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Mapping the darkness : the visionary scientists who unlocked the mysteries of sleep
Journalist Kenneth Miller weaves science with history to tell the story of four outsider academics who carried the study of sleep from fringe discipline to mainstream obsession. In the 1920s Nathaniel Kleitman founded the world's first dedicated sleep lab, with breakthrough experiments in 1938. Kleitman mentored Eugene Aserinsky who discovered REM sleep, and William Dement, who became known as the father of sleep medicine. Dement, in turn, mentored Mary Carskadon, who uncovered an epidemic of sleep deprivation among teenagers.-- Adapted from book jacket flap.
Book
The Sleep of Others and the Transformation of Sleep Research
Examining a vast historical period of 2500 years, Kroker separates the problems associated with the history of dreaming from those associated with sleep itself and charts sleep-related diseases such as narcolepsy, insomnia, and sleep apnea.
eBook
Adolescents’ Electronic Media Use at Night, Sleep Disturbance, and Depressive Symptoms in the Smartphone Age
Adolescence is a time of increasing vulnerability for poor mental health, including depression. Sleep disturbance is an important risk factor for the development of depression during adolescence. Excessive electronic media use at night is a risk factor for both adolescents’ sleep disturbance and depression. To better understand the interplay between sleep, depressive symptoms, and electronic media use at night, this study examined changes in adolescents’ electronic media use at night and sleep associated with smartphone ownership. Also examined was whether sleep disturbance mediated the relationship between electronic media use at night and depressive symptoms. 362 adolescents (12–17 year olds, M = 14.8, SD = 1.3; 44.8 % female) were included and completed questionnaires assessing sleep disturbance (short sleep duration and sleep difficulties) and depressive symptoms. Further, participants reported on their electronic media use in bed before sleep such as frequency of watching TV or movies, playing video games, talking or text messaging on the mobile phone, and spending time online. Smartphone ownership was related to more electronic media use in bed before sleep, particularly calling/sending messages and spending time online compared to adolescents with a conventional mobile phone. Smartphone ownership was also related to later bedtimes while it was unrelated to sleep disturbance and symptoms of depression. Sleep disturbance partially mediated the relationship between electronic media use in bed before sleep and symptoms of depression. Electronic media use was negatively related with sleep duration and positively with sleep difficulties, which in turn were related to depressive symptoms. Sleep difficulties were the more important mediator than sleep duration. The results of this study suggest that adolescents might benefit from education regarding sleep hygiene and the risks of electronic media use at night.
Journal Article
Neurodegenerative Disorder Risk in Idiopathic REM Sleep Behavior Disorder: Study in 174 Patients
To estimate the risk for developing a defined neurodegenerative syndrome in a large cohort of idiopathic REM sleep behavior disorder (IRBD) patients with long follow-up.
Using the Kaplan-Meier method, we estimated the disease-free survival rate from defined neurodegenerative syndromes in all the consecutive IRBD patients diagnosed and followed-up in our tertiary referal sleep center between November 1991 and July 2013.
The cohort comprises 174 patients with a median age at diagnosis of IRBD of 69 years and a median follow-up of four years. The risk of a defined neurodegenerative syndrome from the time of IRBD diagnosis was 33.1% at five years, 75.7% at ten years, and 90.9% at 14 years. The median conversion time was 7.5 years. Emerging diagnoses (37.4%) were dementia with Lewy bodies (DLB) in 29 subjects, Parkinson disease (PD) in 22, multiple system atrophy (MSA) in two, and mild cognitive impairment (MCI) in 12. In six cases, in whom postmortem was performed, neuropathological examination disclosed neuronal loss and widespread Lewy-type pathology in the brain in each case.
In a large IRBD cohort diagnosed in a tertiary referal sleep center, prolonged follow-up indicated that the majority of patients are eventually diagnosed with the synucleinopathies PD, DLB and less frequently MSA. IRBD represented the prodromal period of these conditions. Our findings in IRBD have important implications in clinical practice, in the investigation of the early pathological events occurring in the synucleinopathies, and for the design of interventions with potential disease-modifying agents.
Journal Article
Sleep Apnea Research in Animals. Past, Present, and Future
Obstructive sleep apnea (OSA) is a common disorder that describes recurrent collapse of the upper airway during sleep. Animal models have been pivotal to the understanding of OSA pathogenesis, consequences, and treatment. In this review, we highlight the history of OSA research in animals and include the discovery of animals with spontaneous OSA, the induction of OSA in animals, and the emulation of OSA using exposures to intermittent hypoxia and sleep fragmentation.
