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.
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.
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.
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.