sPDGFRß and neuroinflammation are associated with AD biomarkers and differ by race: The ASCEND Study.

INTRODUCTION: There remains an urgent need to identify preclinical pathophysiological mechanisms of Alzheimer's disease (AD) development in high-risk, racially diverse populations. We explored the relationship between cerebrospinal fluid (CSF) markers of vascular injury and neuroinflammation with AD biomarkers in middle-aged Black/African American (B/AA) and non-Hispanic White (NHW) participants. METHODS: Adults (45-65 years) with a parental history of AD were enrolled (n = 82). CSF and blood biomarkers were collected at baseline and year 2. RESULTS: CSF total tau (t-tau), phosphorylated tau (p-tau), and amyloid beta (Aß)40 were elevated at year 2 compared to baseline. CSF soluble platelet-derived growth factor receptor ß (sPDGFRß) levels, a marker of pericyte injury, correlated positively with t-tau, p-tau, Aß40 markers of vascular injury, and cytokines at baseline and year 2. CSF sPDGFRß and tau were significantly lower in B/AA than NHW. DISCUSSION: Vascular dysfunction and neuroinflammation may precede cognitive decline and disease pathology in the very early preclinical stages of AD, and there are race-related differences in these relationships. HIGHLIGHTS: Cerebrospinal fluid (CSF) Alzheimer's disease (AD) biomarkers changed over 2 years in high-risk middle-aged adults. Markers of vascular dysfunction were associated with the CSF biomarkers amyloid beta and tau. AD biomarkers were lower in Black compared to non-Hispanic White individuals. Markers of vascular dysfunction were lower among Black individuals.

The wrist is not the brain: Estimation of sleep by clinical and consumer wearable actigraphy devices is impacted by multiple patient- and device-specific factors.

Clinical actigraphy devices provide adequate estimates of some sleep measures across large groups. In practice, providers are asked to apply clinical or consumer wearable data to individual patient assessments. Inter-individual variability in device performance will impact such patient-specific interpretation. We assessed two devices, clinical and consumer, to determine the magnitude and predictors of this individual-level variability. One hundred and two patients (55 [53.9%] female; 56.4 [±16.3] years old) undergoing polysomnography wore Jawbone UP3 and/or Actiwatch2. Device total sleep time, sleep efficiency, wake after sleep onset and sleep latency were compared with polysomnography. Demographics, sleep architecture and clinical measures were compared to device performance. Actiwatch overestimated total sleep time by 27.2 min (95% confidence limits [CL], 138.3 min over to 84.0 under), overestimated sleep efficiency by 6.8% (95% CL, 34.1% over to 20.5% under), overestimated sleep onset latency by 2.6 min (95% CL, 63.3 over to 58.2 under) and underestimated wake after sleep onset by 50.7 min (95% CL, 162.5 under to 61.2 over). Jawbone overestimated total sleep time by 59.1 min (95% CL, 208.6 min over to 90.5 under) and overestimated sleep efficiency by 14.9% (95% CL, 52.6% over to 22.7% under). In multivariate models, age, sleep onset latency, wake after sleep onset, % N1 and apnea-hypopnea index explained only some of the variance in device performance. Gender also affected performance. Actiwatch and Jawbone mis-estimate sleep measures with very wide confidence limits and accuracy varies with multiple patient-level characteristics. Given these large individual inaccuracies, data from these devices must be applied only with extreme caution in clinical practice.

Hypocretin measurement: shelf age of radioimmunoassay kit, but not freezer time, influences assay variability.

The hypothalamic peptide hypocretin 1 (orexin A) may be assayed in cerebrospinal fluid to diagnose narcolepsy type 1. This testing is not commercially available, and factors contributing to assay variability have not previously been comprehensively explored. In the present study, cerebrospinal fluid hypocretin concentrations were determined in duplicate in 155 patient samples, across a range of sleep disorders. Intra-assay variability of these measures was analyzed. Inter-assay correlation between samples tested at Emory and at Stanford was high (r = 0.79, p < 0.0001). Intra-assay correlation between samples tested in duplicate in our center was also high (r = 0.88, p < 0.0001); intra-assay variability, expressed as the difference between values as a percentage of the higher value, was low at 9.4% (SD = 7.9%). Although both time the sample spent in the freezer (r = 0.16, p = 0.04) and age of the kit used for assay (t = 3.64, p = 0.0004) were significant predictors of intra-kit variability in univariate analyses, only age of kit was significant in multivariate linear regression (F = 4.93, p = 0.03). Age of radioimmunoassay kit affects intra-kit variability of measured hypocretin values, such that kits closer to expiration exhibit significantly more variability.

