Circadian clocks are internal molecular time-keeping mechanisms that enable organisms to adjust their behavior and physiology to the 24-h environment. In addition to the circadian system, the stress system effectively restores the internal dynamic equilibrium of living organisms, called homeostasis, in light of any threatening stimulus (i.e., stressor). Any dysregulation in either system or disturbance of their molecular interrelation might lead to severe health effects. Importantly, both systems communicate with and feedback on each other at various physiological and neuronal levels. Thus, any disturbance or uncoupling possibly contributes to the development of several somatic and affective disorders. In this chapter, we discuss the biological function of the circadian and the stress system, their interactions, and the clinical implications of their uncoupling or dysregulation. For the sake of clarity and focus, we will only address the mammalian central circadian clock in the brain.


All inhabitants of our planet are exposed to recurrent environmental changes generated by the rotation of the earth in the solar system. In order to anticipate these predictable fluctuations, organisms have evolved an evolutionary conserved internal time-keeping system, i.e., the circadian clock. In mammals, the circadian system is organized in a hierarchical fashion: a central pacemaker is located in the bilateral suprachiasmatic nucleus (SCN) of the hypothalamus, whereas subsidiary peripheral clocks exist in virtually all tissues and organs (see Fig. 38.1) (for review see Ref. 7). Importantly, most species are also exposed to unpredictable changes in the environment, such as decreased food resources, increased predator numbers, or sudden changes in social states. To adapt to these sudden alterations, the acute activation of the stress response system comprising the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic nervous system (SNS) represents a fundamental survival mechanism. In contrast, chronic activation of the stress system might result in severe somatic and affective disorders (for review see Ref. 5). At first glance, the circadian and the stress system seem to represent two separate bodily control systems that are involved in adaptation to predictable and unpredictable stimuli, respectively. However, both systems are fundamental for survival and, thus, communicate with each other at various physiological and neuronal levels.

The central molecular clock

The mammalian SCN is formed by a heterogeneous bilateral network of 10,000–50,000 single neurons14 and serves as a master pacemaker in the control of a wide array of behavioral and physiological rhythms (e.g., sleep-wake, locomotion, cardiovascular function, endocrine processes) (see Box 38.1 and Fig. 38.1) (for review see Ref. 7). According to peptide expression, projection patterns, and neuronal morphology, each unilateral SCN can be divided into two subregions: a dorsomedial shell and a ventrolateral core region. Shell neurons produce primarily arginine-vasopressin (AVP) and are mainly innervated by limbic areas, the hypothalamus, and the core region. In contrast, vasoactive intestinal peptide (VIP) is mainly synthesized in the core region that receives most of the input from the retina and brain regions that receive photic input.32

Gabriella Lundkvist - Figure of oscillator network
Organization of the mammalian circadian system. The circadian system consists of three major components: the inputs (socalled Zeitgebers), the rhythm generator in the oscillator network, and the outputs. Furthermore, it is organized in a hierarchical fashion with the bilateral suprachiasmatic nucleus (SCN) being the master pacemaker and subsidiary peripheral clocks functioning as slave clocks. The SCN is synchronized by the external 24 h cycle or other nonphotic Zeitgebers and produces sustained and synchronous cellular rhythmicity to coordinate rhythms in both central and peripheral tissues. This, in turn, results in rhythmic behavioral and physiological outputs, such as the sleep-wake cycle. The multioscillator network is synchronized through several lines of communication. While light is the primary input for the SCN (via the RHT), peripheral oscillators are synchronized by timing cues from the SCN and in some cases other timing cues such as food availability. AVP, arginine-vasopressin; CNS, central nervous system; RHT, retinohypothalamic tract; VIP, vasoactive intestinal peptide.


A series of electrical lesion studies in rodents in the 1970s provided clear evidence that the SCN possesses a primary role in the generation of mammalian circadian rhythms. Following selective disruption of the master SCN clock, locomotor activity, drinking behavior, body temperature, and GC secretion was completely absent.31,44 Despite the lack of neuronal connections between the grafted SCN and the host brain, transplantation of donor SCN tissue into hosts with lesioned SCN remarkably restored these rhythms, suggesting that a diffusible secreted factor might be responsible for transmitting the circadian signal from the SCN.40 However, while circadian rhythms of locomotor activity, drinking behavior, and body temperature could be restored by SCN transplants, circadian GC secretion was not, implicating that, in addition to secreted factors, neuronal efferents are required for generation of certain circadian rhythms.30


