Objective
To examine associations between subjectively-reported sleep and objectively-measured sleep (i.e., actigraphy) with different domains of cognitive functioning, and determine whether age may moderate these associations.
Method
In this cross-sectional study, a total of 489 participants (mean age = 45.4 years; SD = 18.8) completed a self-reported sleep measure and one week of actigraphy. Participants also completed a battery of cognitive tests measuring episodic memory, social cognition, executive functioning, and complex cognition (i.e., reasoning, visuospatial, and language abilities).
Results
Multiple regression analyses revealed that greater objective sleep quality and longer onset latencies were both associated with better performance on measures of conceptual flexibility. In contrast, subjective sleep quality was not associated with performance in any cognitive domain after accounting for objective sleep variables. Age moderated sleep–cognition relationships in differing ways based on cognitive domain and facet of sleep assessed. For example, whereas poorer subjective sleep quality was associated with poorer complex cognition in younger, but not older adults, poorer objective sleep quality was associated with poorer conceptual flexibility in older, but not younger adults.
Conclusions
Objectively-measured and self-reported sleep are associated with differing aspects of executive functioning, with the latter related to executive functioning broadly and the former associated with conceptual flexibility in particular. Age moderates sleep–cognition relationships differentially depending on the method by which sleep quality and quantity are measured.
Parkinson's disease (PD) is a neurodegenerative disorder most notable for its motoric symptoms (e.g., bradykinesia, resting tremor, rigidity). Although cognitive deficits, anxiety, and depression are also widely reported in PD, there is limited research addressing these symptoms. Current interventions are almost exclusively targeted toward motor symptoms and are largely pharmacological in nature, despite issues with long-term efficacy and medication management. The aim of this pilot study was to describe the preliminary effects of a combined cognitive-behavioral therapy and attention training intervention in a small sample of older adults with PD, an anxiety disorder, and self-reported problems with executive functions (n ϭ 10). According to indices of reliable change on outcome measures, improvement in anxiety and depressive symptomatology as well as cognitive domains was observed. Moreover, 50% of participants were free of diagnosed anxiety disorders following treatment. Despite limitations, this study adds to the literature on nonpharmacological interventions for neuropsychiatric symptoms in PD.
Clinical Impact StatementAs a result of the burgeoning elderly population, the need for research on nonmotoric symptoms and nonpharmacological interventions in Parkinson's disease is evident. Ten patients with Parkinson's disease showed improvement in anxiety, depression, and complex cognitive abilities after completing cognitive-behavioral therapy augmented with an attention enhancement program. These findings point to the potential benefit of incorporating cognitive remediation into interventions for depressed and anxious adults with Parkinson's disease.
The Apolipoprotein E (APOE)-ε4 allele is the strongest genetic risk factor for Alzheimer’s disease (AD) and other neurodegenerative dementias. Cross-sectional case-control studies suggest that the effect of APOE-ε4 decreases in old age. However, since APOE- ε4 is associated with mortality, these studies might be prone to bias due to selective survival. Therefore, we used multi-state-modeling in longitudinal cohort studies to examine the effect of APOE-ε4 on the transition through cognitive states (i.e. cognitively normal, mild cognitive impairment (MCI) and dementia) while taking death as a competing risk into account. Results from the German AgeCoDe study (n=3000, aged 75-101 years) showed that APOE-ε4 increases the risk for cognitive deterioration in all disease stages. Contrary to results from cross-sectional studies, the effect of APOE-ε4 on the transition from MCI to dementia increased with increasing age (HR=1.044, 95%-CI=1.001-1090). The direction of this effect was confirmed in a smaller sample from the Einstein Aging Study (n=744, HR=1.032, 95%-CI=0.949-1.122). To examine the pathophysiological basis of these results, generalized additive models were used to study AD biomarkers in the liquor of 1045 patients with MCI or AD-dementia. Here, increased amyloid (Abeta1-42) pathology was associated with increased tau pathology (pTau181), consistent with the amyloid-cascade-hypothesis. Interestingly, higher age and presence of the APOE-ε4 synergistically lowered the amount of amyloid required to exacerbate tau pathology (interaction p=0.012). Taken together, our results suggest that the effect of APOE-ε4 on disease progression increases with advancing age. An altered neuroinflammatory response to neurodegeneration should be further explored as potential underlying mechanism.
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