Developmental myelination deficits and impaired fine motor function in a mouse model of pediatric obstructive sleep apnea
Hedayatpour MJ, Ailani R, Williamson MR, Pedersen SE, Pautler R, Nicot-Cartsonis MS, Adler AC, Kheradmand F, Deneen B, Harmanci AS, Lee HK and Chandrakantan A
Developmental myelination deficits and impaired fine motor function in a mouse model of pediatric obstructive sleep apnea
Hedayatpour MJ, Ailani R, Williamson MR, Pedersen SE, Pautler R, Nicot-Cartsonis MS, Adler AC, Kheradmand F, Deneen B, Harmanci AS, Lee HK and Chandrakantan A
Our primary objective was to characterize the mechanism that underlies fine motor deficits in Pediatric obstructive sleep apnea (POSA) using a preclinical mouse model of the disease. Our goal was to use a systematic approach to characterize neuroanatomical lesions in POSA mice and identify potential molecular drivers of the fine motor changes in this preclinical model of POSA.
Clinically significant night-to-night variability in overnight oximetry screening for obstructive sleep apnoea in children with Down syndrome: a retrospective review of screening data
Garde AJB, Wen Yi Ong J, Howarth Z, James J, Wilkinson TL, Yuen HM, Hill CM and Evans HJ
Clinically significant night-to-night variability in overnight oximetry screening for obstructive sleep apnoea in children with Down syndrome: a retrospective review of screening data
Garde AJB, Wen Yi Ong J, Howarth Z, James J, Wilkinson TL, Yuen HM, Hill CM and Evans HJ
To understand the extent and implications of night-to-night variability (NTNV) in obstructive sleep apnoea (OSA) screening for children with Down syndrome (DS).
Comparative characteristics of mental health networks in older adults across care models: A cross-sectional study of community home-based and institutional care
Chen B, Wang Y, Hu J, Feng W, Wu M and Wu J
Comparative characteristics of mental health networks in older adults across care models: A cross-sectional study of community home-based and institutional care
Chen B, Wang Y, Hu J, Feng W, Wu M and Wu J
Care models significantly impact older adults' mental health, yet the dynamic interplay among symptoms remains unclear. This study compared the integrated sleep-psychological-social support networks between older adults in community home-based and institutional care.
Sleep timing regulates mood: A multilevel-EEG study of daily life
Pierson-Bartel R and Ujma PP
Sleep timing regulates mood: A multilevel-EEG study of daily life
Pierson-Bartel R and Ujma PP
Sleep and mood are homeostatically regulated systems essential for mental and physical health. Understanding how sleep timing and mood dynamically influence each other, and which individual traits moderate this coupling, can clarify mechanisms of mood regulation. Our objective was to examine bidirectional associations between sleep and daily mood under naturalistic conditions using objective sleep measurements and to identify personality and psychiatric traits that moderate these relationships.
