Investigation of neurochemical correlates of Alzheimer's disease (AD) has led to the development of current treatment strategies. The cholinergic system has profound loss of the acetylcholine synthesis enzyme choline acetyltransferase (ChAT) and neurons in the forebrain's nucleus basalis of Meynert (origin of major cortical cholinergic projections). Loss of ChAT activity is the most consistent finding in post-mortem AD brains and the degree of cognitive impairment has been found to correspond with the extent of deficit. Reductions in acetylcholine release, muscarinic (mAChR) and nicotinic (nAChR) acetylcholine receptors are other cholinergic features of AD; this accumulating evidence has led to the ‘cholinergic hypothesis’ of dementia. There are indications that loss of glutamate activity also correlates with cognitive impairment. Changes in monoamine activity are implicated in the behavioural symptoms of AD. The principal therapeutic agents in AD are cholinesterase inhibitors, which inhibit acetylcholine breakdown. Further treatment targets include mAChRs, nAChRs and glutamate receptors.