Clarithromycin in γ-aminobutyric acid-Related hypersomnolence: A randomized, crossover trial.

OBJECTIVE: Some central hypersomnolence syndromes are associated with a positive allosteric modulator of γ-aminobutyric acid (GABA)-A receptors in cerebrospinal fluid. Negative allosteric modulators of GABA-A receptors, including clarithromycin, have been reported to reduce sleepiness in these patients. We sought to systematically assess the effects of clarithromycin on objective vigilance and subjective sleepiness. METHODS: This was a 5-week, randomized, placebo-controlled, double-blind, crossover trial of clarithromycin 500mg with breakfast and lunch, in patients with hypersomnolence syndromes (excluding narcolepsy with cataplexy) and evidence for abnormal cerebrospinal fluid potentiation of GABA-A receptors. The study occurred at a university-affiliated medical center. The primary outcome measure was median reaction time on the psychomotor vigilance task (PVT) at week 2 in each condition. Secondary outcomes included the Epworth Sleepiness Scale, Stanford Sleepiness Scale, Functional Outcomes of Sleep Questionnaire, Pittsburgh Sleep Quality Index, SF-36, and additional PVT measures. RESULTS: Twenty-three patients began treatment. Three patients dropped out, and final analyses were performed on 20 complete cases. Median reaction time was not significantly different between clarithromycin and placebo. Subjective measures of sleepiness were significantly improved on clarithromycin versus placebo. Altered taste perception occurred, but was the only side effect more common on clarithromycin than placebo. No serious adverse events occurred. INTERPRETATION: Subjective sleepiness, but not psychomotor vigilance, improved during a 2-week course of clarithromycin. Although additional studies are needed, this suggests that clarithromycin may be a reasonable treatment option in patients with treatment-refractory hypersomnolence. This trial was registered at ClinicalTrials.gov (NCT01146600) and supported by the American Sleep Medicine Foundation.

Melatonin for Sleep Disorders in Patients with Neurodegenerative Diseases.

In patients with neurodegenerative diseases, sleep disorders are common; they impair the quality of life for patients and caregivers and are associated with poorer clinical outcomes. Melatonin has circadian, hypnotic, and free radical-scavenging effects, and preclinical data suggest benefits of melatonin on neurodegeneration. However, randomized, controlled trials of melatonin in patients with neurodegenerative diseases have not shown strong effects. Trials in Alzheimer's patients demonstrate a lack of benefit on sleep quantity. Subjective measures of sleep quality are mixed, with possible symptomatic improvements seen only on some measures or at some time points. Benefits on cognition have not been observed across several studies. In Parkinson's patients, there may be minimal benefit on objective sleep measures, but a suggestion of subjective benefit in few, small studies. Effective treatments for the sleep disorders associated with neurodegenerative diseases are urgently needed, but current data are insufficient to establish melatonin as such a treatment.

A case of lithium-induced parkinsonism presenting with typical motor symptoms of Parkinson's disease in a bipolar patient.

Lithium is a mood stabilizer rarely associated with drug-induced parkinsonism (DIP). We present a case of an elderly woman with bipolar disorder who developed parkinsonian symptoms after chronic lithium administration despite therapeutic serum levels. Upon evaluation, classic parkinsonian signs of muscle rigidity, tremor, bradykinesia, freezing of gait, and cognitive decline were observed. Initially, she was diagnosed with Parkinson's disease (PD); however, DaTscan SPECT imaging clarified the diagnosis as DIP. As the daily lithium dosage was reduced, the patient's motor symptoms improved. This report emphasizes close monitoring of lithium levels in geriatric populations and the need to consider lithium-induced parkinsonism when PD symptoms appear in chronic lithium users.

Fluctuations in cognition and alertness vary independently in dementia with Lewy bodies.