The Molecular Clockwork

In order to adjust to the environmental changes, cellular rhythms of roughly 24 h are generated in every single cell by transcriptional–translational autoregulatory loops that drive recurrent molecular oscillations in mRNA and protein levels of the so-called clock genes (see Fig. 38.2). In the SCN, the single neuronal oscillators are coupled to each other by paracrine and synaptic interaction to produce a coherent rhythmic output and to prevent the single oscillators from desynchronizing. In this way, the clock machinery, which also includes ion fluxes such as calcium, electrical activity, and cAMP, drives the biological activities in the body, such as daily hormonal fluctuations, the sleep-wake cycle, and the immune system activity (for review see Ref. 15). The transcription factors circadian locomotor output cycles kaput (CLOCK) and brain and muscle aryl hydrocarbon receptor nuclear translocator-like protein 1 (BMAL1) constitute the positive limb of the feedback loop. Independent of an organism’s activity phase, the CLOCK:BMAL1 heterodimer binds, via PAS domains, to the E-box promoter elements of clock genes and clockcontrolled genes at the beginning of a circadian day, thus activating their transcription. The clock genes Period (Per; isoforms Per1 and Per2) and Cryptochrome (Cry; isoforms Cry1 and Cry2), in turn, constitute the negative limb: their mRNA is translated into proteins in the cytoplasm of the cell over the course of the day. Upon reaching a certain threshold, the protein products form heterodimers and homodimers that feedback to the nucleus by binding to the CLOCK:BMAL1 protein complex to autorepress the expression of their own genes at the beginning of the circadian night. Thereafter, constitutive degradation decreases the PER and CRY protein levels and as soon as these levels fall below a defined threshold required for sufficient autorepression, a new transcriptional cycle can be initiated. Several posttranslational modifications like histone acetylation, phosphorylation, ubiquitination, and methylation seem to be required for the delay between transcriptional activation and repression which is essential for a precise and functional circadian rhythm. In addition to this central molecular loop, multiple accessory regulatory loops contribute to a proper clock function. One of those loops is composed of nuclear receptors from the reverse erythroblastosis virus (REV-ERB) and retinoic acid receptor-related orphan receptor (ROR), families that are transcriptionally regulated by the positive limb and, in turn, activate (ROR) or repress (REV-ERB) transcription of Bmal1. The PER2 protein fine-tunes this process by interacting with REVERB to synchronize the negative and positive limbs of the transcriptional–translational feedback loops. In general, all these clock-related transcription factors impact a broad spectrum of physiological functions like sleepwake behavior, thermoregulation, or nutrition by regulating the transcription rate of several clock-responsive genes (for review see Ref. 37). The internal clock machinery works autonomously and relatively precisely in each cell. However, in order to stay tuned to geophysical time the internal “clock time” needs to be adjusted and reset daily by environmental signals, a process called entrainment. Changes in illumination (occur for instance at dawn and dusk) and ambient temperature are the most important environmental synchronizers, the so-called Zeitgebers. In addition, nutrition, social factors, or even stress are further entrainment factors and might dominate the solar cycle in certain situations (for review see Ref. 7).
Gabriella Lundkvist - figure degradation
A simplified view of the molecular circadian clock. The mammalian clock relies on two interlocked transcriptional and translational feedback loops. The positive limb is formed by the transcription factors CLOCK and BMAL1 that bind to E-box sequences in the promoters of clock genes like Per, Cry, and Rev-Erb, thus activating their transcription at the beginning of a circadian day. As a result, PER proteins accumulate in the cytoplasm and become phosphorylated by kinases like casein kinases ε and δ and glycogen synthase kinase 3β. The phosphorylated forms of PER proteins are unstable and are degraded. Late in the subjective day, CRY accumulates in the cytoplasm and promotes the formation of stable CKI/PER/CRY complexes that enter the nucleus at the beginning of a circadian night and repress CLOCK:BMAL1- mediated transcription. To initiate a new circadian cycle, PER and CRY proteins get degraded and the CLOCK:BMAL1-mediated transcription starts again. The interacting positive and negative feedback loops of circadian genes warrant low levels of PER and CRY and, concomitantly, high levels of BMAL1 at the beginning of a new circadian day. Additional regulation of Bmal1 further tunes the loop. The CLOCK:BMAL1 heterodimer inhibits Bmal1 transcription, and the REV-ERB protein enters the nucleus to suppress the transcription of the Bmal1 gene during the day. At night, REV-ERB protein levels are low, allowing Bmal1 transcription to take place. ROR, another nuclear receptor, competes with the REV-ERB for the RORE binding site and activates the tran cription of Bmal1. BMAL1, brain and muscle aryl hydrocarbon receptor nuclear translocator-like protein; CCGs, clock-controlled genes; CKI, casein kinase; CLOCK, circadian locomotor output cycles kaput; Cry, cryptochrome; E-box, enhancer box; P, phosphorylated; Per, Period; REV-ERB, reverse erythroblastosis virus; ROR, retinoic acid receptor-related orphan receptor; RORE, retinoic acid receptor-related orphan receptor response element. Italic notation for genes, capital notation for respective proteins.


