The Interaction between Obstructive Sleep Apnea and Parkinson’s Disease: Possible Mechanisms and Implications for Cognitive Function

Kamińska, Marta; Lafontaine, Anne‐Louise; Kimoff, R. John

doi:10.1155/2015/849472

Cited by 38 publications

(40 citation statements)

References 151 publications

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“…[ 20 21 22 ] OSA has a relatively high prevalence among patients with neurodegenerative diseases. [ 14 18 19 ] Many studies report down-regulation of Wnt signaling in the pathogenesis of PD, and also highlight the importance of this pathway in neuroprotection. [ 20 ] Godin et al .…”

Section: Discussionmentioning

confidence: 99%

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Altered Wnt Signaling Pathway in Cognitive Impairment Caused by Chronic Intermittent Hypoxia

Pan

Deng

Xie

et al. 2016

Chinese Medical Journal

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Background:Cognitive impairment is a severe complication caused by obstructive sleep apnea (OSA). The mechanisms of causation are still unclear. The Wnt/β-catenin signaling pathway is involved in cognition, and abnormalities in it are implicated in neurological disorders. Here, we explored the Wnt/β-catenin signaling pathway abnormalities caused by chronic intermittent hypoxia (CIH), the most characteristic pathophysiological component of OSA.Methods:We divided 32 4-week-old male C57/BL mice into four groups of eight each: a CIH + normal saline (NS) group, CIH + LiCl group, sham CIH + NS group, and a sham CIH + LiCl group. The spatial learning performance of each group was assessed by using the Morris water maze (MWM). Protein expressions of glycogen synthase kinase-3β (GSK-3β) and β-catenin in the hippocampus were examined using the Western blotting test. EdU labeling and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling staining methods were used, respectively, to determine the proliferation and apoptosis of neurons in the hippocampal dentate gyrus region.Results:Mice exposed to CIH showed impaired spatial learning performance in the MWM, including increased mean escape latencies to reach the target platform, decreased mean times passing through the target platform and mean duration in the target quadrant. The GSK-3β activity increased, and expression of β-catenin decreased significantly in the hippocampus of the CIH-exposed mice. Besides, CIH significantly increased hippocampal neuronal apoptosis, with an elevated apoptosis index. Meanwhile, LiCl decreased the activity of GSK-3β and increased the expression of β-catenin and partially reversed the spatial memory deficits in MWM and the apoptosis caused by CIH.Conclusions:Wnt/β-catenin signaling pathway abnormalities possibly play an important role in the development of cognitive deficits among mice exposed to CIH and that LiCl might attenuate CIH-induced cognitive impairment via Wnt/β-catenin signaling pathway.

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Section: Discussionmentioning

confidence: 99%

“…Kaminska et al . [ 14 ] reported that sleep disturbances were frequent in Parkinson's disease (PD). These include insomnia, hypersomnia, sleep architecture, and circadian abnormalities.…”

Section: Introductionmentioning

confidence: 99%

Altered Wnt Signaling Pathway in Cognitive Impairment Caused by Chronic Intermittent Hypoxia

Pan

Deng

Xie

et al. 2016

Chinese Medical Journal

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“…Sleep apnea may have central, obstructive/peripheral or mixed causes. It has been hypothesized that sleep apneainduced chronic intermittent hypoxia may increase oxidative stress and inflammation [33], which may contribute to the pathophysiology of PD [34]. A recent 3-year nationwide retrospective populationbased study of 1,944 Taiwanese patients with sleep apnea and 9,720 matched control subjects showed a higher risk of incident PD diagnosis (0.9%) in the apneic patients compared to 0.4% in the controls [35].…”

Section: Sleep Apnea and Incident Pd: Intermittent Hypo-oxygenation Amentioning

confidence: 99%

Sleep Disturbance as Potential Risk and Progression Factor for Parkinson’s Disease