Fluctuations in mental status are 1 of the core diagnostic criteria for dementia with Lewy bodies (DLB) and are thought to reflect variability in daytime alertness. Previous attempts to study fluctuations have been limited to caregiver reports, observer rating scales, short segments of electroencephalography, or motor-dependent, reaction time tests. Concordance among such measures is often poor, and fluctuations remain difficult to quantify. We compared fluctuations in cognition and alertness in patients with DLB (n = 13) and idiopathic Parkinson's disease (PD) (n = 64), a condition associated with deficits in daytime alertness. We systematically and repeatedly collected cognitive and physiologic measures during a 48-hour inpatient protocol in a sound-attenuated sleep laboratory in a geriatric hospital. Cognitive fluctuations were analyzed using coefficients of variation (COVs) derived from performance on a bedside examination familiar to clinicians (digit span). Alertness fluctuations were assessed objectively using COVs from the polysomnographically-based Maintenance of Wakefulness Test. Despite predictably lower mean digit span performances, DLB patients demonstrated significantly greater cognitive fluctuations than PD patients (P < 0.001), even when groups were matched on general cognitive impairment. There were no group differences in alertness fluctuations, although DLB patients were less alert than PD patients not receiving dopaminergics. The prevailing assumption that fluctuations in cognition in DLB are reflected in fluctuations in daytime alertness was not supported by objective, physiological measurements. Fluctuating mental status in DLB patients can be detected with repeated administration of a simple bedside exam that can be adapted to a clinic setting.

Magnesium citrate monotherapy improves restless legs syndrome symptoms and multiple suggested immobilization test scores in an open-label pilot study.

STUDY OBJECTIVES: An estimated 3% of the population has clinically significant restless legs syndrome. Given the limited pharmacological options in the arsenal, there is a need for a therapeutic agent with a better side effect profile. METHODS: Twelve treatment naive adults (10 women and 2 men with a median age of 41.5 [32-48.5] years) with primary restless legs syndrome were recruited in our open-label pilot study; magnesium citrate 200 mg was administered daily for 8 weeks. Serum magnesium levels, International Restless Legs Syndrome Study Group Rating Scale, Kohnen quality of life scale, and multiple suggested immobilization tests (three 1-hour tests) were performed before and after supplementation. Paired t tests and Wilcoxon signed-rank tests were used for data analysis. Pearson and Spearman's analyses assessed the association between magnesium levels and restless legs syndrome variables. RESULTS: Participants had a significant reduction in International Restless Legs Syndrome Study Group Rating Scale scores (6.67 [2.33-11] P = .006) and improved Kohnen quality of life scores (8.5 [2.09-14], P = .014) without notable differences in serum magnesium levels (P = .3). The median periodic limb movements during wakefulness index (30.40 [5.20, 122.40] to 8.63 [0.32, 17.47] P = .043) and self-reported discomfort score (19 [14, 30.5] to 6 [0, 8] P = .0010) of all 3 multiple suggested immobilization test trials also demonstrated improvement. Serum magnesium levels negatively correlated with multiple suggested immobilization test self-reported scores and the periodic limb movements during wakefulness indices. CONCLUSIONS: Despite the limitations of open-label design, our study's positive results indicate the need for a placebo-controlled trial with a larger sample size. CLINICAL TRIAL REGISTRATION: Registry: ClinicalTrials.gov; Name: The Effect of Magnesium Citrate Supplementation in Restless Legs Syndrome (RLS); URL: https://clinicaltrials.gov/ct2/show/study/NCT04462796; Identifier: NCT04462796. CITATION: Gorantla S, Ravisankar A, Trotti LM. Magnesium citrate monotherapy improves restless legs syndrome symptoms and multiple suggested immobilization test scores in an open-label pilot study. J Clin Sleep Med. 2024;20(8):1357-1361.

Sleep and sleep disorders in people with Parkinson's disease.

Sleep disorders are common in people with Parkinson's disease. These disorders, which increase in frequency throughout the course of the neurodegenerative disease and impair quality of life, include insomnia, excessive daytime sleepiness, circadian disorders, obstructive sleep apnoea, restless legs syndrome, and rapid eye movement (REM) sleep behaviour disorder. The causes of these sleep disorders are complex and multifactorial, including the degeneration of the neural structures that modulate sleep, the detrimental effect of some medications on sleep, the parkinsonian symptoms that interfere with mobility and comfort in bed, and comorbidities that disrupt sleep quality and quantity. The clinical evaluation of sleep disorders include both subjective (eg, questionnaires or diaries) and objective (eg, actigraphy or video polysomnography) assessments. The management of patients with Parkinson's disease and a sleep disorder is challenging and should be individualised. Treatment can include education aiming at changes in behaviour (ie, sleep hygiene), cognitive behavioural therapy, continuous dopaminergic stimulation at night, and specific medications. REM sleep behaviour disorder can occur several years before the onset of parkinsonism, suggesting that the implementation of trials of neuroprotective therapies should focus on people with this sleep disorder.

