Deep Sleep, Olfactory Loss, and Cognition in Early-stage Parkinson's Disease: Pilot Study Results.

Individuals with Parkinson's disease (PD) have a higher risk of developing dementia compared to age-matched controls. Rapid eye movement sleep behavior disorder (RBD) and hyposmia can influence symptoms severity. We report associations between polysomnography-assessed sleep architecture, olfactory identification, and cognition. Twenty adults with early-stage PD (mean age 69 ± 7.9; 25% female) completed cognitive assessments, the Brief Smell Identification Test (BSIT), and overnight in-clinic polysomnography. A global cognitive score was derived from principal component analysis. Linear regression models examined associations between sleep variables, BSIT performance, and cognition. Cognitive performance was compared between participants with and without RBD. Deep sleep attainment (ß ± SE: 1.18 ± 0.45, p = .02) and olfactory identification (0.37 ± 0.12, p = .01) were associated with better cognition. Light sleep, REM sleep, arousal index, and sleep efficiency were not (all p > .05). Participants with RBD had significantly worse cognition (t-test = -1.06 ± 0.44, p = .03) compared to those without RBD; none entered deep sleep. Deep sleep attainment was associated with better memory (1.20 ± 0.41, p = .01) and executive function (2.94 ± 1.13, p = .02); sleep efficiency was associated with executive function (0.05 ± 0.02, p = .02). These findings suggest interrelationships between lack of deep sleep, hyposmia, and poorer cognition in PD, particularly among individuals with RBD. Assessing these markers together may improve early identification of high-risk individuals and access to interventions.

Performance of the Dreem 2 EEG headband, relative to polysomnography, for assessing sleep in Parkinson's disease.

GOAL AND AIMS: To pilot the feasibility and evaluate the performance of an EEG wearable for measuring sleep in individuals with Parkinson's disease. FOCUS TECHNOLOGY: Dreem Headband, Version 2. REFERENCE TECHNOLOGY: Polysomnography. SAMPLE: Ten individuals with Parkinson's disease. DESIGN: Individuals wore Dreem Headband during a single night of polysomnography. CORE ANALYTICS: Comparison of summary metrics, bias, and epoch-by-epoch analysis. ADDITIONAL ANALYTICS AND EXPLORATORY ANALYSES: Correlation of summary metrics with demographic and Parkinson's disease characteristics. CORE OUTCOMES: Summary statistics showed Dreem Headband overestimated several sleep metrics, including total sleep, efficiency, deep sleep, and rapid eye movement sleep, with an exception in light sleep. Epoch-by-epoch analysis showed greater specificity than sensitivity, with adequate accuracy across sleep stages (0.55-0.82). IMPORTANT SUPPLEMENTAL OUTCOMES: Greater Parkinson's disease duration and rapid eye movement behavior were associated with more wakefulness, and worse Parkinson's disease motor symptoms were associated with less deep sleep. CORE CONCLUSION: The Dreem Headband performs similarly in Parkinson's disease as it did in non-Parkinson's disease samples and shows promise for improving access to sleep assessment in people with Parkinson's disease.

Biological aging processes underlying cognitive decline and neurodegenerative disease.

Alzheimer's disease and related dementias (ADRD) are among the top contributors to disability and mortality in later life. As with many chronic conditions, aging is the single most influential factor in the development of ADRD. Even among older adults who remain free of dementia throughout their lives, cognitive decline and neurodegenerative changes are appreciable with advancing age, suggesting shared pathophysiological mechanisms. In this Review, we provide an overview of changes in cognition, brain morphology, and neuropathological protein accumulation across the lifespan in humans, with complementary and mechanistic evidence from animal models. Next, we highlight selected aging processes that are differentially regulated in neurodegenerative disease, including aberrant autophagy, mitochondrial dysfunction, cellular senescence, epigenetic changes, cerebrovascular dysfunction, inflammation, and lipid dysregulation. We summarize research across clinical and translational studies to link biological aging processes to underlying ADRD pathogenesis. Targeting fundamental processes underlying biological aging may represent a yet relatively unexplored avenue to attenuate both age-related cognitive decline and ADRD. Collaboration across the fields of geroscience and neuroscience, coupled with the development of new translational animal models that more closely align with human disease processes, is necessary to advance novel therapeutic discovery in this realm.