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Abstract Introduction The ability to remember the face and name of a person we have recently met is a critical skill often impacted by cognitive impairment and Alzheimer’s disease. We used a forced desynchrony protocol to explore whether recall of recently-learned face-name pairs is affected by time awake and/or circadian phase in healthy adults. Methods 13 healthy, cognitively normal adults (20-70yrs; 7F) participated in a 39-day inpatient protocol with 3 baseline days (10h time-in-bed/24h) and a 3-week forced desynchrony (FD) segment, where they lived on a 28-h day with sleep restriction (6.5h time-in-bed/28h, equivalent to 5.6h/24h). Core body temperature was collected throughout to estimate circadian period and phase. The face-name test was administered every 4h, beginning 3h after wake. Each test included a learning session with 6 novel face-name pairs. Recall was tested 2h later, when each face was presented twice in random order, once with a correct and once with an incorrect name. Participants were asked to respond whether each face-name pair was correct. Data were averaged across 4-h circadian phase or time awake bins and normalized as a percentage of each participant’s baseline performance. Results Face-name recall varied by time awake (p<0.05), with performance deteriorating ~12% over the course of 12h of wakefulness. Face-name recall also varied by circadian phase (p<0.05), with a ~10% difference in recall performance from the peak at circadian phase 240° (corresponding to the early biological evening) to the nadir at circadian phase 60° (corresponding to the early biological morning). Conclusion Both duration of prior wake and biological time of day impact the ability to correctly recall face-name pairs. Under normal entrained conditions, opposing circadian- and wake- dependent effects on memory for face-name associations may interact to produce stable performance across the day. Support Study supported by P01 AG009975 and conducted at Brigham and Women’s Hospital Center for Clinical Investigation, part of Harvard Clinical and Translational Science Center supported by UL1 TR001102. Authors supported by T32HL007901 and F32HL143893 (RKY); fellowships from the Novartis Foundation, the W.&T. La-Roche Foundation, and Jazz Pharmaceuticals (MYM); a fellowship from the Natural Sciences and Engineering Research Council of Canada (SWC).

\"Bellen Woodard adores ballet and always looks forward to reaching new heights. Though as she moves through dance, she begins to notice that pink leotards, pink shoes, and pink or white tights--often referred to as ballet pink--are synonymous with ballet. But what about brown tights and shoes? When her dance studio doesn't act, Bellen takes matters into her own hands and creates a way for all of us to see the 'many beautiful colors of dance'--and she names it ballet brown\"-- Provided by publisher.

Abstract Introduction Social jet lag is associated with contemporary lifestyle with harmful impacts on health, predisposing individuals to obesity, diabetes, cardiovascular diseases and cognitive impairment. Knowing that this condition is influenced by chronotype and that these are reflected in rhythmicity markers, a better understating of mechanisms and factors related to this condition are helpful to raise awareness to the society, to prevent and treat its consequences. Our goal was to evaluate if chronotype has a moderating effect on social jet lag, investigate if activity-rest rhythm could be affected by social jet lag and whether it could be related to nighttime light exposure. Methods 13 subjects (10 women) aged between 23 and 59 years answered Morningness-Eveningness Questionnaire and record activity and rest rhythm by actimetry. Results We observed that chronotype is a predictor of social jet lag (p < 0.05) and eveningness leads to greater social jet lag. Sleep duration and time of sleep offset were higher on free days (p < 0.05) and, as expected, higher activity at night was related to greater social jet lag (p < 0.05). We did not find relation between level and time of exposure to light at night and social jet lag (p ≥ 0.05). None of these differences were chronotype-dependent. Conclusion Our work was one of the first that addressed the relationship between social jet lag and a rhythmicity marker, the activity-rest rhythm. We also demonstrated the importance of a better understanding of the evening types, that are more affected by social obligations. Support Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES), Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) e Associação Fundo de Incentivo à Pesquisa (AFIP).

Jet-lag symptoms arise from temporal misalignment between the internal circadian clock and external solar time. We found that circadian rhythms of behavior (locomotor activity), clock gene expression, and body temperature immediately reentrained to phase-shifted light-dark cycles in mice lacking vasopressin receptors V1a and V1b (V1a⁻ / ⁻ V1b⁻ / ⁻). Nevertheless, the behavior of V1a⁻ / ⁻ V1b⁻ / ⁻ mice was still coupled to the internal clock, which oscillated normally under standard conditions. Experiments with suprachiasmatic nucleus (SCN) slices in culture suggested that interneuronal communication mediated by V1a and V1b confers on the SCN an intrinsic resistance to external perturbation. Pharmacological blockade of V1a and V1b in the SCN of wild-type mice resulted in accelerated recovery from jet lag, which highlights the potential of vasopressin signaling as a therapeutic target for management of circadian rhythm misalignment, such as jet lag and shift work.