Impact of intermittent hypoxia on cognitive impairment in sleep apnea models of rodents
Lu Z, Zhang W, Shen Y, Ou X, Wang H and Liu S
Impact of intermittent hypoxia on cognitive impairment in sleep apnea models of rodents
Lu Z, Zhang W, Shen Y, Ou X, Wang H and Liu S
Do Physical Exercises and Physical Activity Generate Positive Effects on Sleep Quality and Urinary Incontinence in Menopausal Women? A Systematic Review with Meta-Analysis
Martins JBB, da Rocha ARA, da Silveira J, da Silva E, Marques-Aleixo I and Guimarães ACA
Do Physical Exercises and Physical Activity Generate Positive Effects on Sleep Quality and Urinary Incontinence in Menopausal Women? A Systematic Review with Meta-Analysis
Martins JBB, da Rocha ARA, da Silveira J, da Silva E, Marques-Aleixo I and Guimarães ACA
This systematic review with meta-analysis aimed to investigate the effects of physical exercise and physical activity on sleep quality and urinary incontinence in menopausal women and to assess the strength of evidence from randomized clinical trials. Following the PRISMA checklist, this study was registered in PROSPERO (CDR42024587503), five databases were searched (i.e., Cochrane Library, Embase, Scopus, Web of Science, and PubMed Central) from October 2017 to November 2017, including randomized clinical trials that assessed certain types of physical exercise and physical activity for urinary incontinence and/or sleep quality in menopausal women, which were written in English and published in the last 10 years. Fourteen articles were selected for this review, which assessed 1,230 women for sleep quality and 482 women for urinary incontinence. A low risk of bias and moderate to high methodological quality were observed in most studies. With regard to sleep quality, the studies showed high heterogeneity (I² = 90%), with a 95% CI of -4.32 to -3.37 ( < 0.01), suggesting favorable results for the groups receiving physical exercise and physical activity interventions. With regard to urinary incontinence, the studies showed high heterogeneity (I² = 97%), with a 95% CI (-0.95 to -0.07, < 0.01), indicating favorable results for specific pelvic floor strengthening exercises. In summary, physical exercise and physical activity were shown to improve sleep quality and urinary incontinence, but caution is needed when assessing the specific effects of different types of exercise on each outcome.
Insomnia phenotypes and neurocognitive biomarkers
Ahmed M, Taj F and Nami M
Insomnia phenotypes and neurocognitive biomarkers
Ahmed M, Taj F and Nami M
Insomnia is increasingly understood as a heterogeneous disturbance of sleep-wake regulation shaped by interacting cognitive, physiological, circadian, neurobiological, and perceptual mechanisms. This chapter develops a phenotype-informed framework for insomnia that distinguishes descriptive clinical presentations from underlying mechanistic dimensions and measurable biomarker domains. Core phenotypes reviewed include cognitive-emotional hyperarousal, objective short sleep duration, paradoxical insomnia and sleep-state misperception, circadian misalignment, autonomic dysregulation, sleep-depth instability, psychiatric comorbidity, and night-to-night sleep variability. Particular attention is given to neurocognitive biomarkers, including attention, executive function, working memory, episodic memory, cognitive variability, and subjective cognitive burden, with emphasis on how outcomes differ across insomnia phenotypes. It also examines electrophysiological and sleep microstructure markers, including high-frequency EEG activity, slow-wave activity, spindles, microarousals, cyclic alternating pattern, cardiopulmonary coupling, and Odds Ratio Product as emerging indicators of sleep depth and state instability. Autonomic, circadian, physiological, neuroimaging, wearable, and AI-enabled multimodal approaches are evaluated for their potential to refine mechanistic understanding and support future precision sleep medicine. Across domains, the chapter emphasizes that no single biomarker currently provides sufficient specificity for diagnosis or treatment selection. Instead, insomnia phenotyping is most useful as an integrative, mechanism-informed approach that can improve clinical formulation, guide individualized treatment emphasis, and identify future research priorities.
Neuromodulation in sleep disorders
Qatanany B, Uzma N, Nizam A, Kaur S, Kamali AM and Nami M
Neuromodulation in sleep disorders
Qatanany B, Uzma N, Nizam A, Kaur S, Kamali AM and Nami M
Sleep disorders are a growing global health issue with profound consequences on cardiovascular health, metabolic functioning, cognitive output and overall quality of life. Although there have been numerous clinical advances in brain-based treatments for sleep disorders, there are still a number of sleep disorders that are not well understood and need new treatment options to address the underlying neural mechanisms of sleep-wake regulation. Recent advances in neuroscience have highlighted neuromodulation as a promising treatment option for the complex neural mechanisms of sleep-wake dysfunction. This chapter provides an overview on the neurobiological basics of neuromodulation in sleep medicine, including neurobiological circuits, circadian processes of sleep, wakefulness and their disorders in brain and potential targeting biomarkers for brain stimulation. Present non-invasive neuromodulation strategies include transcranial magnetic stimulation (TMS), transcranial direct current stimulation (tDCS), transcranial alternating current stimulation (tACS), vagus nerve stimulation, etc.; new and invasive neuromodulation strategies such as deep brain stimulation (DBS) for insomnia, obstructive sleep apnea (OSA) and periodic leg movement disorder (PLMD). In this paper, we review the current level of evidence and provide an overview on the road ahead to bring brain stimulation to the daily practice of sleep medicine.
