Cognitive rehabilitation (CR) is a promising treatment approach for older adults with dementia because it aims at supporting the management of day-to-day problems. There is insufficient evidence regarding whether CR provides clinically meaningful benefits. In this study, we evaluated the feasibility, acceptance, efficacy, and usefulness of a CR intervention in a multicenter, randomized, controlled trial on 201 patients with mild dementia in Alzheimer disease and their carers. The intervention comprised 12 individual weekly sessions and combined 4 established strategies adopted from neurorehabilitation and psychotherapy. Activities of daily living were chosen as the primary outcome. The results show that the feasibility, treatment adherence, and carer commitment were excellent. However, no effect of the intervention was demonstrable on everyday functioning. There were improvements favoring the intervention on quality of life and treatment satisfaction and a significant antidepressant effect in female participants. The lack of impact on everyday activities may be due to methodological limitations including insufficient personalization, short treatment duration, poor transfer into the real-life setting, and low sensitivity of assessment instruments. The findings of this study may be helpful for designing further studies that are needed to determine the potential of CR in older adults with dementia.
The intracellular signaling mechanism of the ischemia-stimulated glucose transporter (GLUT) translocation in the heart is not yet characterized. It has been suggested that catecholamines released during ischemia may be involved in this pathway. The purpose of this study was to evaluate the contribution of alpha-adrenoceptors and beta-adrenoceptors to ischemia-mediated GLUT4 and GLUT1 translocation in the isolated, Langendorff-perfused rat heart. Additionally, GLUT translocation was studied in response to catecholamine stimulation with phenylephrine (Phy) and isoproterenol (Iso). The results were compared with myocardial uptake of glucose analogue [18F]fluorodeoxyglucose (FDG). Subcellular analysis of GLUT4 and GLUT1 protein on plasma membrane vesicles (PM) and intracellular membrane vesicles (IM) using membrane preparation and immunoblotting revealed that alpha- and beta-receptor agonists stimulated GLUT4 translocation from IM to PM (2.5-fold for Phy and 2.1-fold for Iso, P<0.05 versus control), which was completely inhibited by phentolamine (Phe) and propranolol (Pro), respectively. Plasmalemmal GLUT1 moderately rose after Iso exposure, and this was prevented by Pro. In contrast, ischemia-stimulated GLUT4 translocation (2.2-fold, P<0.05 versus control) was only inhibited by alpha-adrenergic antagonist Phe but not by beta-adrenergic antagonist Pro. Similarly, Phe but not Pro inhibited ischemia-stimulated GLUT1 translocation. GLUT data were confirmed by FDG uptake monitored using bismuth germanate detectors. The catecholamine-stimulated FDG uptake (6.9-fold for Phy and 8.9-fold for Iso) was significantly inhibited by Phe and Pro; however, only Phe but not Pro significantly reduced the ischemia-induced 2.5-fold increase in FDG uptake (P<0.05 versus ischemia). This study suggests that alpha-adrenoceptor stimulation may play a role in the ischemia-mediated increase in glucose transporter trafficking leading to the stimulation of FDG uptake in the isolated, perfused rat heart, whereas beta-adrenergic activation does not participate in this signaling pathway.
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