Cholinesterase inhibitors and memantine for symptomatic treatment of dementia

A 78 year old woman is assessed in the memory clinic. Her family feel that she has become increasingly forgetful over the past two years, misplacing objects around the house and forgetting her drugs. Her speech is repetitive, and she struggles with day to day activities such as cooking. Routine blood tests are normal, and she scores 21/30 on the mini-mental state examination (MMSE) with deficits in orientation, attention and concentration, and recall. Magnetic resonance imaging, performed to exclude other pathology, reveals global cerebral atrophy consistent with Alzheimer’s disease. In discussion with her and her family, a management plan is formulated that includes referral to the local dementia advisor and social services for day opportunities as well as prescription of a cholinesterase inhibitor. The most common types of dementia are Alzheimer’s disease, vascular dementia, mixed dementia, dementia with Lewy bodies, and frontotemporal dementia. At present, four drugs are licensed in the UK for the management of Alzheimer’s disease, the cholinesterase inhibitors (donepezil, rivastigmine, and galantamine) and memantine, a partial antagonist of NMDA receptors (table 1⇓). The use of these drugs in other types of dementia has been investigated, with the most convincing evidence coming from studies of dementia with Lewy bodies and Parkinson’s disease dementia. There is currently no evidence to support the use of cholinesterase inhibitors or memantine in frontotemporal dementia or mild cognitive impairment. View this table: Table 1  Licensed indications for cholinesterase inhibitors and memantine in the UK Cholinesterase inhibitors increase the availability of acetylcholine at the synaptic cleft by preventing its breakdown by the enzyme acetylcholinesterase. Galantamine also modulates nicotinic acetylcholine receptors, and rivastigmine inhibits butylcholinesterase, but the importance of these additional properties is unknown. Memantine is believed to act by reducing glutamate mediated excitotoxicity. In this review we summarise the evidence and current guidance related to the use of …