Validation and performance of the sleep inertia questionnaire in central disorders of hypersomnolence.

BACKGROUND: Optimal measurement tools for problematic sleep inertia, common in some central disorders of hypersomnolence (CDH), have not yet been determined. We evaluated the performance of the Sleep Inertia Questionnaire (SIQ) in CDH, and how well it distinguished hypersomnolent groups from controls, and IH (idiopathic hypersomnia) from narcolepsy type 1 (NT1). METHODS: This prospective, bi-centric study included 63 control, 84 IH, 16 NT1, 18 narcolepsy type 2 (NT2), and 88 subjective excessive daytime sleepiness (sEDS) participants, using ICSD-3 criteria. 126 (47.2 %) participants were on any medication at the time of SIQ completion. We assessed construct validity of SIQ scores, and sleep inertia duration (SID), and compared them across diagnoses, controlling for age and center. We derived cutpoints to distinguish hypersomnolent patients from controls and IH from NT1. Sensitivity analyses for depression, chronotype, and medication were performed. RESULTS: The SIQ sum and composite score were significantly lower in controls than in other groups (p < 0.0001), demonstrating outstanding ability to distinguish patients from controls (AUCs 0.92), without differences among hypersomnolent groups. SID (AUC 0.76) was significantly shorter in controls than in all hypersomnolent groups except NT1, and was shorter in NT1 than in IH or sEDS. Optimal SIQ sum cutpoint was 42 (J = 0.71) for patients versus controls. Optimal SID cutpoint in distinguishing IH from NT1 was 25 min (J = 0.39). CONCLUSION: The SIQ has excellent ability to distinguish hypersomnolent patients from healthy controls, after controlling for depression, eveningness, and medication. SID is best at distinguishing IH from NT1.

Restless legs syndrome, periodic limb movements of sleep, and subclinical cardiovascular disease.

Restless legs syndrome (RLS) and periodic limb movements of sleep (PLMS) have been variably implicated in risk for cardiovascular disease (CVD), but there is lack of consensus on these relationships. We sought to assess subclinical CVD measures and RLS/PLMS in a large cohort to further evaluate these associations. The Emory Center for Health Discovery and Well Being cohort is composed of employed adults, with subclinical CVD measures including endothelial function (flow-mediated vasodilation), microvascular function (reactive hyperemia index, RHI), arterial stiffness (pulse wave velocity and augmentation index), and carotid intima-media thickness (cIMT). Participants were grouped based on presence (N = 50) or absence (N = 376) of RLS and subclinical CVD measures compared between groups. A subset of participants (n = 40) underwent ambulatory monitoring for PLMS and obstructive sleep apnea. PLMS association with subclinical CVD measures was assessed. RLS status was significantly associated with flow-mediated dilation in univariate analyses but not after controlling for potential confounders; RLS was not associated with other subclinical CVD measures. PLMS were significantly correlated with the RHI, augmentation index, and cIMT in univariate analyses; only the association between PLMS and cIMT remained significant (p = 0.04) after controlling for RLS status, age, apnea-hypopnea index, hyperlipidemia, and hypertension. The observed association between higher PLMS and greater cIMT suggests that PLMS may be a marker of subclinical CVD. Further work is needed to determine the relationship between PLMS and CVD risk. Supplementary Information: The online version contains supplementary material available at 10.1007/s41105-023-00497-7.

Permanent standard time is the optimal choice for health and safety: an American Academy of Sleep Medicine position statement.