Journal Article
Effect of Rapid Eye Movement Sleep Behavior Disorder on Obstructive Sleep Apnea Severity and Cognition of Parkinson's Disease Patients
Background: Rapid eye movement (REM) sleep behavior disorder (RBD) and obstructive sleep apnea (OSA) are the most common sleep disorders in Parkinson's disease (PD). The aim of this study was to identify whether RBD could alleviate OSA severity in PD patients and its effect on cognitive impairment.
Methods: From February 2014 to May 2017, we recruited 174 PD patients from the Second Affiliated Hospital of Soochow University, all of whom underwent polysomnography (PSG). We collected clinical data, PSG results, and compared information between patients with and without RBD or OSA by analysis of covariance. We also investigated the effect of these sleep disorders on cognitive impairment using linear regression.
Results: We grouped participants as follows: PD only (n = 53), PD + OSA (n = 29), PD + RBD (n = 61), and PD + RBD + OSA (n = 31). Minimum oxygen saturation (SaO2) during whole sleep and in REM sleep was higher in PD + RBD + OSA patients than that in PD + OSA patients. PD + RBD patients had worse Mini-Mental Status Examination and Montreal Cognitive Assessment (MoCA) scores than those in the PD group (P < 0.001), especially in visuospatial/executive, attention, and memory functions. The PD + OSA group performed worse than the PD group in the delayed recall domain. After adjusting for age, sex, body mass index, education, disease severity, and other sleep disorders, MoCA was negatively associated with OSA (β = −0.736, P = 0.043) and RBD (β = −2.575,P < 0.001). The severity of RBD (tonic/phasic electromyography activity) and OSA (apnea-hypopnea index/oxygen desaturation index/minimum SaO2) were also associated with MoCA. The adjusted β values of RBD-related parameters were higher than that for OSA.
Conclusions: We found that RBD alleviated OSA severity; however, RBD and OSA together exacerbated PD cognitive impairment. Further studies are needed to evaluate whether OSA treatment can improve cognition in PD.
Journal Article
Long-term sleep disturbance and prescription sleep aid use among cancer survivors in the United States
Purpose
Insomnia and related sleep disorders are common complaints among cancer patients, and use of prescription sleep aids can be high in the treatment setting. The prevalence of sleep disturbance and prescription sleep aid use in the community-dwelling cancer survivorship population, however, remains relatively unexplored. We aim to ascertain the extent to which a cancer diagnosis is associated with sleep disturbances and prescription sleep aid use as measured in several cross sections of individuals across multiple disease sites and time since cancer diagnosis.
Methods
We used data from five cross-sectional cycles of the National Health and Nutrition Evaluation Survey (NHANES) from 2005 to 2014. We identified a total of 2371 individuals who reported a diagnosis of cancer (averaging 61 years old) and 25,788 individuals who did not report a cancer diagnosis (averaging 45 years old). We considered several patient-reported sleep-related outcomes. Multivariate regression analyses, as well as propensity score matching, were used to clarify the relationship between sleep disturbances, prescription sleep aid use, and cancer diagnosis, stratified by time since diagnosis and primary disease site.
Results
Reported sleep disturbance was common in cancer survivors, with approximately 34% of patients with a history of cancer reporting having ever been told they had trouble sleeping, compared to 23% of non-cancer patients in the general population with no history of cancer (
p
< 0.001). Propensity score matching supported a significantly higher rate of trouble sleeping among cancer survivors compared to matched controls. Compared to the general adult population without cancer, cancer survivors 11 or more years past diagnosis were more likely to report being diagnosed with trouble sleeping or a sleep disorder. Further, patients with gynecological cancers were more likely to report prescription sleep aid use, sleep disorders, and trouble sleeping compared to adults without a history of cancer.
Conclusions
Sleeping problems are common in the cancer survivorship population, especially in patients with a long survivorship history and a history of gynecological cancers. Consideration of symptoms of insomnia and sleep disturbance may be helpful in the follow-up care of these patients.
