Misunderstanding the therapeutic aims is a hazard in evaluating efficacy of drug therapy. Dementia therapies, for example, are used to alleviate the symptoms of the condition or to modify the underlying disease process. The researcher should identify which of these primary therapeutic goals to address, and then design the eligibility criteria for the systematic review accordingly. A recent systematic review examined the ability of drugs used to treat dementia in order to delay disease onset and prevent the progression of the disease (5). The difference between the 2 therapeutic aims (in the context of dementia) is conceptualized in Figures 1 and 2, which show hypothetical responses of patients with dementia to 2 similar drug interventions (I and II) relative to placebo. In these examples, the cognitive abilities of the untreated patients (those who received placebo) with Alzheimer disease decline over time in a manner described by Stern and colleagues (6). For simplicity's sake, the decline in cognition is assumed to be fairly linear; however, the literature has suggested that the rate of decline varies between the different types of dementia and within each of these groups as a function of disease severity (7–8). In Figures 1 and 2, the titration period of 8 weeks (the minimum time required for the drug to be brought to the expected dosage for optimal effect) and the washout period are identical. In both hypothetical scenarios, the drugs are withdrawn from patients at 6 months and the washout periods (during which the drug can no longer be acting) have ended at 8 months. Figure 1 exemplifies the therapeutic aim of symptom relief. Within the active treatment period (first 6 months), the response to drug I depicts the maintenance or stabilization of cognitive function relative to the untreated or placebo; in contrast, the response to drug II suggests improvement (or restoration) of cognition for a short period. Upon withdrawal for patients exposed to either drug I or drug II (following the washout period), the cognition scores declined rapidly to the same rate as that in the untreated (placebo) group; thus, disease progression was not delayed. In contrast, Figure 2 shows a delayed rate of decline relative to placebo after the withdrawal of the pharmacologic intervention and, as such, exemplifies disease modification. Comparison of the slopes of the decline of cognition would indicate a greater rate of decline for drug II relative to drug I, but both show delay in progression of the disease effects. Theoretically, the rates of decline in the treatment group will never meet the rate in the untreated group when the pharmacologic agent has truly modified the disease.