ABSTRACT Typical content themes in dreams still defy clear explanation. While a series of studies administering typical dream theme questionnaires mainly to college students point to a surprising consistency in the prevalence of such themes over gender, age, culture, and time, it is still unclear how generalizable such findings are to the larger population. We used a validated online questionnaire, the Typical Dreams Questionnaire (TDQ), to assess the responses of 30,686 individuals who varied in age (10–85 years), gender, and student status. Results replicated several findings from an earlier study with a much smaller sample size. This included strong evidence that the number of typical themes reported decreases with age, that the prevalence of some themes differs between males and females, and that the questionnaire items tend to group into a smaller number of factors similar to those found in the previous study. Overall evidence of strong rank‐order correlations between different groups (males/females; students/non‐students) for such a large sample suggests that this version of the TDQ is highly generalizable to the larger population.
Study Objectives Excessive cerebral iron deposition has been implicated in cognitive dysfunction across several neurological disorders. We evaluated severity-dependent patterns of cerebral iron accumulation in obstructive sleep apnea (OSA) using quantitative susceptibility mapping (QSM) and assessed their potential role in mediating cognitive impairment. Methods The cohort comprised 139 OSA patients, stratified by severity (68 mild-moderate [OSA-M: apnea-hypopnea index (AHI) 5-30 events/hour] and 71 severe [OSA-S: AHI > 30 events/hour]), and 48 healthy controls. All underwent polysomnography, Montreal Cognitive Assessment, and 3 T MRI with multi-echo gradient echo sequences for QSM analysis. Whole-brain voxel-wise comparisons characterized iron deposition patterns. Correlation analysis and mediation models evaluated associations between OSA severity, regional iron content, and cognition. Results With increasing OSA severity, iron content increased in the bilateral precentral gyri, bilateral medial superior frontal gyri, right putamen and middle cingulate gyrus. Notably, higher QSM values in the left precentral gyrus and right putamen were negatively correlated with cognitive impairment, particularly visuospatial function (p < .05). Mediation analysis demonstrated iron deposition in the right putamen partially mediated associations between AHI, N3 sleep stage proportion, percentage of total sleep time with oxygen saturation < 90%, and cognitive function, particularly visuospatial and executive abilities. Conclusion Cerebral iron overload may contribute to cognitive dysfunction across OSA severity levels. The partial mediating effect of putaminal iron supports chronic intermittent hypoxia-induced iron dysregulation as a potential neuropathological mechanism. These findings, predominantly from a male cohort, identify cerebral iron deposition as a potential therapeutic target for mitigating cognitive decline in OSA.
Chronic intermittent hypoxia (CIH), a defining feature of obstructive sleep apnea, is strongly associated with cognitive impairment and increased risk of neurodegenerative disease, yet the underlying mechanisms linking hypoxic stress to disrupted brain homeostasis remain poorly defined. Impaired glymphatic clearance has been reported in patients with obstructive sleep apnea, but whether and how intermittent hypoxia directly alters glymphatic function is unknown. Here, we investigated the effects of acute and chronic intermittent hypoxia on cerebrospinal fluid-interstitial fluid exchange in male mice and examined the molecular mechanisms governing these effects. Using tracer-based influx and efflux assays, in vivo two-photon imaging, behavioral testing, and genetic and pharmacological manipulation, we show that intermittent hypoxia exerts a duration-dependent, biphasic effect on glymphatic function. Acute exposure transiently enhanced glymphatic influx and efflux, whereas prolonged CIH progressively impaired glymphatic transport, disrupted perivascular aquaporin-4 (AQP4) polarization, reduced vascular pulsatility, and impaired spatial working memory. CIH was associated with reduced extracellular adenosine levels, suppression of cerebral energy metabolism, and altered expression of equilibrative nucleoside transporters (ENTs). Genetic ablation of AQP4 abolished CIH-induced glymphatic impairment, confirming its essential role in hypoxia-induced glymphatic dysfunction. Importantly, pharmacological inhibition or genetic deletion of ENT1 and deletion of ENT2 restored adenosine availability, normalized AQP4 polarization and vascular dynamics, and rescued glymphatic dysfunction and cognitive deficits under CIH. These findings identify ENT-dependent dysregulation of adenosine signaling as a key mechanism by which chronic intermittent hypoxia compromises glymphatic clearance, providing mechanistic insight into how sleep-disordered breathing disrupts brain waste removal and cognitive function.
ABSTRACT Are sleep duration and sleep intensity manifestations of the same phenotype, or are they distinct, complementary traits? We addressed this question by removing two major constraints on phenotype expression: limited sleep opportunity and prior sleep deficit. Across 105 baseline 8‐h nights and 420 extended 14‐h nights in 15 individuals, sleep duration and NREM intensity behaved as two largely independent traits. Baseline expression of each parameter predicted its own subsequent expression during chronic sleep abundance but failed to predict the companion trait either within or between conditions. We then evaluated external evidence from chronic 4‐ and 6‐h sleep restriction alongside extreme natural sleep‐duration phenotypes, interpreting these findings through the wave model of sleep dynamics. In this framework, sleep duration reflects the geometry of sleep‐cycle oscillations, determined primarily by the width of the sleep‐state stability landscape (formally represented as a Morse potential well). Conversely, NREM intensity reflects oscillation amplitude, providing a visible signature of deviation from homeostatic equilibrium. While acute perturbation alters amplitude, chronic perturbation induces adaptive changes in landscape width, preserving a characteristic deviation from equilibrium despite severe shifts in underlying state instability and allostatic strain.
