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Major Depressive Disorder (MDD) is one of the most common psychiatric disorders, with a large global impact on both the individual and the society. In this narrative review, we summarize neurocognitive deficits during acute and (partially) remitted states of depression. Furthermore, we outline the potential negative effect of cognitive impairment (CI) on functional recovery, and discuss the role of several variables in the development of CI for MDD patients. Though there is cumulating evidence regarding persistent CI in unipolar depression, research on treatment options specific for this patient group is still scarce. Hence the central aim of our review is to present non-pharmacological interventions, which are thought to reduce CI in affected MDD patients. We discuss cognitive remediation therapy (CRT), physical exercise, yoga, mindfulness-based therapy, and modern neuromodulation approaches like neurostimulation and neurofeedback training. In conclusion, we propose future directions for research on CI in depression. Looking further ahead, we suggest creative interventional designs that include a direct comparison of different non-pharmacological treatment approaches on neurocognition and functional outcome of MDD. Furthermore, additive and synergistic effects of CRT with other treatment approaches should be examined and compared to create multimodal and even personalized intervention programs.

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Cerebellar involvement in major depressive disorder (MDD) has been demonstrated by a growing number of studies, but it is unknown whether cognitive functioning in depressed individuals is related to cerebellar gray matter volume (GMV) abnormalities. Impaired attention and executive dysfunction are characteristic cognitive deficits in MDD, and critically, they often persist despite remission of mood symptoms. In this study, we investigated cerebellar GMV in patients with remitted MDD (rMDD) that showed persistent cognitive impairment. We applied cerebellum-optimized voxel-based morphometry in 37 patients with rMDD and with cognitive deficits, in 12 patients with rMDD and without cognitive deficits, and in 36 healthy controls (HC). Compared with HC, rMDD patients with cognitive deficits had lower GMV in left area VIIA, crus II, and in vermal area VIIB. In patients with rMDD, regression analyses demonstrated significant associations between GMV reductions in both regions and impaired attention and executive dysfunction. Compared with HC, patients without cognitive deficits showed increased GMV in bilateral area VIIIB. This study supports cerebellar contributions to the cognitive dimension of MDD. The data also point towards cerebellar area VII as a potential target for non-invasive brain stimulation to treat cognitive deficits related to MDD.