta plaques and intracellular neurofibrillary tangles (hyperphosphorylated tau protein), leading to neuronal loss, brain atrophy (particularly hippocampi and temporal lobes), and cholinergic neurotransmitter deficiency. Mixed dementia (AD + vascular) is very common, especially in older patients.
Epidemiology
Approximately 900,000 people in the UK live with dementia, projected to exceed 1 million by 2030. Prevalence doubles approximately every 5 years after age 65. Risk factors for AD include advancing age (strongest risk factor), female sex, Down syndrome, family history, ApoE4 allele (strongest genetic risk factor for late-onset AD), cardiovascular risk factors (hypertension, diabetes, obesity, smoking), low educational attainment, social isolation, and hearing loss. Early-onset dementia (<65 years) accounts for ~5% of cases.
Clinical Features
Symptoms
Progressive short-term (episodic) memory loss — asking repetitive questions, losing items, forgetting recent events
Difficulty with word-finding (anomia) and language (progressive aphasia)
Visuospatial dysfunction — getting lost in familiar places, difficulty judging distances
Impaired executive function — poor planning, decision-making, problem-solving
Changes in personality and behaviour — apathy, social withdrawal, disinhibition
Difficulty with activities of daily living (dressing, cooking, finances)
Behavioural and psychological symptoms: agitation, aggression, delusions, wandering, sleep disturbance
Signs
Impaired performance on cognitive testing: ACE-III <88/100 or MMSE <24/30 suggests dementia
Often well-presented and socially appropriate early in disease ("facade" effect)
Disorientation to time and place
Neurological examination often normal early — no focal signs (unlike vascular dementia)
Late stages: myoclonus, seizures, primitive reflexes, dysphagia
Investigations
First-line
Cognitive assessmentAddenbrooke's Cognitive Examination (ACE-III) or MMSE. Also 6-CIT or GPCOG in primary care for initial screening
BloodsTo exclude reversible causes of cognitive impairment: FBC, U&Es, LFTs, calcium, glucose, TFTs, B12, folate, HIV (if risk factors). Not all cognitive decline is dementia
MRI brainStructural imaging recommended for all (NICE NG97). AD: medial temporal lobe and hippocampal atrophy. Also excludes structural causes (tumour, subdural, NPH)
Second-line
FDG-PET or SPECT (perfusion)If diagnosis uncertain — shows temporo-parietal hypometabolism/hypoperfusion in AD
CSF biomarkersLow amyloid-beta 42, raised total tau and phospho-tau support AD diagnosis — used in specialist centres
Specialist
Amyloid PETDemonstrates amyloid deposition in vivo — mainly research tool, but used in diagnostic uncertainty
Neuropsychological assessmentDetailed cognitive profiling — especially useful in young-onset or atypical presentations
1
Pharmacological
- Mild-moderate AD: acetylcholinesterase inhibitor (AChEI) — donepezil 5 mg OD (increase to 10 mg after 4–6 weeks), or rivastigmine, or galantamine
- Moderate-severe AD: memantine 5 mg OD titrated to 20 mg OD (NMDA receptor antagonist). Can be used alone or with AChEI
- AChEIs should NOT be used in frontotemporal dementia
- Review response at 3–6 months — continue if clinically beneficial
2
Non-pharmacological
- Cognitive stimulation therapy (group-based) — recommended for mild-moderate dementia
- Physical exercise — evidence for slowing cognitive decline
- Music therapy, art therapy, reminiscence therapy
- Environmental modifications: good lighting, clear signage, reduce fall hazards
3
Managing behavioural and psychological symptoms (BPSD)
- Non-pharmacological approaches FIRST: identify triggers, person-centred care, reassurance, distraction
- Antipsychotics (risperidone) only for severe distress or risk of harm — use lowest dose for shortest time. Increased mortality and stroke risk in dementia
- Avoid benzodiazepines where possible (increased falls, paradoxical agitation)
4
Support and planning
- Advance care planning, lasting power of attorney — discuss while capacity retained
- Carer assessment and support — refer to local Alzheimer's Society and carer services
- DVLA notification — formal driving assessment may be needed. Group 2 licence revoked at diagnosis
- Regular comprehensive review including medication review, carer wellbeing, safety, and social care needs
Complications
- Aspiration pneumonia: Leading cause of death — dysphagia develops in advanced stages
- Falls and fractures: Visuospatial impairment, gait disturbance, polypharmacy
- Delirium: People with dementia are highly susceptible — any acute illness can precipitate delirium
- Carer burden: Depression, anxiety, social isolation in carers — must be assessed and supported
- Wandering and risk: Getting lost, accidents, vulnerability to harm
- Weight loss and malnutrition: Forgetting to eat, dysphagia in later stages
UKMLA Exam Tips
- 1Alzheimer's: insidious onset, progressive short-term memory loss, temporal lobe atrophy on MRI. Vascular: stepwise decline, vascular risk factors, multi-infarct pattern on MRI
- 2Donepezil (AChEI) = first-line for mild-moderate AD. Memantine for moderate-severe (or intolerant of AChEIs)
- 3ALWAYS exclude reversible causes: hypothyroidism, B12 deficiency, depression, normal pressure hydrocephalus, subdural haematoma
- 4Delirium vs dementia: delirium = acute onset, fluctuating, inattention. Dementia = chronic, progressive, stable attention (until late). They frequently coexist
- 5Do NOT use antipsychotics routinely for BPSD — increased stroke risk and mortality in dementia patients
- 6ApoE4 allele is the strongest genetic risk factor for late-onset AD (not diagnostic)
- 7Down syndrome: almost all develop AD pathology by age 40 — amyloid precursor protein gene on chromosome 21
practicetest your knowledge on alzheimer's disease and dementiaApply what you've learnt with UKMLA-style questions from the iatroX Q-Bank — neurology and beyond.
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