Alzheimer’s disease is a chronic progressive disease affecting higher intellectual functioning. The clinical diagnosis is made when the onset of illness is insidious, the course slowly progressive and all the treatable causes of dementia have been ruled out. The use of more stringent criteria has improved clinical diagnosis, but at best only 80% of patients are accurately diagnosed. Ultimately the diagnosis depends upon pathological confirmation. The neuritic plaques and neurofibrillary tangles described by Alzheimer, although not pathognomonic for the disease, continue to be the basis for pathological diagnosis. The aetiology and pathophysiology of Alzheimer’s disease are presently unknown. Epidemiological studies have suggested a genetic basis for the disorder, and many biochemical studies have linked it to degeneration of central cholinergic neurons, and possibly to abnormalities of other neurotransmitter systems. A marker which would permit accurate diagnosis early in the course of disease would be of major importance to researchers and clinicians alike. No marker has been found to date, although recent research results are promising. Various pharmacological strategies have been employed in the treatment of Alzheimer’s disease. More recently attempts have focused on enhancing central cholinergic transmission. Despite the well-founded rationale for these studies, results have been modest.