Educational scope notice: This is a study note for medical students, not medical advice, diagnosis, or treatment guidance. Clinical management should follow local protocols and current guidelines.
Non-pharmacological care is the foundation of dementia management, not an afterthought:
- Physiotherapy maintains mobility and breaks the deconditioning spiral toward falls;
- social and cognitive engagement keeps surviving circuits active;
- day centres and consistent routines supply the structure patients can no longer organise;
- occupational therapy adapts tasks to remaining abilities;
- environmental simplification with clear signage and less clutter lowers the demand on failing executive function.
Early hospitalisation is avoided where possible, because unfamiliar surroundings, broken sleep, infection risk, and medication changes can precipitate delirium in a brain with little reserve.
Cholinesterase inhibitors
Alzheimer disease destroys cholinergic neurons of the basal forebrain, and the resulting acetylcholine shortfall drives much of the early cognitive loss. Donepezil, rivastigmine, and galantamine slow acetylcholine breakdown at the synapse, preserving whatever transmission remains. They do not replace dead neurons or slow degeneration; their benefit is modest, roughly delaying functional decline by months. Donepezil is the most commonly used, starting at 5 mg daily and titrating to 10 mg; rivastigmine also comes as a transdermal patch that eases gastrointestinal effects. In vascular dementia these drugs play at most a supporting role, since the primary treatment is vascular risk factor control, though a trial is reasonable when mixed Alzheimer pathology cannot be excluded. That means treating hypertension, diabetes, and hyperlipidaemia as dementia therapy, not background care.
Memantine
Memantine blocks pathological NMDA receptor overactivation by excess glutamate, which would otherwise drive calcium influx and excitotoxic damage in surviving neurons, while preserving normal transmission. It is used in moderate to severe Alzheimer disease, alone or with donepezil, a combination that can show early improvement followed by slower decline than donepezil alone. It has no benefit in mild disease, where the cholinergic deficit dominates. Common effects include dizziness, headache, and constipation.
Anti-amyloid antibodies
The first generation of anti-amyloid strategies did not succeed: the antibodies bapineuzumab and solanezumab showed no benefit, amyloid vaccination failed, and BACE inhibitors, which lower amyloid production, worsened cognition and daily function on some measures versus placebo. That last result matters conceptually, because it suggests amyloid may sit downstream of the true driver rather than upstream.
Newer antibodies (lecanemab, donanemab) have received FDA approval for early Alzheimer disease with confirmed amyloid pathology. They slow decline modestly, by roughly a quarter on standard rating scales, and carry a boxed warning for amyloid-related imaging abnormalities. Risk is stratified by ApoE e4 status, with MRI surveillance during treatment. Anticoagulant use excludes patients until more safety data accrue. Neither antibody is recommended for routine NHS use: benefits were judged small against cost and risk, with appeals pending.
Symptomatic and family therapy
Depression, agitation, anxiety, and psychosis frequently complicate dementia and drive institutionalisation. Depression deserves treatment in its own right since it worsens cognition independently; agitation may need cautious neuroleptic use, except in Lewy body dementia, where antipsychotic sensitivity can be fatal and cholinesterase inhibitors, particularly rivastigmine with its dual enzyme inhibition, are the supported option. Physiotherapy, occupational therapy, and structured family support with education, respite, and counselling complete the plan; caregiver burnout predicts placement more accurately than disease severity, so treating the caregiver keeps the patient home longer. Practical planning covers driving cessation, finances, and advance directives, discussed early.
In cerebral amyloid angiopathy, antiplatelets and anticoagulants are generally avoided because fragile amyloid-laden vessels carry a high lobar haemorrhage risk: a rare reversal of the usual vascular-protective reflex.
Evidence anchors
- NICE. Dementia: assessment, management and support (NG97): https://www.nice.org.uk/guidance/ng97