- Sleep architecture changes in the APP23 mouse model manifest at onset of cognitive deficits. [Journal Article]
- BBBehav Brain Res 2019 Jul 17; :112089
- Alzheimer's disease (AD), which accounts for most of the dementia cases, is, aside from cognitive deterioration, often characterized by the presence of non-cognitive symptoms such as activity and sle…
Alzheimer's disease (AD), which accounts for most of the dementia cases, is, aside from cognitive deterioration, often characterized by the presence of non-cognitive symptoms such as activity and sleep disturbances. AD patients typically experience increased sleep fragmentation, excessive daytime sleepiness and night-time insomnia. Here, we sought to investigate the link between sleep architecture, cognition and amyloid pathology in the APP23 amyloidosis mouse model for AD. By means of polysomnographic recordings the sleep-wake cycle of freely-moving APP23 and wild-type (WT) littermates of 3, 6 and 12 months of age was examined. In addition, ambulatory cage activity was assessed by interruption of infrared beams surrounding the home cage. To assess visuo-spatial learning and memory a hidden-platform Morris-type Water Maze (MWM) experiment was performed. We found that sleep architecture is only slightly altered at early stages of pathology, but significantly deteriorates from 12 months of age, when amyloid plaques become diffusely present. APP23 mice of 12 months old had quantitative reductions of NREM and REM sleep and were more awake during the dark phase compared to WT littermates. These findings were confirmed by increased ambulatory cage activity during that phase of the light-dark cycle. No quantitative differences in sleep parameters were observed during the light phase. However, during this light phase, the sleep pattern of APP23 mice was more fragmented from 6 months of age, the point at which also cognitive abilities started to be affected in the MWM. Sleep time also positively correlated with MWM performance. We also found that spectral components in the EEG started to alter at the age of 6 months. To conclude, our results indicate that sleep architectural changes arise around the time the first amyloid plaques start to form and cognitive deterioration becomes apparent. These changes start subtle, but gradually worsen with age, adequately mimicking the clinical condition.
- The effect of sex and body weight on lung volumes during sleep. [Journal Article]
- SSleep 2019 Jul 19
- CONCLUSIONS: Reductions in FRC while supine and with increased body weight may contribute to worsened OSA in these conditions, but low lung volumes appear unlikely to explain the worsening of OSA in REM and in men versus women.
- Short Average Duration of NREM/REM Cycle Is Related to Cognitive Decline in an Elderly Cohort: An Exploratory Investigation. [Journal Article]
- JAJ Alzheimers Dis 2019 Jul 15
- Prospective studies concerning sleep architecture and cognitive function have focused on individual sleep measures per se, without considering the complementary role of non-REM (NREM) and REM sleep. …
Prospective studies concerning sleep architecture and cognitive function have focused on individual sleep measures per se, without considering the complementary role of non-REM (NREM) and REM sleep. We explored the association between NREM/REM cycle-related sleep architecture and cognitive decline. Community-dwelling elderly people in Korea from the Korean Longitudinal Study on Cognitive Aging and Dementia were enrolled. They were cognitively normal and underwent an overnight polysomnography at baseline. A NREM/REM cycle is a sequence of NREM and REM sleep, uninterrupted by a waking period of >2 min. After 4 years, the development of mild cognitive impairment (MCI) or dementia was related to the measures of sleep architecture, including NREM/REM cycle parameters by logistic regression analyses. Of 235 participants (mean [SD] age 68  years; 60% female) at baseline, 14 (5.9%) developed MCI/dementia at follow-up. A short average cycle length (OR, 0.97 [95% CI, 0.94-0.99]; p = 0.02) was significantly associated with cognitive decline. When its substructure and NREM and REM sleep outside of cycles were considered simultaneously, the average REM sleep duration per cycle (OR, 0.87 [95% CI, 0.76-0.98]; p = 0.03) was significantly related to the outcome. In conclusion, a short average duration of NREM/REM cycles, especially average REM sleep duration in each cycle, in cognitively normal elderly might be used as an early marker of cognitive decline.
- The Many Roads to Sleep. [Journal Article]
- NNeuron 2019 Jul 17; 103(2):181-183
- Recent studies have expanded our understanding of sleep regulation by elucidating multiple neural circuits that promote sleep. In this issue of Neuron, Ma et al. (2019) identify a novel thalamo-amygd…
Recent studies have expanded our understanding of sleep regulation by elucidating multiple neural circuits that promote sleep. In this issue of Neuron, Ma et al. (2019) identify a novel thalamo-amygdalar circuit which uses neurotensin to initiate and sustain NREM sleep.
- Sleep microstructure in Parkinson's disease: cycling alternating pattern (CAP) as a sensitive marker of early NREM sleep instability. [Journal Article]
- SMSleep Med 2019 Apr 20
- CONCLUSIONS: The main result of our study consists in the disclosure of altered NREM sleep microstructure in PD even at an early stage of the disease, suggesting an early alteration of the central pathways involved in the NREM sleep building-up and stability.