Journal Article
Protective role of brain derived neurotrophic factor (BDNF) in obstructive sleep apnea syndrome (OSAS) patients
Obstructive sleep apnea syndrome (OSAS) is a common disorder characterized by repeated episodes of upper airways collapse during the sleep. The following intermittent hypoxia triggers a state of chronic inflammation, which also interests the nervous system leading to neuronal damage and increased risk of cognitive impairment. Brain derived neurotrophic factor (BDNF) is a growth factor often associated with neuroplasticity and neuroprotection whose levels increase in several condition associated with neuronal damage. However, whether patients affected by OSAS have altered BDNF levels and whether such alteration may be reflective of their cognitive impairment is still controversial. Here we show that, when compared to healthy control volunteers, OSAS patients have increased serum levels of BDNF. Moreover, OSAS patients with the higher levels of BDNF also have reduced neurocognitive impairment as measured by The Montreal Cognitive Assessment (MoCA) questionnaire. Treatment with standard non-invasive mechanical ventilation (CPAP) also was able to ameliorate the level of cognitive impairment. Altogether our results indicate that BDNF levels represent a neuroprotective response to intermittent hypoxia in OSAS patients.
Journal Article
Association of rapid eye movement sleep latency with multimodal biomarkers of Alzheimer's disease
INTRODUCTION Sleep disturbances are associated with Alzheimer's disease (AD) and Alzheimer's disease and related dementias (ADRD), but the relationship between sleep architecture, particularly rapid eye movement (REM) sleep, and AD/ADRD biomarkers remains unclear. METHODS We enrolled 128 adults (64 with Alzheimer's disease, 41 with mild cognitive impairment [MCI], and 23 with normal cognition [NC]), mean age 70.8 ± 9.6 years, 56.9% female, from a tertiary hospital in China. Participants underwent overnight polysomnography (PSG), amyloid β (Aβ) positron emission tomography (PET), and plasma biomarker analysis: phosphorylated tau at threonine 181 (p‐tau181), neurofilament light (NfL), and brain‐derived neurotrophic factor (BDNF). RESULTS After adjusting for demographics, apolipoprotein E (APOE) ε4 status, cognition, and comorbidities, the highest tertile of REM latency was associated with higher Aβ burden (β = 0.08, 95% confidence interval [CI]: 0.03 to 0.13, p = 0.002), elevated p‐tau181 (β = 0.19, 95% CI: 0.02 to 0.13, p = 0.002), and reduced BDNF levels (β = ‐0.47, 95% CI: –0.68 to –0.13, p = 0.013), compared to the lowest tertile. DISCUSSION Prolonged REM latency may serve as a novel marker or risk factor for AD/ADRD pathogenesis. Highlights Rapid eye movement latency (REML) may be a potential marker for Alzheimer's disease and Alzheimer's disease and related dementias (AD/ADRD) pathogenesis. Prolonged REML was associated with higher amyloid beta (Aβ) burden, phosphorylated tau‐181 (p‐tau181), and lower brain‐derived neurotrophic factor (BDNF) levels. Intervention trial is needed to determine if targeting REML can modify AD/ADRD risk. Slow‐wave sleep was not associated with AD/ADRD biomarkers.
Journal Article
Evolution of canonical circadian clock genes underlies unique sleep strategies of marine mammals for secondary aquatic adaptation
To satisfy the needs of sleeping underwater, marine mammals, including cetaceans, sirenians, and pinnipeds, have evolved an unusual form of sleep, known as unihemispheric slow-wave sleep (USWS), in which one brain hemisphere is asleep while the other is awake. All aquatic cetaceans have only evolved USWS without rapid eye movement (REM) sleep, whereas aquatic sirenians and amphibious pinnipeds display both bihemispheric slow-wave sleep (BSWS) and USWS, as well as REM sleep. However, the molecular genetic changes underlying USWS remain unknown. The present study investigated the evolution of eight canonical circadian genes and found that positive selection occurred mainly within cetacean lineages. Furthermore, convergent evolution was observed in lineages with USWS at three circadian clock genes. Remarkably, in vitro assays showed that cetacean-specific mutations increased the nuclear localization of zebrafish clocka , and enhanced the transcriptional activation activity of Clocka and Bmal1a. In vivo , transcriptome analysis showed that the overexpression of the cetacean-specific mutant clocka ( clocka -mut) caused the upregulation of the wakefulness-promoting glutamatergic genes and the differential expression of multiple genes associated with sleep regulation. In contrast, the GABAergic and cholinergic pathways, which play important roles in promoting sleep, were downregulated in the bmal1a -mut-overexpressing zebrafish. Concordantly, sleep time of zebrafish overexpressing clocka -mut and bmal1a -mut were significantly less than the zebrafish overexpressing the wild-type genes, respectively. These findings support our hypothesis that canonical circadian clock genes may have evolved adaptively to enhance circadian regulation ability relating to sleep in cetaceans and, in turn, contribute to the formation of USWS.
Journal Article