Indicated for moderate to severe dementia of the Alzheimer’s type.
Most common adverse events are dizziness, confusion, headache and constipation.
Memantine is an oral medication used to treat moderate-to-severe Alzheimer’s disease.
Trade name Namenda
Pregnancy category
US: B (No risk in non-human studies)
Bioavailability 100%
Metabolism Liver <10%?
Elimination half-life 60–100 hours
Excretion Kidney
Common side effects include headache, constipation, sleepiness, and dizziness.
Severe side effects may include blood clots, psychosis, and heart failure.
It is believed to work by blocking NMDA receptors.
Used to treat moderate-to-severe Alzheimer’s disease, especially for people who are intolerant of or have a contraindication to acetylcholinesterase inhibitors.
Use associated with a modest improvement in Alzheimer’s disease with small positive effects on cognition, mood, behavior, and the ability to perform daily activities in moderate-to-severe.
There does not appear to be any benefit in mild disease.
Common adverse drug reactions (≥1% of people) include: confusion, dizziness, drowsiness, headache, insomnia, agitation, and/or hallucinations.
Less common adverse effects include vomiting, anxiety, hypertonia, cystitis, and increased libido.
Alzheimer’s disease is related to a
dysfunction of glutamatergic neurotransmission, and manifests as neuronal excitotoxicity.
It is a low-affinity voltage-dependent uncompetitive antagonist at glutamatergic NMDA receptors.
It binds to the NMDA receptor with a higher affinity than Mg2+ ions, and is able to inhibit the prolonged influx of Ca2+ ions, particularly from extrasynaptic receptors, which forms the basis of neuronal excitotoxicity.
Its low affinity, uncompetitive nature, and rapid off kinetics at the level of the NMDA receptor-channel, preserves the function of the receptor at synapses, as it can still be activated by physiological release of glutamate following depolarization of the postsynaptic neuron.
Its interaction with NMDA receptors plays a major role in the symptomatic improvement in Alzheimer’s disease.
No evidence it has a disease-modifying effect in Alzheimer’s.
Acts as a non-competitive antagonist at the 5-HT3 receptor, with a potency similar to that for the NMDA receptor.
The number of nicotinic receptors in the brain are reduced in Alzheimer’s disease, even in the absence of a general decrease in the number of neurons.
It acts as an agonist at the dopamine D2 receptor with equal or slightly higher affinity than to the NMDA receptors.
Whole brain radiation therapy (WBRT) associated with cognitive decline in 50-60% of patients 4 months after treatment, and Memantine delays cognitive decline in patients treated with WBRT