The symptomatic drugs used for the treatment of Alzheimer disease (AD) are considered to exert their effect by suppressing the progression of dementia symptoms. Although clinical trials conducted on the drugs in Japan have revealed statistically significant differences in assessments of change in cognitive function, three of the four drugs have not shown any statistically significant differences in the clinician's global impression. There are many overseas reports indicating the efficacy of these drugs, whereas many other reports also indicate that the assessment procedures themselves are difficult and have many limitations. In order to determine the efficacy of the drugs in clinical practice, physicians need to determine whether the progression of dementia symptoms is inhibited. However, AD symptoms vary and are affected by the patient's living environment, personal relationships, and other factors. Although there are certain trends in the time of symptom onset according to disease stages, the symptoms progress by the year and greatly vary among patients. Comparison of progression rates to the average rate is a primary requirement for measurement of the drugs' inhibitory effects on progression. However, because progression rates greatly vary among patients, it is difficult to determine the average rate. In principle, drug therapy should be discontinued if it is not effective. However, because it is difficult to determine whether the drugs are effective, they are likely to be unnecessarily prescribed even when there is a lack of efficacy. The typical adverse effects of cholinesterase inhibitors (ChEIs) include gastrointestinal, neuropsychiatric, extrapyramidal, and cardiovascular symptoms. Transdermal patch formulations of ChEIs may cause pruritus. N-methyl-_D-aspartic acid receptor antagonists may also cause various adverse effects. Patients with AD often have impaired ability to recognize psychosomatic changes and to inform people around them of the changes. Thus, detection of adverse effects is likely to be delayed. If the somatic symptoms caused by adverse effects appear as a lack of animation or irritation, the changes due to adverse effects will be likely misunderstood as symptoms caused by progression of AD, behavioral and psychological symptoms. Since the four symptomatic drugs became available, there have been more opportunities to discuss how the use of the drugs can be differentiated. However, the need for using these drugs should be reevaluated before differentiation of their use.
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