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Re: RedShoulder post# 276508

Friday, 10/16/2020 11:30:36 AM

Friday, October 16, 2020 11:30:36 AM

Post# of 470067
Sleep - a few of many papers released within the last year:


ORIGINAL RESEARCH ARTICLE
Front. Neurol., 21 April 2020 | https://doi.org/10.3389/fneur.2020.00292
Nonmotor Symptoms Affect Sleep Quality in Early-Stage Parkinson's Disease Patients With or Without Cognitive Dysfunction
Jun Zhu1, Min Zhong2, Jun Yan1, Xu Jiang2, Zhuang Wu2, Yang Pan1, Bo Shen1, Lili Zhang1, Jingde Dong1 and Li Zhang1*
1Nanjing Brain Hospital Affiliated to Nanjing Medical University, Nanjing, China
2Nanjing Medical University, Nanjing, China
Purpose: Parkinson's disease (PD) patients frequently present with sleep disorders. This study was designed to assess the impact of nonmotor symptoms (NMSs) on sleep quality in early-stage PD patients with and without cognitive dysfunction.

Materials and Methods: A sample of 389 early-stage PD patients (modified Hoehn and Yahr score ≤ 2.5, duration ≤ 5 years) was recruited for the present study. The Non-Motor Symptoms Questionnaire (NMS-Quest) was used to screen for global NMSs. Depressive symptoms were assessed using the Hamilton Rating Scale for Depression (HAMD). PD motor symptoms were measured with the Unified PD Rating Scale (UPDRS), part III. The Montreal Cognitive Assessment (MoCA) was used to evaluate global cognitive status, and the PD Sleep Scale (PDSS) was used to quantify sleep quality. Polysomnography (PSG) was used for objective assessment of sleep.

Results: In our sample, approximately one-quarter of the PD patients suffered from sleep disturbances (23.7%). Our results also confirmed the high prevalence of cognitive dysfunction in patients with PD (39.8%). In patients with cognitive dysfunction, higher percentage of sleep disorders (34.8 vs. 16.2%, P < 0.01) was observed. They also with lower PDSS score, sleep efficiency (SE) and longer sleep lantency (SL) and wake after sleep onset (WASO) (All P < 0.05). In total, the patients who suffered from NMSs, such as depressive symptoms, anxiety symptoms, urinary tract symptoms and hallucinations/delusions, had poorer sleep quality. Better cognition may predict better sleep quality. In patients with cognitive dysfunction, the NMS-Hallucinations/delusions score was the most important risk factor for sleep disorders. In patients without cognitive dysfunction, NMSs such as anxiety and cognition and medication were related to sleep disorder.

Conclusions: NMSs in early-stage PD are highly associated with and are determinants of subjective sleep quality. Future studies should focus on elucidating the pathophysiology of these symptoms.



https://www.frontiersin.org/articles/10.3389/fneur.2020.00292/full



Sleep dysregulation, memory impairment, and CSF biomarkers during different levels of neurocognitive functioning in Alzheimer’s disease course
Claudio Liguori, Fabio Placidi, Francesca Izzi, Matteo Spanetta, Nicola Biagio Mercuri & Alessandra Di Pucchio
Alzheimer's Research & Therapy volume 12, Article number: 5 (2020) Cite this article


Abstract
Background
Alzheimer's disease (AD) is frequently accompanied by sleep impairment, which can induce AD-related neurodegeneration. We herein investigated the sleep architecture, cognition, and cerebrospinal fluid (CSF) biomarkers (tau proteins and ß-amyloid42) during AD progression from subjective cognitive impairment (SCI) to mild cognitive impairment (MCI) and eventually to AD dementia, and compared the results with cognitively normal (CN) subjects.

Methods
We included patients affected by SCI, MCI, mild AD, and moderate-to-severe AD in our study along with CN subjects as controls. All the subjects underwent nocturnal polysomnography to investigate sleep, neuropsychological testing to evaluate cognition, and lumbar puncture for CSF AD biomarkers assessment.

Results
Sleep (both rapid eye movement (REM) and non-REM sleep) and memory function are both progressively impaired during the course of AD from SCI to mild and subsequently to moderate AD. Further, sleep dysregulation appears earlier than cognitive deterioration, with a reduction of CSF ß-amyloid42 level.

Conclusion
Sleep, memory, and CSF AD biomarkers are closely interrelated in AD progression from the earliest asymptomatic and preclinical stages of the disease related in AD since the earliest and preclinical stages of the disease.



https://alzres.biomedcentral.com/articles/10.1186/s13195-019-0571-3



INTRODUCTION
Sleep-wake disturbances are among the most prevalent and persistent sequelae of traumatic brain injury (TBI) [1-3]. Patients suffering from TBI of any severity, in both the acute and chronic phases, commonly report excessive daytime sleepiness, increased sleep need, insomnia, and sleep fragmentation [4-6]. Identification and treatment of sleep disorders in patients with TBI is important and can complement other efforts to promote maximum functional recovery.

The clinical features, evaluation, and treatment of sleep-wake disorders in patients with TBI are discussed here. The classification of TBI and management of other complications of head injury, including the postconcussion syndrome, are reviewed separately.
.....

Actigraphy — Actigraphy records rest-activity patterns using an accelerometer to detect motion, often combined with a light detector, usually worn on the nondominant wrist or waist. Actigraphy results are an objective counterpart to data obtained from a sleep diary. (See "Actigraphy in the evaluation of sleep disorders".)

