The diagnosis of dysthymic disorder was created in DSM-III and maintained in DSM-IV to describe a depressive syndrome of mild to moderate severity of at least two years’ duration that did not meet criteria for major depressive disorder. The prevalence of dysthymic disorder is approximately 2% in the elderly population where subsyndromal depressions of lesser severity are more common. Dysthymic disorder was replaced in DSM-V by the diagnosis of “persistent depressive disorder” that includes chronic major depression and dysthymic disorder. In older adults, epidemiological and clinical evidence supports the use of the term “dysthymic disorder.” In contrast to young adults with dysthymic disorder, older adults with dysthymic disorder commonly present with late age of onset, without major depression and other psychiatric disorders, and with a low rate of family history of mood disorders. They often have stressors such as loss of social support and bereavement, and some have cerebrovascular or neurodegenerative pathology. A minority has chronic depression dating from youth with psychiatric comorbidity similar to young adults with dysthymic disorder. In older adults, both dysthymic disorder and subsyndromal depression increase disability and lead to poor medical outcomes. Elderly patients with dysthymic disorder are seen mainly in primary care where identification and treatment are often inadequate. Treatment with antidepressant medication shows marginal superiority over placebo in controlled trials, and problem-solving therapy shows similar efficacy. Combined treatment and collaborative care models show slightly better results, but cost effectiveness is a concern. Further work is needed to clarify optimal approaches to the treatment of dysthymic disorder in elderly patients.

Background: Cognitive training (CT) may be effective as a therapeutic strategy to prevent cognitive decline in older adults. This review evaluates CT as a preventive tool at various stages of a prevention hierarchy with specific reference to healthy older adults, “at risk” and clinical populations. It also considers the underlying mechanism of CT, namely that which suggests that CT acts via promoting neuroplasticity.

Methods: Evidence for CT in healthy, “at risk” and clinical populations has been systematically reviewed elsewhere. This review re-examines several studies in each group to clarify the potential of CT as a preventive technique, with a key focus on the secondary level of prevention.

Results: Studies in healthy older adults and those with mild cognitive impairment are largely positive and suggest that CT has the potential to improve cognition. However, findings in relation to Alzheimer's disease are mixed. Limitations of existing research include diverse methodologies and CT programs, small samples, insufficient focus on functional outcomes, sustainability and generalization of effects and the need for imaging data to delineate mechanisms of change. Additionally, there is limited data on those with late-life depression, despite this being an independent risk factor for dementia.

Conclusions: CT offers promise as a preventive therapeutic technique in healthy older adults and particularly as a secondary prevention method for “at risk” groups. Future investigations need to focus on methodological constraints and delineating possible neuroplastic mechanisms of action. Nonetheless, CT programs may represent a viable, non-pharmacological early intervention strategy, as they are easily-implemented, engaging and promote social interaction in group settings.