  • => The circadian system is our control system for predictable environmental changes (e.g., day/ night, seasons). It consists of the central clock in the hypothalamic suprachiasmatic nucleus (SCN) and subsidiary peripheral clocks


  • => The stress system is our control system for unforeseen changes in the environment (e.g., predators). It comprises the hypothalamicpituitary- adrenal (HPA) axis and the sympathetic nervous system (SNS)

  • => Both systems are fundamental for survival and communicate with each other at various levels; disruptions in either system can lead to somatic and affective disorders

  • => The central circadian clock activates the HPA axis, thereby controlling the daily glucocorticoid release from the adrenal cortex

  • => Acute and chronic stress can affect core clock components within the SCN; disruptions of the molecular circadian clockwork is often related to depressive-like behavior


In order to retain a constant internal environment in response to external environmental changes, organisms maintain a complex dynamic equilibrium, also called homeostasis. If this equilibrium state is disrupted by a threatening stimulus, i.e., stressor, a stress response is generated to regain homeostasis. This includes the activation of the SNS and the HPA axis.39 Upon activation of the SNS, large quantities of the catecholamines norepinephrine and epinephrine are secreted into nearby capillaries within seconds. Once released into the blood, these hormones amplify the “fight or flight” reaction in order to provide sufficient energy (for review see Ref. 10). While the neuronal innervation of end organs through the SNS provides an immediate response to stressor exposure, activation of the HPA axis is slower (within minutes) and more persistent in its actions. In response to stressful stimuli, parvocellular neurons of the paraventricular nucleus of the hypothalamus (PVN) secrete releasing hormones, such as corticotropin-releasing hormone (CRH) and AVP into the portal circulation at the median eminence. These releasing hormones then act synergistically on the anterior pituitary by binding to their respective receptors (CRH-R1 and AVP-R1b), thereby triggering the secretion of adrenocorticotropic hormone (ACTH) from preformed granules into the peripheral circulation. Upon reaching the adrenal cortex, ACTH activates the synthesis and secretion of glucocorticoids (GC) (see Fig. 38.3). Once released, circulating GC modulate the expression of approximately 10% of our genes and exert widespread actions in the body which are essential for the maintenance of homeostasis and enable an organism to prepare for, respond to, and cope with physical and emotional stress (for review see Ref. 26). GC exert
Gabriella Lundkvist - the circadian system
Interactions between the circadian system and the HPA axis. The hypothalamic PVN receives homeostatic/stress inputs from the brain stem and limbic areas. Upon activation, parvocellular CRH/AVP-secreting neurons project to the median eminence where they terminate in close proximity to a capillary plexus. CRH and AVP are directly secreted into these vessels and transported via the hypophyseal portal system to corticotropes in the anterior pituitary gland. As a result, ACTH is released into the venous circulation. When ACTH reaches the adrenal cortex, it activates the synthesis and secretion of GC that, in turn, act on different levels of the HPA axis via negative feedback. The circadian system and the HPA axis communicate with each other at various levels. The central mammalian clock in the SCN controls the daily activity of the HPA axis, thus leading to a circadian and ultradian GC release from the adrenal cortex. The SCN also controls the diurnal sensitivity of the adrenal gland to the incoming ACTH message. The local adrenal clock contributes to the rhythmic GC secretion. Secreted GC resets peripheral clocks via GRs. Acute/chronic stressor exposure might affect core clock components in the SCN. This process, however, appears to be dependent on the time of day when the stressor occurs. The stress effects on the SCN might lead to increased susceptibility for affective and somatic disorders. ACTH, adrenocorticotropi hormone; AVP, arginine-vasopressin; CRH, corticotropin-releasing hormone; DMH, dorsomedial hypothalamic nucleus; GC, glucocorticoid(s); GR, glucocorticoid receptor; HPA axis, hypothalamic-pituitary-adrenal axis; PVN, paraventricular nucleus of the hypothalamus; SCN, suprachiasmatic nucleus; subPVZ, subparaventricular zone; VIP, vasoactive intestinal peptide.

