Treatment of Mild Cognitive Impairment

Opinion statement

It is increasingly evident that early identification of cognitive impairment in older adults presents opportunities for interventions that aim to mitigate the impact of cognitive symptoms on daily function and that attempt to delay (or ultimately prevent) progression from mild cognitive impairment (MCI) to dementia. To date, no intervention has proven protective in ultimately preventing conversion to dementia. However, several lifestyle, dietary, and pharmacologic interventions have suggested symptomatic benefit for those having MCI. A number of diet and lifestyle recommendations have been associated with decreased risk of dementia both in cognitively intact older adults and in those having mild cognitive impairment. Thus, these recommendations may be appropriate for both people presenting with subjective cognitive concerns and for those having objective evidence of memory problems. It remains less certain whether adopting these lifestyle habits in later life confers the benefits seen in epidemiological cohorts (where people have likely practiced them for many years). Discussion of starting on a cholinesterase inhibitor is appropriate for those having MCI, particularly those in whom the MCI is thought to have a vascular etiology or to represent the prodromal stage of a neurodegenerative disease. Recent meta-analyses exploring the use of cholinesterase inhibitors in patients having MCI have concluded that there is no evidence to support this practice. Although meta-analytic techniques seemingly strengthen the confidence in a recommendation via the incorporation of a large number of subjects analyzed, the technique is not capable of overcoming any inherent weaknesses of the individual studies included in the analysis. It is arguable whether studies in MCI may have employed endpoints poorly adapted to investigating effect of cholinesterase inhibitors. Most studies have used cognitive screening examinations, all of which stretch their detection ability to identify subjects with MCI, let alone discriminate subtle differences between them. Some have used conversion from MCI to dementia as an endpoint, which may not be the best measure for a symptomatic treatment. Further, once conversion to dementia has occurred, a cholinesterase inhibitor would be started in most (if not all) clinical settings, a reality not well reflected in most study designs. Additionally, several large studies have not permitted subject stratification by APOE carrier status, another important defect in assessing outcome. In clinical practice, our center typically does recommend cholinesterase inhibitors for patients having MCI. Despite the modest effect size, many patients do wish to start on treatment. It appears that this is a generally accepted practice and experience, as most clinical trials for prodromal Alzheimer’s disease specify that participants should be taking a cholinesterase inhibitor.