Synopsis
Recognise typical and atypical Alzheimer phenotypes, establish a clinical and biomarker-supported diagnosis where appropriate, use cognitive medicines safely, and provide longitudinal functional, behavioural, carer and advance-care support.
- Typical Alzheimer disease causes insidious progressive episodic memory impairment followed by broader language, orientation, executive and visuospatial difficulty that interferes with independent function.
- Atypical phenotypes include posterior cortical atrophy with visuospatial dysfunction and a logopenic language syndrome; young-onset disease deserves specialist review rather than dismissal because memory is not the first complaint.
- Diagnosis integrates progressive history, collateral functional evidence, cognitive profile, neurological examination and structural imaging after delirium, depression, medicine effects and systemic contributors are addressed.
- MRI may show disproportionate medial temporal and parietal atrophy but a normal or non-specific scan does not exclude early disease; patterns support rather than replace clinical diagnosis.
- CSF amyloid and tau or amyloid imaging can increase confidence in uncertain, young-onset or atypical cases when a result will alter management or access to a specialist therapy.
- Donepezil, galantamine or rivastigmine are NICE options for mild to moderate Alzheimer disease; choose around adherence, comorbidity, interactions and adverse-effect profile.
- Memantine is an option as monotherapy for severe disease or moderate disease when cholinesterase inhibitors are contraindicated or not tolerated, and may be added to an inhibitor in moderate or severe disease.
- Do not stop a cholinesterase inhibitor solely because dementia has become severe; review benefit, adverse effects, swallowing, adherence and the person’s goals.
- Distress and behavioural change first require pain, delirium, environment, communication and unmet-needs assessment; antipsychotics are reserved for risk of harm or severe distress and need frequent review.
- Driving, capacity, medication support, nutrition, continence, falls, carer wellbeing, lasting power of attorney and advance care planning are integral treatment, not post-diagnostic extras.
Key red flags
Hours-to-days worsening, inattention, drowsiness or agitation signals delirium, medication toxicity, pain or another acute illness rather than sudden Alzheimer progression.
Investigation priorities
Establish an insidious progressive amnestic or atypical syndrome and its effect on independence.
Management branches
Progressive cognitive and functional decline remains after initial reversible-factor assessment.
- 1. Reconstruct onset, progression and domain sequence with the patient and informant, separating chronic decline from any current delirium.
- 2. Use adapted cognitive testing, neurological examination and structural imaging to formulate typical Alzheimer, atypical Alzheimer, mixed or uncertain disease.
- 3. Request CSF or amyloid imaging through specialist services when uncertainty, age or treatment eligibility makes molecular confidence useful.
- 4. Communicate diagnosis and limits, assess emotional response and safety, and offer a named memory-service or primary-care contact for follow-up.
Key medicines
DonepezilStart 5 mg orally once daily, commonly at night, and after at least one month consider 10 mg once daily if tolerated and clinically appropriate under the memory-service or shared-care plan.Check bradycardia, syncope, conduction disease, ulcer or bleeding risk, asthma, weight loss, sleep disturbance and interactions. Monitor gastrointestinal effects and falls; an ECG is indicated when the cardiovascular history warrants it.
MemantineStart 5 mg once daily and increase by 5 mg at weekly intervals to a usual 20 mg once daily if tolerated, using a lower maximum in significant renal impairment.Review dizziness, headache, constipation, confusion, blood pressure and renal function. Adjust for renal impairment and evaluate continued global and functional benefit rather than cognition alone.