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

Bohnen, Nicolaas I.; Hu, Michele T.M.

doi:10.3233/jpd-191627

Cited by 96 publications

(90 citation statements)

References 61 publications

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“…Interestingly, epilepsy and myoclonus have recently been reported in A53T α-syn mice which was associated with reduced NREM sleep and more time spent in the awake state (Peters et al, 2020). Ours and other data, therefore, support the idea that early interventions aimed at improving sleep cycle regulation and sleep-related oscillations could be beneficial, not only in AD (Mander et al, 2016) and PD (Bohnen and Hu, 2019), but also in patients with DLB.…”

Section: The Clinical Significance Future Directions and Limitationssupporting

confidence: 81%

“…Abnormal slow wave sleep activity is thought to prevent the clearance of pathological forms of amyloid-β and tau, and even promote excess production of these peptides (Mander et al, 2016). If the same were also true for α-syn clearance, then the sleep oscillation impairments we have observed in A30P mice could set off a cycle of increasing levels of α-syn and sleep disruption, as has been suggested might occur in PD (Bohnen and Hu, 2019).…”

Section: Functional Consequences Of α-Syn Mediated So and Spindle Dysmentioning

confidence: 59%

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Early Disruption of Cortical Sleep-Related Oscillations in a Mouse Model of Dementia With Lewy Bodies (DLB) Expressing Human Mutant (A30P) Alpha-Synuclein

et al. 2020

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Changes in sleep behavior and sleep-related cortical activity have been reported in conditions associated with abnormal alpha-synuclein (α-syn) expression, in particular Parkinson's disease (PD) and dementia with Lewy bodies (DLB). Notably, changes can occur in patients years before the onset of cognitive decline. Sleep-related network oscillations play a key role in memory function, but how abnormal α-syn impacts the generation of such activity is currently unclear. To determine whether early changes in sleep-related network activity could also be observed, prior to any previously reported cognitive dysfunction, we used mice that over-express human mutant α-syn (A30P). Recordings in vivo were performed under urethane anesthesia in the medial prefrontal cortex (mPFC) and CA1 region of the hippocampus in young male (2.5-4 months old) A30P and age-matched wild type (WT) mice. We found that the slow oscillation (SO) < 1 Hz frequency was significantly faster in both the mPFC and hippocampus in A30P mice, and Up-state-associated fast oscillations at beta (20-30 Hz) and gamma (30-80 Hz) frequencies were delayed relative to the onset of the Up-state. Spindle (8-15 Hz) activity in the mPFC was also altered in A30P mice, as spindles were shorter in duration and had reduced density compared to WT. These changes demonstrate that dysregulation of sleep-related oscillations occurs in young A30P mice long before the onset of cognitive dysfunction. Our data suggest that, as seen in patients, changes in sleep-related oscillations are an early consequence of abnormal α-syn aggregation in A30P mice.

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Section: The Clinical Significance Future Directions and Limitationssupporting

confidence: 81%

Section: Functional Consequences Of α-Syn Mediated So and Spindle Dysmentioning

confidence: 59%

Early Disruption of Cortical Sleep-Related Oscillations in a Mouse Model of Dementia With Lewy Bodies (DLB) Expressing Human Mutant (A30P) Alpha-Synuclein

et al. 2020

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“…38,39 Sleep efficiency, the percentage of time spent asleep in bed, has also been observed to decrease in individuals with synucleinopathies. [38][39][40] Other specific sleep dimensions, such as sleep disturbances, medication taking, and daytime sleepiness, though showed non-significant associations with CSF a-syn in our study, were reported associated with a-syn propagation in the nervous system, 40,41 Figure 2. Linear associations of global sleep quality and score of characteristics in PSQI with CSF a-syn.…”

Section: Discussionmentioning

confidence: 77%

Associations of sleep characteristics with alpha‐synuclein in cerebrospinal fluid in older adults

