Erfan Bashar
Back to Alzheimer Disease

Alzheimer Disease — Treatment

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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.

There is currently no curative treatment for Alzheimer disease or for neurodegenerative diseases generally. Available therapies slow the rate of decline. They do not stop, reverse, or substantially alter the trajectory. Each drug’s rationale follows from the neurotransmitter deficit it targets.

Acetylcholinesterase inhibitors: boosting a fading signal

These drugs slow the enzyme that breaks down acetylcholine in the synaptic cleft. Whatever the surviving neurons still release stays active longer. The signal keeps fading, but what remains is amplified. Benefit is modest and symptomatic, across cognition, function, and behaviour. It persists for months to a few years before decline overtakes the drug effect.

  • Donepezil is the most commonly prescribed, taken once daily.
  • Rivastigmine comes oral and as a transdermal patch. The patch bypasses first-pass metabolism and delivers drug steadily, which reduces the gastrointestinal intolerance seen with oral dosing. Rivastigmine also inhibits butyrylcholinesterase alongside acetylcholinesterase.
  • Galantamine additionally modulates nicotinic receptors. Its clinical difference from donepezil is modest, and it is not first-line at most centres.

Class side effects follow the cholinergic mechanism: nausea, vomiting, diarrhoea, bradycardia with possible syncope, and muscle cramps. Starting low and titrating slowly reduces them.

Memantine: blocking excitotoxic damage

Memantine is a low-to-moderate affinity NMDA receptor antagonist. It preferentially blocks sustained pathological activation of NMDA receptors by excess glutamate. It permits the brief physiological activation needed for learning and memory. This dampens calcium-driven intracellular damage.

Memantine is indicated for moderate-to-severe Alzheimer disease, not early disease. In practice it is added to donepezil as the disease passes the mild stage. Combination gives a brief lift before gradual decline resumes. Side effects are generally mild: dizziness, headache, and rarely confusion.

Anti-amyloid monoclonal antibodies: the new frontier

These antibodies remove amyloid plaques and modestly slow decline in early disease. The clinical significance of the slowing remains debated. They are studied only in early symptomatic disease with confirmed amyloid pathology. Treatment starts only in that studied population.

  • Lecanemab received full FDA approval after its phase 3 trial showed roughly a 27% reduction in the rate of decline over 18 months, equivalent to a delay of several months in progression. The main safety concern is ARIA (amyloid-related imaging abnormalities): brain swelling or microbleeds visible on MRI. ARIA occurs more often in APOE ε4 carriers, so APOE testing precedes treatment. Anticoagulant-associated brain bleeding needs added caution.
  • Donanemab received FDA approval in July 2024 for early symptomatic Alzheimer disease with confirmed amyloid pathology, with a similar benefit profile and the same ARIA concern. APOE testing precedes treatment here as well.
  • Aducanumab, the first antibody granted accelerated approval, has been discontinued as an Alzheimer treatment. Imaging confirmed plaque removal, but cognitive benefit was marginal and the approval controversial.

These drugs represent a genuine shift toward disease-directed treatment with limited magnitude of benefit, and the field continues to evolve.

Non-pharmacological management: essential, not adjunctive

Drugs are only one part of care:

  • Cognitive stimulation — structured activities, memory exercises, social engagement — builds on cognitive reserve and may slow functional decline.
  • Caregiver support is part of treatment itself: support groups, respite care, and education about each stage. Burden and burnout are the norm as dependence progresses from finances and cooking to dressing, bathing, and recognition of family.
  • Safety measures (locks, door alarms, supervised outings) address dangerous wandering.
  • Environmental modification (familiar settings, consistent routines, simplified tasks, clear signage) lets the patient function at the highest level remaining cognition permits.

What not to use, and why

Antipsychotics for behavioural symptoms are a last resort at the lowest dose for the shortest time. They increase mortality and stroke risk in elderly patients with dementia. Benzodiazepines worsen cognition, increase fall risk, and accelerate functional decline. Any centrally depressing drug makes Alzheimer symptoms worse. This includes many anticholinergic medications (bladder antispasmodics, first-generation antihistamines, tricyclic antidepressants), which directly oppose the cholinergic mechanism these treatments try to support.

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