- Clinical neurophysiology of NREM parasomnias. [Journal Article]
- HCHandb Clin Neurol 2019; 161:397-410
- The nonrapid eye movement (NREM) parasomnias range from age-related developmental phenomena in children to aggressive and injurious motor behaviors in all age groups. These parasomnias are commonly r…
The nonrapid eye movement (NREM) parasomnias range from age-related developmental phenomena in children to aggressive and injurious motor behaviors in all age groups. These parasomnias are commonly referred to as disorders of arousal and are an important cause of sleep-related injury. Genetic predisposition plays a role in the disorders of arousal, most evident in sleepwalking. Important concepts guiding our current understanding of the pathophysiology of the NREM parasomnias include sleep state instability (a propensity for arousal during NREM sleep), sleep inertia (incomplete awakening from NREM sleep), state dissociation (an ability to simultaneously straddle both NREM sleep and wakefulness), and activation of central pattern generators (permitting expression of subcortically determined motor behaviors without conscious higher cortical input). Management is multifaceted with an emphasis on education and nonpharmacologic measures. The purpose of this chapter is to review wake and NREM neurobiology and update our current understanding of NREM parasomnia pathophysiology, epidemiology, genetics, clinical features, precipitating factors, neurophysiologic evaluation, diagnosis, and clinical management.
- Clinical neurophysiology of apnea. [Journal Article]
- HCHandb Clin Neurol 2019; 161:345-352
- Understanding the clinical neurophysiology of apnea generation encompasses discussion of the neuroanatomic aspects of central respiratory rhythm and pattern generation, including the central respirat…
Understanding the clinical neurophysiology of apnea generation encompasses discussion of the neuroanatomic aspects of central respiratory rhythm and pattern generation, including the central respiratory control networks, central and peripheral chemoreceptors, mechanisms of respiratory muscles, and sleep state dependent differences. Anatomical and functional links to apnea also involve central respiratory motor output recruited from the hypoglossal nerve, which has led to novel treatments for obstructive sleep apnea. Autonomic fluctuations occur in relation to sleep-wake and sleep states (i.e., REM vs NREM sleep), with both parasympathetic and sympathetic contributions. Finally, our understanding of the pathophysiology of obstructive sleep apnea now includes concepts of critical closing pressure of the upper airway, increased loop gain as reflected by high responsiveness to external perturbations, inadequate responsiveness of upper airway muscle recruitment, and reductions in arousal threshold leading to ventilatory instability. In turn, these concepts have led to the development of novel therapies such as hypoglossal nerve stimulation and targeting key culprit physiologic mechanisms specific to the individual.
- Sleep and neurological autoimmune diseases. [Review]
- NNeuropsychopharmacology 2019 Jul 14
- Neurological autoimmune diseases are characterized by an inappropriate immune response that by mistake targets the nervous system. As a result, patients experiment a number of neurological manifestat…
Neurological autoimmune diseases are characterized by an inappropriate immune response that by mistake targets the nervous system. As a result, patients experiment a number of neurological manifestations that may include insomnia, excessive daytime sleepiness, cataplexy, central hypoventilation, and REM sleep behavior disorder. Polysomnographic evaluation may reveal disorganized sleep architecture involving both NREM and REM sleep, and REM sleep intrusions into wakefulness. The study of sleep disorders in the setting of autoimmune diseases (e.g., narcolepsy, anti-IgLON5 disease, paraneoplastic neurological syndromes) shows that an abnormal immune-mediated (humoral or cellular) response target the neuronal structures (e.g., brainstem, hypothalamus) and neurotransmitters systems (e.g., hypocretin) that regulate sleep resulting in sleep impairment. It is a window to examine the link between the autoimmune system and the sleep regulation at the molecular, cellular, and anatomic level.
- Sleep fragmentation as an important clinical characteristic of sleep disorders in Parkinson's disease: a preliminary study. [Journal Article]
- CMChin Med J (Engl) 2019 Jul 05
- CONCLUSIONS: This preliminary study supported that sleep fragmentation was an important clinical characteristic of sleep disorders in PD. Whether sleep fragmentation is a potential quantifiable marker in PD needs to be further investigated in the future study.
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- Optogenetic Manipulation of Neural Circuits During Monitoring Sleep/wakefulness States in Mice. [Journal Article]
- JVJ Vis Exp 2019 Jun 19; (148)
- In recent years, optogenetics has been widely used in many fields of neuroscientific research. In many cases, an opsin, such as channel rhodopsin 2 (ChR2), is expressed by a virus vector in a particu…
In recent years, optogenetics has been widely used in many fields of neuroscientific research. In many cases, an opsin, such as channel rhodopsin 2 (ChR2), is expressed by a virus vector in a particular type of neuronal cells in various Cre-driver mice. Activation of these opsins is triggered by application of light pulses which are delivered by laser or LED through optic cables, and the effect of activation is observed with very high time resolution. Experimenters are able to acutely stimulate neurons while monitoring behavior or another physiological outcome in mice. Optogenetics can enable useful strategies to evaluate function of neuronal circuits in the regulation of sleep/wakefulness states in mice. Here we describe a technique for examining the effect of optogenetic manipulation of neurons with a specific chemical identity during electroencephalogram (EEG) and electromyogram (EMG) monitoring to evaluate the sleep stage of mice. As an example, we describe manipulation of GABAergic neurons in the bed nucleus of the stria terminalis (BNST). Acute optogenetic excitation of these neurons triggers a rapid transition to wakefulness when applied during NREM sleep. Optogenetic manipulation along with EEG/EMG recording can be applied to decipher the neuronal circuits that regulate sleep/wakefulness states.