Distributed lag non-linear models (DLNMs) are a modelling tool for describing potentially non-linear and delayed dependencies. Here, we illustrate an extension of the DLNM framework through the use of penalized splines within generalized additive models (GAM). This extension offers built-in model selection procedures and the possibility of accommodating assumptions on the shape of the lag structure through specific penalties. In addition, this framework includes, as special cases, simpler models previously proposed for linear relationships (DLMs). Alternative versions of penalized DLNMs are compared with each other and with the standard unpenalized version in a simulation study. Results show that this penalized extension to the DLNM class provides greater flexibility and improved inferential properties. The framework exploits recent theoretical developments of GAMs and is implemented using efficient routines within freely available software. Real-data applications are illustrated through two reproducible examples in time series and survival analysis.

Jet lag encompasses a range of psycho- and physiopathological symptoms that arise from temporal misalignment of the endogenous circadian clock with external time. Repeated jet lag exposure, encountered by business travelers and airline personnel as well as shift workers, has been correlated with immune deficiency, mood disorders, elevated cancer risk, and anatomical anomalies of the forebrain. Here, we have characterized the molecular response of the mouse circadian system in an established experimental paradigm for jet lag whereby mice entrained to a 12-hour light/12-hour dark cycle undergo light phase advancement by 6 hours. Unexpectedly, strong heterogeneity of entrainment kinetics was found not only between different organs, but also within the molecular clockwork of each tissue. Manipulation of the adrenal circadian clock, in particular phase-shifting of adrenal glucocorticoid rhythms, regulated the speed of behavioral reentrainment. Blocking adrenal corticosterone either prolonged or shortened jet lag, depending on the time of administration. This key role of adrenal glucocorticoid phasing for resetting of the circadian system provides what we believe to be a novel mechanism-based approach for possible therapies for jet lag and jet lag-associated diseases.

Social jetlag, the misalignment between internal circadian rhythms and socially imposed schedules, is increasingly recognized as a risk factor for metabolic disorders such as obesity, type 2 diabetes (T2D), and cardiovascular disease. Recent evidence implicates the gut microbiota as a key mediator in this relationship, operating through a microbiota–gut–metabolic axis that influences host metabolism, immune function, and circadian regulation. Mechanistic studies reveal that social jetlag disrupts microbial rhythmicity, reduces short-chain fatty acid (SCFA) production, impairs intestinal barrier function, and promotes systemic inflammation, which contribute to insulin resistance and metabolic dysfunction. Clinical and preclinical interventions, including time-restricted feeding (TRF)/time-restricted eating (TRE), probiotics or melatonin supplementation, and fecal microbiota transplantation (FMT), demonstrate the potential to restore microbial and metabolic homeostasis by realigning host and microbial rhythms. This review synthesizes mechanistic insights with emerging human and clinical evidence, highlighting the gut microbiota as a novel target for chronotherapeutic strategies aimed at mitigating the metabolic consequences of circadian disruption. Recognizing and treating circadian–microbiome misalignment may provide a clinically actionable pathway to prevent or reverse chronic metabolic diseases in modern populations.

Flavonoids are natural polyphenols that are widely found in plants. The effects of flavonoids on obesity and numerous diseases such as cancer, diabetes, and Alzheimer's have been well studied. However, little is known about the relationships between flavonoids and the circadian clock. In this study, we show that continuous or transient application of flavonoids to the culture medium of embryonic fibroblasts from PER2::LUCIFERASE (PER2::LUC) mice induced various modifications in the circadian clock amplitude, period, and phase. Transient application of some of the tested flavonoids to cultured cells induced a phase delay of the PER2::LUC rhythm at the down slope phase. In addition, continuous application of the polymethoxy flavonoids nobiletin and tangeretin increased the amplitude and lengthened the period of the PER2::LUC rhythm. The nobiletin-induced phase delay was blocked by co-treatment with U0126, an ERK inhibitor. In summary, among the tested flavonoids, polymethoxy flavones increased the amplitude, lengthened the period, and delayed the phase of the PER2::LUC circadian rhythm. Therefore, foods that contain polymethoxy flavones may have beneficial effects on circadian rhythm disorders and jet lag.

Detection of internal body time (BT) via a few-time-point assay has been a longstanding challenge in medicine, because BT information can be exploited to maximize potency and minimize toxicity during drug administration and thus will enable highly optimized medication. To address this challenge, we previously developed the concept, \"molecular-timetable method,\" which was originally inspired by Linné's flower clock. In Linné's flower clock, one can estimate the time of the day by watching the opening and closing pattern of various flowers. Similarly, in the molecular-timetable method, one can measure the BT of the day by profiling the up and down patterns of substances in the molecular timetable. To make this method clinically feasible, we now performed blood metabolome analysis and here report the successful quantification of hundreds of clock-controlled metabolites in mouse plasma. Based on circadian blood metabolomics, we can detect individual BT under various conditions, demonstrating its robustness against genetic background, sex, age, and feeding differences. The power of this method is also demonstrated by the sensitive and accurate detection of circadian rhythm disorder in jet-lagged mice. These results suggest the potential for metabolomics-based detection of BT (\"metabolite-timetable method\"), which will lead to the realization of chronotherapy and personalized medicine.