The period of the year from spring to fall, when clocks in most parts of the United States are set one hour ahead of standard time, is called daylight saving time, and its beginning and ending dates and times are set by federal law. The human biological clock is regulated by the timing of light and darkness, which then dictates sleep and wake rhythms. In daily life, the timing of exposure to light is generally linked to the social clock. When the solar clock is misaligned with the social clock, desynchronization occurs between the internal circadian rhythm and the social clock. The yearly change between standard time and daylight saving time introduces this misalignment, which has been associated with risks to physical and mental health and safety, as well as risks to public health. In 2020, the American Academy of Sleep Medicine (AASM) published a position statement advocating for the elimination of seasonal time changes, suggesting that evidence best supports the adoption of year-round standard time. This updated statement cites new evidence and support for permanent standard time. It is the position of the AASM that the United States should eliminate seasonal time changes in favor of permanent standard time, which aligns best with human circadian biology. Evidence supports the distinct benefits of standard time for health and safety, while also underscoring the potential harms that result from seasonal time changes to and from daylight saving time. CITATION: Rishi MA, Cheng JY, Strang AR, et al. Permanent standard time is the optimal choice for health and safety: an American Academy of Sleep Medicine position statement. J Clin Sleep Med. 2024;20(1):121-125.

Nocturia and overnight polysomnography in Parkinson disease.

AIM: Characterize clinical factors related to nocturia and sleep disruption in Parkinson disease (PD) using polysomnography (PSG). METHODS: Sixty-three PD patients were recruited regardless of sleep or voiding complaints from a university-based movement disorders clinic for a 48 hr inpatient PSG protocol. Nocturia frequency and bother related to urinary symptoms were assessed using the International Prostate Symptom Score (IPSS) and were corroborated by measurements of PSG-defined sleep made immediately preceding and subsequent to each in-lab voiding episode. PSG measures included whole-night total sleep time (TST), sleep efficiency (SE), apnea/hypopnea index (AHI), and time to PSG-defined sleep following nocturia episodes. Differences between groups were assessed using Mantel-Haenszel chi-square, t-tests, or Wilcoxon signed rank tests. Linear regression was used to assess factors associated with reported nocturia frequency. RESULTS: Sixty patients completed the IPSS. Thirty-seven (61%) reported at least two nocturia episodes nightly; those individuals demonstrated lower PSG-defined SE (P = 0.01) and TST (P = 0.02) than patients with 0-1 episodes. Participants reporting 2-3 episodes of nocturia with high bother on the IPSS (n = 12) demonstrated lower whole-night TST (280.5 ± 116.1 min vs. 372.5 ± 58.7 min, P = 0.03) and worse SE (59.2 ± 22.7% vs. 75.9 ± 11.2%, P = 0.04) when compared to participants with 2-3 episodes of nocturia with low bother (n = 13). CONCLUSIONS: These results verify objectively that PD patients with nocturia have poor sleep. Furthermore, among individuals with comparable levels of reported nocturia, higher bother is associated with poorer sleep as defined on PSG. Neurourol. Urodynam. Published 2013. This article is a U.S. Government work and is in the public domain in the USA.

Nocturnal sleep enhances working memory training in Parkinson's disease but not Lewy body dementia.

Working memory is essential to higher order cognition (e.g. fluid intelligence) and to performance of daily activities. Though working memory capacity was traditionally thought to be inflexible, recent studies report that working memory capacity can be trained and that offline processes occurring during sleep may facilitate improvements in working memory performance. We utilized a 48-h in-laboratory protocol consisting of repeated digit span forward (short-term attention measure) and digit span backward (working memory measure) tests and overnight polysomnography to investigate the specific sleep-dependent processes that may facilitate working memory performance improvements in the synucleinopathies. We found that digit span backward performance improved following a nocturnal sleep interval in patients with Parkinson's disease on dopaminergic medication, but not in those not taking dopaminergic medication and not in patients with dementia with Lewy bodies. Furthermore, the improvements in patients with Parkinson's disease on dopaminergic medication were positively correlated with the amount of slow-wave sleep that patients obtained between training sessions and negatively correlated with severity of nocturnal oxygen desaturation. The translational implication is that working memory capacity is potentially modifiable in patients with Parkinson's disease but that sleep disturbances may first need to be corrected.

A prospective photographic study of the ocular fundus in obstructive sleep apnea.

