Background: Affective temperaments have been considered antecedents of major depressive disorder (MDD). However, little is known about how the covariation between alterations in brain activity and distinct affective temperaments work collaboratively to contribute to MDD. Here, we focus on the insular cortex, a critical hub for the integration of subjective feelings, emotions, and motivations, to examine the neural correlates of affective temperaments and their relationship to depressive symptom dimensions.Methods: Twenty-nine medication-free patients with MDD and 58 healthy controls underwent magnetic resonance imaging scanning and completed the Temperament Evaluation of Memphis, Pisa, Paris and San Diego (TEMPS). Patients also received assessments of the Hamilton Depression Rating Scale (HDRS). We used multivariate analyses of partial least squares regression and partial correlation analyses to explore the associations among the insular activity, affective temperaments, and depressive symptom dimensions.Results: A profile (linear combination) of increased fractional amplitude of low-frequency fluctuations (fALFF) of the anterior insular subregions (left dorsal agranular–dysgranular insula and right ventral agranuar insula) was positively associated with an affective-temperament (depressive, irritable, anxious, and less hyperthymic) profile. The covariation between the insula-fALFF profile and the affective-temperament profile was significantly correlated with the sleep disturbance dimension (especially the middle and late insomnia scores) in the medication-free MDD patients.Conclusions: The resting-state spontaneous activity of the anterior insula and affective temperaments collaboratively contribute to sleep disturbances in medication-free MDD patients. The approach used in this study provides a practical way to explore the relationship of multivariate measures in investigating the etiology of mental disorders.

(1) Background: Cognitive decline is associated with instrumental activities of daily living (IADL) disability. Intervention targeting the mediators of this association will provide a path to avoid cognition-related IADL disability. (2) Methods: This study used data of wave 2008 (baseline) and wave 2014 of Chinese Longitudinal Healthy Longevity Surveys. Structural equation modeling was conducted to examine the mediating effect of social interaction, lifestyle (fruit and vegetable intake; exercise habits), and depressive status on the association between four baseline cognitive function dimensions (measured by the Chinese version of the Mini-Mental State Examination) and five (2014) IADL dimensions (visiting neighbors, shopping, preparing meals, washing clothes, and taking public transportation). (3) Results: Among 1976 older adults, 29.1% developed IADL disability 6 years later. The cognition–disability association was completely mediated by social interaction (estimate = −0.095, p < 0.001), lifestyle (estimate = −0.086, p < 0.001), and depressive status (estimate = −0.017, p = 0.003). The mediating effects of social interaction (46.3% variances explained) and lifestyle (42.0% variances explained) were both larger than that of depressive status (8.3% variances explained). (4) Conclusions: The development of interventions aimed at improving social interaction, depression, and lifestyle could be of value to prevent cognition-related IADL disability.

Under a “cocktail-party” listening condition with multiple-people talking, healthy people, but not people with schizophrenia, can benefit from the use of visual-speech (lipreading) priming (VSP) cues to improve speech recognition. The neural mechanisms underlying the unmasking effect of VSP remain unknown. This study investigated the brain substrates underlying the unmasking effect of VSP in healthy listeners and the schizophrenia-induced changes in the brain substrates. Using functional magnetic resonance imaging, brain activation and functional connectivity for the contrasts of the VSP listening condition versus the visual non-speech priming (VNSP) condition were examined in 16 healthy listeners (27.4 ± 8.6 years old, 9 females) and 22 listeners with schizophrenia (29.0 ± 8.1 years old, 8 females). The results showed that in healthy listeners, the VSP-induced activation (against the VNSP condition) of the left posterior inferior temporal gyrus (pITG) was significantly correlated with the VSP-induced improvement in target-speech recognition against speech masking. Compared to healthy listeners, listeners with schizophrenia showed significantly lower VSP-induced activation of the left pITG and reduced functional connectivity of the left pITG with the bilateral Rolandic operculum, bilateral STG, and left insular. Thus, the left pITG and its functional connectivity are the most critical brain substrates underlying the unmasking effect of VSP, assumedly through enhancing both the processing of target visual-speech signals and the inhibition of masking-speech signals. In people with schizophrenia, the vanished unmasking effect of VSP on speech recognition is associated with a schizophrenia-related reduction of VSP-induced activation and functional connectivity of the left pITG.