Sites of interaction between the circadian clock system and the stress system

The Circadian and Ultradian Release of Glucocorticoids
In addition to the aforementioned stress-related secretion of GCs, these cholesterol-derived molecules are further released in a circadian manner under nonstressed conditions with an increased concentration prior to the active period of the day (early morning in humans, early evening in rats and mice).4,47 Furthermore, the circadian pattern is overlaid by an ultradian rhythm, i.e., a rhythm with a period significantly shorter than 24 h, with a pulse frequency (the rate of hormonal release) averaging between 60 and 90 min.47,48 The daily GC rhythm is controlled by the central circadian clock in a multimodal fashion: (1) the SCN controls the activity of the HPA axis by conveying excitatory and inhibitory information through synaptic contacts to the medioparvocellular PVN, where the CRH- and AVPexpressing neurons are located18; (2) the clock control over GC secretion operates via the sympathetic input to the adrenal gland, thereby modulating the sensitivity of the target organ to the incoming ACTH message35,45; and(3) the peripheral autonomous adrenal clock itself confers rhythmic expression of several clock genes as well as encoding molecules involved in the steroidogenic pathway and the ACTH signal transduction cascade in the zona glomerulosa and zona fasciculata of the adrenal gland. Thereby, mechanisms (2) and (3) are the main routes of SCN control over GC secretion. However, each of these paths might dominate under different conditions. The adrenal clockwork, for instance, appears to be essential for circadian GC production in mice in constant darkness, while under normal light–dark conditions ligh information is capable of regulating daily changes in GC production even in the absence of a functional local adrenal clock.43
The ultradian pulses that underlie the circadian GC rhythm occur with a relatively constant, roughly hourly, frequency, whereas the pulse amplitude (the amount of hormonal release) is variable. Besides the circadian input, homeostatic as well as stress-related signals impact the amplitude of these secretory episodes. The rising GC levels at the beginning of the active phase result from increases in the amplitude of the pulses, reaching its maximum just before awakening and declining thereafter to reach a trough early in the sleep phase (for review see Ref. 19). It has been demonstrated that the pulsatility of GC secretion is crucial for the appropriate stress response. The time of stressor application, for instance, determines the physiological stress response depending on the phase of an endogenous basal pulse. Rats that were exposed to white noise for 10 min responded with additional GC secretion if endogenous basal GC levels increased just prior to stressor exposure. In contrast, no or neglected GC responses were noticeable when basal endogenous GC levels were falling at stressor initiation. 48 These findings suggest that the basal GC pulsatility dynamically interacts with the ability of an organism to mount a stress response. Termination of the rising phase of the GC pulse by rapid feedback inhibition via the GR and MR may be essential in the generation of such pulses. While the GR mediates the acute effects of GC, the MR has an approximately 10-fold higher affinity than the GR and is involved in permissive or long-term activation during the peak of circadian GC concentration (for review see Ref. 21).

Circadian Responsiveness of the Hypothalamic-Pituitary-Adrenal Axis to Stress

Besides the ultradian pulsatility of the GC rhythm, the stress response might also be influenced by the fluctuating sensitivity of the HPA axis over the day. In addition, the type of stressor seems to play a crucial role. While psychological stressors, such as novel environment or restraint, elicit the largest HPA axis response during the inactive phase of rats (i.e., early day), physical stressors like hypoglycemic shock provoke greater stress responses at the onset of activity (i.e., early evening). One likely explanation for these differences might be the fact that physical stress is relayed to the PVN mainly via the brain stem, while processing psychological stress information requires the interpretation from higher brain centers involving the limbic system. The central clock in the SCN might differentially interfere with these signals from different brain areas by enhancing input from psychological stressors during day and inhibiting physical stress input at the same time (for review see Ref. 8).
Besides the commonly accepted interaction of the stress response and the time of day of stressor exposure in relation to psychological and physical stressors, recent studies suggest that this also applies for psychosocial stressors such as social defeat. Exposure of mice to 19 days of social defeat at the beginning of the active phase at Zeitgeber time (ZT)13–15 (ZT0 is defined as the time when lights are turned on) results in a more negative outcome (decreased social preference, reduced home–cage activity during the dark phase, more severe chemically induced colitis effects) as compared to stressor exposure at ZT1–3.2 In contrast, stress responses to intruder/resident confrontations of golden hamsters during the rest period (ZT2) as measured by heart rate, core body temperature, and general activity were significantly stronger compared to stressor exposure during the activity time (ZT14).12
Although we and others began to study the interactions between the type and duration of stressors and the time of the day and their effects on parameters like HPA axis activity, physiological rhythms, or the immune status, the exact mechanisms underlying the diurnal differences in the stress response remain to be elucidated.