Bohnen

2019

JPD

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Sleep disturbances are common and a major source of disability in Parkinson's disease (PD). Primary and secondary insomnia, rapid eye movement sleep behavior disorder (RDB), central sleep apnea, restless legs, and nocturnal akinesia are common sleep disturbances in PD. Prodromal presence of RBD is associated with a more severe motor and non-motor PD subtype implying a significant disease-modifying effect of this parasomnia. Other disease-modifying mechanisms of sleep disturbances in PD include impaired glymphatic clearance, endoplasmic reticulum stress, nocturnal brain deoxygenation and inflammatory processes among others. Impairments of neural circuit switching and imbalance between inhibitory and excitatory neuronal populations are likely responsible for episodic sleep disturbances, in particular RBD. As neural circuits may predict patterns of ␣-synuclein propagation in the nervous system, impairments of such circuits are of high relevance for PD pathophysiology. Future research is needed to determine whether appropriate treatment for disturbed sleep might slow progression of PD.

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“…Recently, De Natale et al [120] showed that abnormalities in brainstem reflexes (vestibular-evoked myogenic potential) were more severe in patients with advanced Parkinson's disease compared with patients in the early phase and were significantly correlated with high scores on RBD Screening Questionnaire, an indicator for RBD severity. Similarly, dysfunction in brainstem ventilatory control mechanisms may be the link for the involvement of Parkinson's disease in the pathogenesis of SDB [93,94]. …”

Section: Sleep-wake Neurobiology In Prodromal Parkinson's Diseasementioning

confidence: 99%

Sleep-wake disturbances in the premotor and early stage of Parkinson's disease

Bargiotas

Schuepbach

Bassetti

2016

Current Opinion in Neurology

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Purpose of reviewReview of recent literature pertaining to frequency, associations, mechanisms, and overall significance of sleep-wake disturbances (SWD) in the premotor and early phase of Parkinson's disease.Recent findings SWD are frequent in Parkinson's disease and their prevalence increases with disease progression. Recent studies confirm previous findings that SWD can appear as initial manifestation of Parkinson's disease even decades before motor signs appear and highlight their clinical associations in these early stages. More intriguingly, new evidence underpins their role as risk factors, predictors, or even as driving force for the neurodegenerative process. As our understanding of sleep-wake neurobiology increases, new hypotheses emerge concerning the pathophysiology of SWD in early Parkinson's disease stages involving dopaminergic and nondopaminergic mechanisms. INTRODUCTIONSleep-wake disturbances (SWD) are frequent in Parkinson's disease and are typically attributed to Parkinson's disease medications, poor sleep hygiene, and other nonmotor symptoms (NMS) such as nocturnal akinesia, pain, cramping, and nycturia. Over the past decade, notable advances have been made in the understanding of the role of the dopaminergic system in circadian mechanisms and sleep-wake physiology [1]. In addition, nondopaminergic systems are involved early in the pathogenesis of SWD in Parkinson's disease [2,3]. These findings suggest that SWD are no longer solely a complication of advanced PD but can emerge, among other NMS, in the premotor stages as a primary manifestation of neurodegeneration [4] and increase in frequency with Parkinson's disease progression (Fig. 1). Considering the importance of early diagnosis and intervention, the possibility that SWD may have prognostic value for the development of Parkinson's disease is intriguing.This review will discuss first the most recent literature on SWD in the context of premotor and early stage of Parkinson's disease and then important recent evidence on the pathophysiology of SWD in early Parkinson's disease. SUBJECTIVE SLEEP DISTURBANCES/ INSOMNIATwo thirds of patients with Parkinson's disease report poor sleep quality [5], many of them very early in the course of the disease [6,7]. Recent studies confirm the high prevalence of subjective sleep disturbances in the early stages of Parkinson's disease and highlight their association with low quality of life [8,9&& ,10 && ] and other NMS such as global cognitive impairment, anxiety, depression and nocturia [8]. Individuals later diagnosed with

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The Interaction between Obstructive Sleep Apnea and Parkinson’s Disease: Possible Mechanisms and Implications for Cognitive Function

Cited by 38 publications

References 151 publications

Altered Wnt Signaling Pathway in Cognitive Impairment Caused by Chronic Intermittent Hypoxia

Altered Wnt Signaling Pathway in Cognitive Impairment Caused by Chronic Intermittent Hypoxia

Sleep Disturbance as Potential Risk and Progression Factor for Parkinson’s Disease

Sleep-wake disturbances in the premotor and early stage of Parkinson's disease

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