Communicative Coping Behavior Checklist: Observation of Persons With Dementia in the Home Environment.

PURPOSE OF THE STUDY: Communication contributes to increased stress, mortality, and decreased quality of life (QOL) for persons with dementia (PWD) and caregivers. PWD use communicative coping behaviors (CCBs) to manage the demands of the disease. However, most assessments neither look for nor give credit to communication behaviors. This is the first study to examine CCBs in the home environment as measured by the Communicative Coping Behavior Checklist (CCBC). DESIGN AND METHODS: This cross-sectional quantitative study included 26 dementia and 18 cognitively normal control dyads. Raters observed their partners' CCBs at home, over several weeks and completed the CCBC. We analyzed the endorsement rates (how often behaviors were observed by a rater) of emotion and activity-focused CCBs in dementia and control dyads. RESULTS: The primary outcome was rate of CCB endorsement. Secondary outcomes included dementia diagnosis, cognitive status, depressive mood, life satisfaction (SWL) and QOL. Dementia dyads endorsed 11 of 23 CCBs significantly more than control dyads. Action-focused CCBs (p < .001) were more frequent than emotion-focused CCBs (p = .004) in dementia dyads. Specific CCBs such as humor correlated with higher caregiver QOL (p = .019) and PWD's SWL (p = .003). Another CCB, general humor, correlated with lower PWD's SWL (p = .024). IMPLICATIONS: This was the first study to examine CCBs in the home environment comparing dementia and control dyads. Higher endorsement rates of action-focused than emotion-focused CCBs were seen in dementia dyads. We conclude that attention to CCBs during treatment and care will improve QOL and SWL of PWD and caregivers.

TAK1 and IKK2, novel mediators of SCF-induced signaling and potential targets for c-Kit-driven diseases.

NF-κB activation depends on the IKK complex consisting of the catalytically active IKK1 and 2 subunits and the scaffold protein NEMO. Hitherto, IKK2 activation has always been associated with IκBα degradation, NF-κB activation, and cytokine production. In contrast, we found that in SCF-stimulated primary bone marrow-derived mast cells (BMMCs), IKK2 is alternatively activated. Mechanistically, activated TAK1 mediates the association between c-Kit and IKK2 and therefore facilitates the Lyn-dependent IKK2 activation which suffices to mediate mitogenic signaling but, surprisingly, does not result in NF-κB activation. Moreover, the c-Kit-mediated and Lyn-dependent IKK2 activation is targeted by MyD88-dependent pathways leading to enhanced IKK2 activation and therefore to potentiated effector functions. In neoplastic cells, expressing constitutively active c-Kit mutants, activated TAK1 and IKKs do also not induce NF-κB activation but mediate uncontrolled proliferation, resistance to apoptosis and enables IL-33 to mediate c-Kit-dependent signaling. Together, we identified the formation of the c-Kit-Lyn-TAK1 signalosome which mediates IKK2 activation. Unexpectedly, this IKK activation is uncoupled from the NF-κB-machinery but is critical to modulate functional cell responses in primary-, and mediates uncontrolled proliferation and survival of tumor-mast cells. Therefore, targeting TAK1 and IKKs might be a novel approach to treat c-Kit-driven diseases.