]. Mis-categorization of individuals with T2D may be relatively socially beneficial in that it relieves individuals of stigmatizing aspects of their own illness identity.The current study investigates perceived blame and self-blame for disease onset, diabetes stigma, and negative affect in response to diabetes mis-categorization in relation to perceived weight status in a sample of adults affected by T1D or T2D .Framework of hypotheses.
Individuals with T2D and a higher weight status will report higher levels on all facets of diabetes stigma than those with a lower weight status. For participants with T1D, individuals with a higher weight status will report higher levels of stigma on the blame and judgment stigma subscale than those with a lower weight status. Due to the qualitative differences in diabetes stigma between T1D and T2D, these facets of stigma cannot be directly compared across disease type.
Individuals who are incongruent with their stereotype will more frequently be mis-categorized compared to those who are congruent with their stereotype.Those with T1D and a higher weight status will report higher levels of negative affect about mis-categorization.
Analyses of covariance were conducted using a univariate general linear model to assess differences in measures by diabetes type and perceived weight status. Covariates included in our models were gender, age, education, and time since diagnosis, where there was difference between demographic groups and theoretical reason to believe a given variable may be a confounder. Bonferroni correction was applied to post-hoc tests assessing significant interactions.
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NREM sleep as a novel protective cognitive reserve factor in the face of Alzheimer's disease pathology - BMC MedicineBackground Alzheimer’s disease (AD) pathology impairs cognitive function. Yet some individuals with high amounts of AD pathology suffer marked memory impairment, while others with the same degree of pathology burden show little impairment. Why is this? One proposed explanation is cognitive reserve i.e., factors that confer resilience against, or compensation for the effects of AD pathology. Deep NREM slow wave sleep (SWS) is recognized to enhance functions of learning and memory in healthy older adults. However, that the quality of NREM SWS (NREM slow wave activity, SWA) represents a novel cognitive reserve factor in older adults with AD pathology, thereby providing compensation against memory dysfunction otherwise caused by high AD pathology burden, remains unknown. Methods Here, we tested this hypothesis in cognitively normal older adults (N=62) by combining 11C-PiB (Pittsburgh compound B) positron emission tomography (PET) scanning for the quantification of β-amyloid (Aβ) with sleep electroencephalography (EEG) recordings to quantify NREM SWA and a hippocampal-dependent face-name learning task. Results We demonstrated that NREM SWA significantly moderates the effect of Aβ status on memory function. Specifically, NREM SWA selectively supported superior memory function in individuals suffering high Aβ burden, i.e., those most in need of cognitive reserve (B=2.694, p=0.019). In contrast, those without significant Aβ pathological burden, and thus without the same need for cognitive reserve, did not similarly benefit from the presence of NREM SWA (B=-0.115, p=0.876). This interaction between NREM SWA and Aβ status predicting memory function was significant after correcting for age, sex, Body Mass Index, gray matter atrophy, and previously identified cognitive reserve factors, such as education and physical activity (p=0.042). Conclusions These findings indicate that NREM SWA is a novel cognitive reserve factor providing resilience against the memory impairment otherwi
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