BACKGROUND: The prevalence of optic nerve and retinal vascular changes within the obstructive sleep apnea (OSA) population are not well-known, although it has been postulated that optic nerve ischemic changes and findings related to an elevated intracranial pressure may be more common in OSA patients. We prospectively evaluated the ocular fundus in unselected patients undergoing overnight diagnostic polysomnography (PSG). METHODS: Demographic data, medical/ocular history, and nonmydriatic fundus photographs were prospectively collected in patients undergoing PSG at our institution and reviewed for the presence of optic disc edema for which our study was appropriately powered a priori. Retinal vascular changes were also evaluated. OSA was defined using the measures of both sleep-disordered breathing and hypoxia. RESULTS: Of 250 patients evaluated in the sleep center, fundus photographs were performed on 215 patients, among whom 127 patients (59%) had an apnea/hypopnea index (AHI) ≥ 15 events per hour, including 36 with severe OSA. Those with AHI <15 served as the comparison group. None of the patients had optic disc edema (95% confidence interval [CI]: 0%-3%). There was no difference in rates of glaucomatous appearance or pallor of the optic disc among the groups. Retinal arteriolar changes were more common in severe OSA patients (odds ratio: 1.09 per 5 unit increase in AHI; 95% CI, 1.02-1.16; P = 0.01), even after controlling for mean arterial blood pressure. CONCLUSIONS: We did not find an increased prevalence of optic disc edema or other optic neuropathies in our OSA population. However, retinal vascular changes were more common in patients with severe OSA, independent of blood pressure.

Novel Objective Measures of Hypersomnolence.

Purpose of review: To provide a brief overview of current objective measures of hypersomnolence, discuss proposed measure modifications, and review emerging measures. Recent findings: There is potential to optimize current tools using novel metrics. High-density and quantitative EEG-based measures may provide discriminative informative. Cognitive testing may quantify cognitive dysfunction common to hypersomnia disorders, particularly in attention, and objectively measure pathologic sleep inertia. Structural and functional neuroimaging studies in narcolepsy type 1 have shown considerable variability but so far implicate both hypothalamic and extra-hypothalamic regions; fewer studies of other CDH have been performed. There is recent renewed interest in pupillometry as a measure of alertness in the evaluation of hypersomnolence. Summary: No single test captures the full spectrum of disorders and use of multiple measures will likely improve diagnostic precision. Research is needed to identify novel measures and disease-specific biomarkers, and to define combinations of measures optimal for CDH diagnosis.

Commonly Used Therapeutics Associated with Changes in Arousal Inhibit GABAAR Activation.

GABAA receptor-positive modulators are well-known to induce sedation, sleep, and general anesthesia. Conversely, GABAA receptor negative allosteric modulators (GABAARNAMs) can increase arousal and induce seizures. Motivated by our studies with patients with hypersomnia, and our discovery that two GABAARNAMs can restore the Excitation/Inhibition (E/I) balance in vitro and arousal in vivo, we chose to screen 11 compounds that have been reported to modulate arousal, to see if they shared a GABA-related mechanism. We determined modulation with both conventional and microfluidic patch clamp methods. We found that receptor activation was variably modulated by all 11 compounds: Rifampicin (RIF), Metronidazole (MET), Minocycline (MIN), Erythromycin (ERY), Ofloxacin (OFX), Chloroquine (CQ), Hydroxychloroquine sulfate (HCQ), Flumazenil (FLZ), Pentylenetetrazol (PTZ), (-)-Epigallocatechin Gallate (EGCG), and clarithromycin (CLR). The computational modeling of modulator-receptor interactions predicted drug action at canonical binding sites and novel orphan sites on the receptor. Our findings suggest that multiple avenues of investigation are now open to investigate large and brain-penetrant molecules for the treatment of patients with diminished CNS E/I balance.

At-home wireless sleep monitoring patches for the clinical assessment of sleep quality and sleep apnea.

Although many people suffer from sleep disorders, most are undiagnosed, leading to impairments in health. The existing polysomnography method is not easily accessible; it's costly, burdensome to patients, and requires specialized facilities and personnel. Here, we report an at-home portable system that includes wireless sleep sensors and wearable electronics with embedded machine learning. We also show its application for assessing sleep quality and detecting sleep apnea with multiple patients. Unlike the conventional system using numerous bulky sensors, the soft, all-integrated wearable platform offers natural sleep wherever the user prefers. In a clinical study, the face-mounted patches that detect brain, eye, and muscle signals show comparable performance with polysomnography. When comparing healthy controls to sleep apnea patients, the wearable system can detect obstructive sleep apnea with an accuracy of 88.5%. Furthermore, deep learning offers automated sleep scoring, demonstrating portability, and point-of-care usability. At-home wearable electronics could ensure a promising future supporting portable sleep monitoring and home healthcare.