Although not widely available for clinical purposes in the United States and moderately expensive, actigraphy can be useful as an objective measure of sleep-wake patterns in patients with a complaint of excessive daytime sleepiness. It also has the advantage over PSG of recording activity patterns over long periods of time (ie, weeks to months). An actigraphy pattern showing much longer sleep times on weekends than weekdays supports a diagnosis of insufficient sleep syndrome in patients with a complaint of daytime sleepiness.

Actigraphy has been used in many studies of adult patients with TBI [11,15,38,43,82,83], though caution should be exercised regarding using activity as a surrogate for sleep in patients with locomotor limitations including spasticity, paresis, depression, and/or agitation.



https://www.uptodate.com/contents/sleep-wake-disorders-in-patients-with-traumatic-brain-injury





Cognitive neurology
Original research
Sleep problems and risk of all-cause cognitive decline or dementia: an updated systematic review and meta-analysis
orcid.org/0000-0002-3310-5875Wei Xu1, Chen-Chen Tan1, Juan-Juan Zou2, Xi-Peng Cao3, Lan Tan1
Author affiliations
Abstract
Objectives To conduct an updated systematic review and meta-analysis of association between sleep and all-cause cognitive disorders.

Methods PubMed and EMBASE were searched from inception to 18 February 2019. Cohort studies exploring longitudinal associations of sleep with cognitive decline or dementia were included. The multivariable-adjusted effect estimates were pooled by random-effects models, with credibility assessment. The robust error meta-regression model was used to conduct the dose–response meta-analysis for sleep duration.

Results 11?155 reports were searched and 51 eligible cohorts with 15 sleep problems were included for our meta-analyses. Ten types of sleep conditions or parameters, including six (insomnia, fragmentation, daytime dysfunction, prolonged latency, rapid eye movement sleep behaviour disorder and excessive time in bed) with moderate-to-high levels of evidence, were linked to higher risk of all-cause cognitive disorders. Furthermore, a U-shaped relationship was revealed for the associations with sleep duration.

Conclusions Sleep management might serve as a promising target for dementia prevention.

http://creativecommons.org/licenses/by-nc/4.0/
This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/.



View Full Text
http://dx.doi.org/10.1136/jnnp-2019-321896




Abstract
Objective Disrupted sleep increases CSF levels of tau and ß-amyloid (Aß) and is associated with an increased risk of Alzheimer disease (AD). Our aim was to determine whether acute sleep loss alters diurnal profiles of plasma-based AD-associated biomarkers.

Methods In a 2-condition crossover study, 15 healthy young men participated in 2 standardized sedentary in-laboratory conditions in randomized order: normal sleep vs overnight sleep loss. Plasma levels of total tau (t-tau), Aß40, Aß42, neurofilament light chain (NfL), and glial fibrillary acidic protein (GFAP) were assessed using ultrasensitive single molecule array assays or ELISAs, in the fasted state in the evening prior to, and in the morning after, each intervention.

Results In response to sleep loss (+17.2%), compared with normal sleep (+1.8%), the evening to morning ratio was increased for t-tau (p = 0.035). No changes between the sleep conditions were seen for levels of Aß40, Aß42, NfL, or GFAP (all p > 0.10). The AD risk genotype rs4420638 did not significantly interact with sleep loss–related diurnal changes in plasma levels of Aß40 or Aß42 (p > 0.10). Plasma levels of Aß42 (-17.1%) and GFAP (-12.1%) exhibited an evening to morning decrease across conditions (p < 0.05).

Conclusions Our exploratory study suggests that acute sleep loss results in increased blood levels of t-tau. These changes provide further evidence that sleep loss may have detrimental effects on brain health even in younger individuals. Larger cohorts are warranted to delineate sleep vs circadian mechanisms, implications for long-term recurrent conditions (e.g., in shift workers), as well as interactions with other lifestyle and genetic factors.



https://n.neurology.org/content/94/11/e1181



The results of studies by researchers at the University of Rochester Medical Center (URMC) have outlined how the complex set of molecular and fluid dynamics that comprise the glymphatic system—the brain’s self-contained waste removal process—are synchronized with the master internal clock that regulates the body’s sleep-wake cycle. The findings suggest that people who rely on sleeping during daytime hours are at greater risk or developing neurological disorders.

The study data have also provided new insights into the function of the glymphatic system, which was discovered in 2012 by researchers in the lab of neuroscientist Maiken Nedergaard, MD, co-director of the Center for Translational Neuromedicine at URMC. “These findings show that glymphatic system function is not solely based on sleep or wakefulness, but by the daily rhythms dictated by our biological clock,” said Nedergaard. The studies are published in Nature Communications, in a paper titled, “Circadian control of brain glymphatic and lymphatic fluid flow.”

Sleep is an “evolutionarily conserved biological function, clearing the brain of harmful metabolites such as amyloid beta, which build up during wakefulness, and consolidating memory,” the authors wrote. Acute sleep deprivation has been shown to impair cognitive function, and sleep disruption is often associated with neurodegenerative diseases. “Sleep quality is highly dependent on both sleep deficit and sleep timing controlled by circadian rhythms, 24-hour cycles in gene transcription, cell signaling, physiology, and behavior,” they continued. “Understanding how circadian rhythms contribute to sleep quality is necessary to promote long-term brain health.”



https://www.genengnews.com/news/sleep-timing-disrupts-brains-waste-disposal-may-increase-risk-of-neurological-disorders/




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