“…20 In addition, experimental evidence using mouse models demonstrated that modulation of NREM qEEG activity may reduce α-synuclein aggregation. 21 As such, these studies may contextualise the finding that qEEG abnormalities in NREM sleep, rather than REM sleep, were associated with increased risk of incident PD in the present study. In the present spectral analysis, reduced α, β, and α/θ, were all found to be associated with increased PD risk (consistent with the characteristic slowing of EEG activity seen in PD during wakefulness).…”
Section: Discussionsupporting
confidence: 51%
“…9 The absolute and relative power of the EEG in different frequency bands throughout the night were computed for REM and non-REM (NREM) separately. In this analysis, the qEEG measures of interest included the mean relative power for the following frequency bands: δ (0.1 -4 Hz), θ (4 -8 Hz), α (8 -12 Hz), β (12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30) and γ (>30 Hz). In addition, using the absolute spectral power for α and θ, the α/θ power ratio (α/θ) -a synoptic index of EEG background slowing down -was calculated.…”
BackgroundParkinson’s disease (PD) is associated with abnormalities of sleep macro- and microstructure as measured using polysomnography (PSG). Whether sleep abnormalities precede the development of PD is unknown. This study investigated the association between PSG measured sleep abnormalities in older adults and the risk of developing PD.Methods2,770 men aged 67 years or older from the ancillary sleep study of the Osteoporotic Fractures in Men Study (MrOS), a population-based cohort from the USA, who were free from PD at baseline (December 2003 – March 2005) and in whom there was PSG data available, were included in this analysis. Incident PD was based on a clinical diagnosis from a medical professional. Multivariable logistic regression was used to estimate odds ratios (OR) for incident PD by quartiles of PSG measures.FindingsDuring a median follow-up of 10.1 years, 70 (2.5%) cases of incident PD were identified. Longer total sleep time, lower rapid eye movement sleep (REM) percentage, a lower α/θ ratio during non-REM sleep and higher minimum oxygen saturations during REM sleep, were independently associated with an increased risk of developing PD during follow-up. Conversely, a higher awakening index was independently associated with a decreased risk of developing PD. The OR for the highest risk quartiles compared to the lowest risk quartiles, ranged from 2.3 to 4.0 (P < 0.05). The associations remained significant when incident PD cases occurring within the first two years of follow-up were excluded from the analyses.ConclusionsMacro- and microstructural sleep abnormalities precede the development of PD by several years and can identify individuals at high risk of developing PD in the future. Future studies are needed to determine whether sleep abnormalities represent preclinical markers of PD or causal risk factors.
“…20 In addition, experimental evidence using mouse models demonstrated that modulation of NREM qEEG activity may reduce α-synuclein aggregation. 21 As such, these studies may contextualise the finding that qEEG abnormalities in NREM sleep, rather than REM sleep, were associated with increased risk of incident PD in the present study. In the present spectral analysis, reduced α, β, and α/θ, were all found to be associated with increased PD risk (consistent with the characteristic slowing of EEG activity seen in PD during wakefulness).…”
Section: Discussionsupporting
confidence: 51%
“…9 The absolute and relative power of the EEG in different frequency bands throughout the night were computed for REM and non-REM (NREM) separately. In this analysis, the qEEG measures of interest included the mean relative power for the following frequency bands: δ (0.1 -4 Hz), θ (4 -8 Hz), α (8 -12 Hz), β (12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30) and γ (>30 Hz). In addition, using the absolute spectral power for α and θ, the α/θ power ratio (α/θ) -a synoptic index of EEG background slowing down -was calculated.…”
BackgroundParkinson’s disease (PD) is associated with abnormalities of sleep macro- and microstructure as measured using polysomnography (PSG). Whether sleep abnormalities precede the development of PD is unknown. This study investigated the association between PSG measured sleep abnormalities in older adults and the risk of developing PD.Methods2,770 men aged 67 years or older from the ancillary sleep study of the Osteoporotic Fractures in Men Study (MrOS), a population-based cohort from the USA, who were free from PD at baseline (December 2003 – March 2005) and in whom there was PSG data available, were included in this analysis. Incident PD was based on a clinical diagnosis from a medical professional. Multivariable logistic regression was used to estimate odds ratios (OR) for incident PD by quartiles of PSG measures.FindingsDuring a median follow-up of 10.1 years, 70 (2.5%) cases of incident PD were identified. Longer total sleep time, lower rapid eye movement sleep (REM) percentage, a lower α/θ ratio during non-REM sleep and higher minimum oxygen saturations during REM sleep, were independently associated with an increased risk of developing PD during follow-up. Conversely, a higher awakening index was independently associated with a decreased risk of developing PD. The OR for the highest risk quartiles compared to the lowest risk quartiles, ranged from 2.3 to 4.0 (P < 0.05). The associations remained significant when incident PD cases occurring within the first two years of follow-up were excluded from the analyses.ConclusionsMacro- and microstructural sleep abnormalities precede the development of PD by several years and can identify individuals at high risk of developing PD in the future. Future studies are needed to determine whether sleep abnormalities represent preclinical markers of PD or causal risk factors.