Wang

Liu

et al. 2020

Ann Clin Transl Neurol

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Objective: Sleep disorders as a preclinical symptom of synucleinopathies become more prevalent in older adults. Synucleinopathies might be caused by the abnormal aggregation of alpha-synuclein in the brain, which was indicated by alpha-synuclein levels in cerebrospinal fluid (CSF). We aimed to investigate associations of sleep characteristics with CSF alpha-synuclein in older adults. Methods: Our study recruited 536 cognitively intact individuals (aged between 40 and 90 years old) from the Chinese Alzheimer's Biomarker and Lifestyle study. Sleep behaviors were assessed by Pittsburgh Sleep Quality Index and total alpha-synuclein in CSF was measured by enzyme-linked immune-sorbent assay. We used multiple linear and non-linear regression models for research. Results: Significant non-linear associations of CSF alpha-synuclein with sleep time and duration were revealed. Individuals who went to bed and fell asleep too early or late tended to have lower CSF alpha-synuclein (reflection point for time to bed and fall asleep were 10:26 p.m. and 10:40 p.m.). Lower CSF alpha-synuclein was also observed in individuals with either excessive or insufficient sleep duration (reflection point: 7.24 hours). Besides, overall poor sleep quality (b = À0.0621; P = 0.0242), longer sleep latency (b = À0.0415; P = 0.0174) and lower sleep efficiency (b = 0.0036; P = 0.0017) showed linear associations with lower CSF alpha-synuclein. Sleep disturbances and daytime dysfunction were not significantly associated with CSF alpha-synuclein. Interpretation: Poor sleep was associated with lower levels of CSF alpha-synuclein in older adults, which may provide new insight into the prevention of synucleinopathies.

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“…In this way, sleep apnea episodes were not significantly present in PD patients, as compared to control groups [ 131 ], despite that other reports demonstrated that almost 50% of PD patients experienced sleep apnea incidents [ 129 ]. In a more recent study, Bohnen and Hu [ 132 ] reported a correlation between sleep apnea which leads to repeated periods of hypoxia and reoxygenation during sleeping and the occurrence of OS and inflammation though a similar mechanism with sleep apnea-induced chronic intermittent hypoxia models. On the other hand, other studies reported that the more common sleep disturbance in PD patients is insomnia [ 131 , 133 ], which is present in 54-60% of cases [ 134 ].…”

Section: Is There An Oxidative Stress Correlation To Sleep Disturmentioning

confidence: 99%

“…However, Gjerstad et al [ 134 ] discussed the results in the context of age, pathological lesions in the upper brainstem and midbrain, depression, nocturia, and medication [ 133 , 135 ]. Thus, the multifactorial etiology of sleep disturbances [ 132 ] could be discussed in this context and also in the context of the possible comorbidity of sleep disturbances in PD. However, the cause-effect relationship between PD and sleep disturbances is not fully understood.…”

Section: Is There An Oxidative Stress Correlation To Sleep Disturmentioning

confidence: 99%

Parkinson’s Disease-Induced Zebrafish Models: Focussing on Oxidative Stress Implications and Sleep Processes

Robea

Balmuș

Ciobîcă

et al. 2020

Oxidative Medicine and Cellular Longevity

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The complex yet not fully understood pathophysiology of Parkinson’s disease includes an important molecular component consisting of oxidative status changes, thus leading to oxidative stress occurrence. While no particular evidence has been reported that describes the relationship between oxidative stress and the molecular mechanisms behind Parkinson’s disease development, animal model studies has shown that oxidative stress induction could modulate Parkinson’s disease symptomatology. Despite the inability to perfectly replicate human disease in animals and despite that Parkinson’s disease has not been reported in any animal species, animal modeling is one of the most important tools in understanding the complex mechanisms of human disorders. In this way, this study is aimed at detailing this particular relationship and describing the molecular mechanisms underlying Parkinson’s disease in animal models, focusing on the potential advantages and disadvantages of zebrafish in this context. The information relevant to this topic was gathered using major scientific database research (PubMed, Google Scholar, Web of Science, and Scopus) based on related keywords and inclusion criteria. Thus, it was observed that oxidative stress possesses an important role in Parkinson’s disease as shown by numerous animal model studies, many of which are based on rodent experimental models. However, an emerging impact of the zebrafish model was observed in the research of Parkinson’s disease pathological mechanisms with regard to disease development factors and the cause-effect relationship between oxidative stress and comorbidities (such as depression, hyposmia, fatigue, sleep disturbances, and cognitive deficits) and also with regard to the pharmacological potential of antioxidant molecules in Parkinson’s disease treatment.

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

Cited by 96 publications

References 61 publications

Early Disruption of Cortical Sleep-Related Oscillations in a Mouse Model of Dementia With Lewy Bodies (DLB) Expressing Human Mutant (A30P) Alpha-Synuclein

Early Disruption of Cortical Sleep-Related Oscillations in a Mouse Model of Dementia With Lewy Bodies (DLB) Expressing Human Mutant (A30P) Alpha-Synuclein

Associations of sleep characteristics with alpha‐synuclein in cerebrospinal fluid in older adults

Parkinson’s Disease-Induced Zebrafish Models: Focussing on Oxidative Stress Implications and Sleep Processes

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