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tion in BD as they persist in remission, appear to be heritable, and hence co-segregate within families [46, 47]. Therefore, our study provides further evidence that working memory could serve as a potential neurocognitive endophenotype in remitted BP.Association between cognition and clinical variablesRegarding the clinical characteristics of our bipolar sam-ple, we found no relationship between test measures and disease characteristics indicating severity of the disorder (e.g. number of episodes, age of onset, bipolar type). How-ever, subclinical mood symptoms and sleep disturbances were associated with cognitive speed, attention, and verbal memory. Although patients with bipolar disorder have his-torically been characterised as returning to full remission between affective episodes, recent studies demonstrated that some residual symptoms may persist [48, 49]. It has been previously demonstrated that subthreshold mood symptoms are associated with impairments in attention and verbal memory [11, 50–52]. In a study by Bonnin et al. , the degree of cognitive functioning was best predicted by subdepressive symptoms, and a meta-analysis reported that more rigorously defined euthymia goes along with smaller cognitive impairments . Therefore, it seems that the neuronal circuitry activated in the modulation of emo-tions overlaps with brain regions involved in neurocogni-tion. Besides subclinical depressive symptoms, 37 % of our remitted bipolar sample reported sleep disturbances like initial or middle insomnia or an abnormal increased sleep-ing time. Rates of sleep disturbances are usually very high in remitted BP [54, 55], and BD is highly associated with sleep and circadian rhythm abnormalities [49, 56, 57]. It is well known that sleep deprivation in healthy people causes cognitive deterioration [58, 59]. Furthermore, it has been demonstrated that sleep and circadian rhythms are involved in the cognitive deficits in BD through overlapping neuro-biological systems . In our bipolar sample, sleep distur-bances were associated with impairments in psychomotor speed, divided attention, and verbal learning. In a recently published study, we reported accordingly that several cog-nitive impairments in euthymic BP were predicted by sleep disorder . Taken together this underscores the need for more extensive research on the influence of sleep dis-turbances on cognitive deficits in BD. In conclusion, our results suggest that residual symptoms negatively affect cognitive functioning in BD. Therefore, an optimised antidepressant treatment and sleep regulation should be enforced in patients complaining about cognitive impair-ments. Even though our results do not disprove the idea of neurodegenerative processes in BD , our data underscore the importance of residual symptoms. This also has impli-cations for future research and calls for the improvement of treatment options for cognitively impaired BP.