“…These associations are presumably attributable to the reduced efficacy of the glymphatic system as a result of sleep disturbance 30 , 31 , as the function of the glymphatic fluid is enhanced by sleep and regulated by circadian rhythms 32 . Previous studies revealed slow-wave sleep is the stage at which glymphatic drainage is enhanced 29 . A recent clinical study indicated that increased brain parenchyma mean water diffusivity was positively related to the proportion of total sleep time spent in the REM phase in healthy people 33 .…”
Section: Discussionmentioning
confidence: 99%
“…5 ). Besides, other pathologies such as neuroinflammation 27 , reactive astroglioses 28 and sleep abnormalities 29 may also induce glymphatic dysfunction, and further animal and human studies are required to elucidate these processes. Fig.…”
Alpha-synucleinopathy is postulated to be central to both idiopathic rapid eye movement sleep behaviour disorder (iRBD) and Parkinson’s disease (PD). Growing evidence suggests an association between the diminished clearance of α-synuclein and glymphatic system dysfunction. However, evidence accumulating primarily based on clinical data to support glymphatic system dysfunction in patients with iRBD and PD is currently insufficient. This study aimed to use diffusion tensor image analysis along the perivascular space (DTI-ALPS) to evaluate glymphatic system activity and its relationship to clinical scores of disease severity in patients with possible iRBD (piRBDs) and those with PD. Further, we validated the correlation between the ALPS index and the prognosis of PD longitudinally. Overall, 168 patients with PD, 119 piRBDs, and 129 healthy controls were enroled. Among them, 50 patients with PD had been longitudinally reexamined. Patients with PD exhibited a lower ALPS index than those with piRBDs (P = 0.036), and both patient groups showed a lower ALPS index than healthy controls (P < 0.001 and P = 0.001). The ALPS index and elevated disease severity were negatively correlated in the piRBD and PD subgroups. Moreover, the ALPS index was correlated with cognitive decline in patients with PD in the longitudinal analyses. In conclusion, DTI-ALPS provided neuroimaging evidence of glymphatic system dysfunction in piRBDs and patients with PD; however, the potential of assessing the pathological progress of α-synucleinopathies as an indicator is worth verifying. Further development of imaging methods for glymphatic system function is also warranted.
“…Various animal models of PD, especially mouse models, are useful for examining the causal relationship between sleep and PD because the core mechanisms underlying the sleep-wake cycle and its regulation are shared between humans and mice ( 43 ). A recent study demonstrated in mouse models of PD that the administration of sodium oxybate enhanced SWS and reduced the accumulation of aggregated α-syn in the brain, although no major symptomatic effects were observed ( 44 ). Further investigations of the causal relationship between sleep disturbances and PD with a particular focus on PD symptoms and pathology are needed.…”
Section: Bidirectional Relationship Between Sleep and Pdmentioning
Parkinson's disease (PD) is the second most common neurodegenerative disease after Alzheimer's disease (AD). Both diseases share common clinical and pathological features: the gradual progression of neurological and psychiatric symptoms caused by neuronal dysfunction and neuronal cell death due to the accumulation of misfolded and neurotoxic proteins. Furthermore, both of them are multifactorial diseases in which both genetic and non-genetic factors contribute to the disease course. Non-genetic factors are of particular interest for the development of preventive and therapeutic approaches for these diseases because they are modifiable; of these, sleep is a particularly intriguing factor. Sleep disturbances are highly prevalent among both patients with AD and PD. To date, research has suggested that sleep disturbances are a consequence as well as a risk factor for the onset and progression of AD, which implies a bidirectional relationship between sleep and AD. Whether such a relationship exists in PD is less certain, albeit highly plausible given the shared pathomechanisms. This review examines the current evidence for the bidirectional relationship between sleep and PD. It includes research in both humans and animal models, followed by a discussion of the current understanding of the mechanisms underlying this relationship. Finally, potential avenues of research toward achieving disease modification to treat or prevent PD are proposed. Although further efforts are crucial for preventing the onset and slowing the progress of PD, it is evident that sleep is a valuable candidate target for future interventions to improve the outcomes of PD patients.
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