Drug treatments for Alzheimer's disease

3. How do they work?

Cholinesterase inhibitors (donepezil, rivastigmine and galantamine)

In the brain of a person with Alzheimer's disease, there are lower levels of a chemical called acetylcholine. Acetylcholine helps to send messages between certain nerve cells. In Alzheimer's there is also a loss of the nerve cells that use acetylcholine. Falling acetylcholine levels and progressive loss of these nerve cells are linked to worsening symptoms.

Donepezil, rivastigmine and galantamine all prevent an enzyme called acetylcholinesterase from breaking down acetylcholine in the brain. As a result, an increased concentration of acetylcholine leads to increased communication between nerve cells. This may temporarily alleviate or stabilise some symptoms of Alzheimer's disease.

All three cholinesterase inhibitors work in a similar way, but one might suit a certain individual better than another, particularly in terms of side effects experienced.

Guidance on the use of drugs in the NHS is issued by the National Institute for Health and Care Excellence (NICE). NICE reviews drugs and decides whether they represent good enough value for money to be available as part of NHS treatment. Drugs considered by NICE will also have been through the UK or European licensing process for new medicines. This means the medicine has been tested and met rigorous standards of safety, quality and effectiveness. The licence will be granted for treatment of a particular health condition.

For the cholinesterase inhibitors, the NICE guidance (2011) suggests that the cheapest drug (currently donepezil) should generally be tried first. See 'NICE guidance: a summary'.


The action of memantine is different from that of donepezil, rivastigmine and galantamine. Glutamate is another chemical that helps to send messages between nerve cells. Glutamate is released in excessive amounts when brain cells are damaged by Alzheimer's disease. This causes the brain cells to be damaged further. Memantine protects brain cells by blocking the effects of excess glutamate.