Neurobiology of sleep apnea and cognitive impairment
Sharafkhaneh A and BaHammam A
Neurobiology of sleep apnea and cognitive impairment
Sharafkhaneh A and BaHammam A
Obstructive sleep apnea (OSA) has a broad and clinically important effect on cognition, most often impairing attention, executive function, memory, processing speed, and visuospatial ability, while language and immediate recall are relatively preserved. A substantial proportion of adults referred to sleep clinics already meet criteria for mild cognitive impairment at initial evaluation, particularly in moderate-to-severe OSA. This cognitive burden reflects multiple interacting mechanisms. Intermittent hypoxia promotes oxidative stress, mitochondrial dysfunction, and hippocampal injury through recurrent ischemia-reperfusion cycles. Sleep fragmentation disrupts slow-wave and REM sleep, impairing memory consolidation and glymphatic clearance. Neuroinflammation, endothelial dysfunction, and structural brain changes, including hippocampal atrophy, white matter hyperintensities, and reduced frontoparietal connectivity, may further compound injury over time. REM-related hypoxemia appears especially important for cerebrovascular injury and memory impairment. Measures such as hypoxic burden and oxygen desaturation indices may better capture brain risk than the apnea-hypopnea index alone. Older age, APOE ε4 genotype, obesity, hypertension, diabetes, depression, and prior cerebrovascular disease increase vulnerability and should guide screening and treatment priorities. Cognitive assessment in OSA should be domain-sensitive rather than based only on a single global cutoff. Effective therapy, especially positive airway pressure with adequate REM-period coverage, can improve alertness and selected cognitive outcomes, although attention may remain impaired despite improved oxygenation. In children, OSA can disrupt memory consolidation and working memory, and adenotonsillectomy often leads to only partial cognitive recovery. Cognition should therefore be considered a primary treatment outcome in both clinical care and future research.
REM sleep behavior disorder and synucleinopathies
Uzma N, Wajdi M, Alhashmi A, Qatanany B, Sharafkhaneh A, Kosagisharaf JR and Nami M
REM sleep behavior disorder and synucleinopathies
Uzma N, Wajdi M, Alhashmi A, Qatanany B, Sharafkhaneh A, Kosagisharaf JR and Nami M
Rapid Eye Movement (REM) Sleep Behavior Disorder (RBD) is a somnipathy characterized by a physiological failure of skeletal muscle atonia during REM sleep. Such a brainstem pathway disruption, which directly affects the pontomedullary reticular formation, disrupts the descending inhibitory pathways that normally cause muscle paralysis. Patients then are much more likely to act out their dreams and will have complex, often violent dream-enactment behaviors that may cause injury and disrupt sleep continuity. Almost two decades of research have shown that RBD is potentially a crucial early indicator for synucleinopathies (brain diseases that are related to the accumulation of alpha-synuclein protein). These diseases include Parkinson's disease (PD), dementia with Lewy bodies (DLB), and multiple system atrophy (MSA). Emerging biomarkers, neuroimaging results, and fluid-based biomarkers are discussed in the context of risk stratification and prediction of phenotypic pathophysiological transformation to overt neurodegenerative disease. Moreover, the chapter discusses how RBD provides a window for testing neuroprotective and disease-modifying therapies that may delay or prevent overt synucleinopathy. It also reviews current symptom management approaches that mix pharmacological treatment with non-pharmacological safety measures for injury prevention and neuromodulation technologies that target disrupted motor circuitry. Understanding the relationship between RBD and synucleinopathies offers a unique window into the earliest stages of neurodegeneration and presents new possibilities for early diagnosis, targeted treatment, and better patient outcomes.