Can Stress Directly Affect the Central Clock?

Several studies have shown that circadian rhythms at the output level are strongly affected by acute and chronic stressor exposure. For instance, altered rhythms in sleep-wake behavior,33 body temperature, 46 locomotor activity,13 and hormone secretion9 have been reported after exposure to chronic mild, shaker, and restraint stress, respectively. An imbalance between normally precisely orchestrated physiological and behavioral rhythms might be either attributable to alterations in SCN activity or might arise from stressinduced changes in peripheral suboscillators. While various studies have examined stress effects on peripheral clocks (see Box 38.2), investigations on the central pacemaker are scarce. This might be ascribed to the fact that, in contrast to peripheral clocks, GR expression could not be detected in the SCN.1


In order to properly adjust to acute stressful situations, peripheral oscillators need to be reset in such situations. In contrast to the SCN, peripheral nonbrain tissues mostly contain GRs and MRs. Clock genes, such as Per1, and possibly Per2, possess a GRE in their promoter region.1,41 Following binding to the GRE, ligand-activated GRs/MRs can phase-shift the expression rhythm of several clock genes and clock-related genes, leading to the resetting of circadian rhythms, for instance in the liver, heart, and kidney (for review see Refs. 34,50) Direct interactions between clock factors and the GR at peripheral target tissues may also occur. CLOCK/BMAL1 can acetylate lysine residues in the hinge region of the GR. This posttranslational modification renders GRs unable to fully interact with GRE, thus modifying the transcription rate of GC-responsive genes. Moreover, CRY has also been shown to prevent GR function via direct binding, resulting in decreased transactivation potential on a GRE-controlled luciferase reporter gene. 23

Acute Stress and the Suprachiasmatic Nucleus

With respect to the acute stressful situation, it is very reasonable that the SCN is devoid of GRs since elsewise the SCN rhythm could be perturbed any time an organism is stressed. In support, early studies indicated that acute social defeat does not perturb the central oscillator in the SCN as measured by body temperature and activity output,29 and it has been assumed that the central SCN clock cannot be affected by acute stress. However, there are strong indications that the SCN brain clock is responsive to stress under certain circumstances and not completely insensitive as initially believed. In early studies it was shown that exogenous GC enhances AVP and VIP mRNA expression in the SCN,24 and AVP release within the master pacemaker was increased following 10 min of forced swim and water immersion,11 strongly suggesting a direct and rapid effect on SCN function. Furthermore, it has been shown that acute exposure to predator scent stress leads to an upregulation of PER1 and PER2 protein expression in the SCN of male rats.22 Although predator scent stress is sensed by the olfactory bulb that contains a self-sustained, SCN-independent clock and the signaling from the olfactory bulb to the SCN might be indirect, this finding clearly shows that a certain type of acute stressor can indeed impact clock gene expression in the SCN.

Chronic Stress and the Suprachiasmatic Nucleus

Also with regard to chronic stressful situations, there is conflicting evidence of stress effects on the central clock. Chronic stressor exposure including forced swim, restraint, and social stress did not affect the central clock although it impinged the amplitude
of the activity rhythm in mice.42 In contrast, a reduction in PER2 oscillation amplitude has been reported in the rat SCN following 4 weeks of chronic unpredictable stress.16 The same stress paradigm also led to a decreased CLOCK and BMAL1 protein expression in the central clock.17 Likewise, seven days of repeated restraint decreased the PER2 protein expression in the mouse SCN.20

Stress Effects on the Suprachiasmatic Nucleus Might be Dependent on the Time of Day

What could be the reason for these contradictory results regarding stress effects on the SCN clock? One explanation might be that the SCN sensitivity to stress follows a circadian rhythm; i.e., mammals may be differentially sensitive/responsive to stress depending on what time of day they are exposed to the stressor. In support, our groups have recently shown that 19 days of repeated social defeat in mice has completely different effects on the SCN clock depending on whether the animals are exposed in the beginning of the active (night) or the nonactive (day) phase. Social defeat at ZT13–15 increased the PER2 rhythm amplitude in the SCN and PER2 protein expression in the posterior part of the central clock, whereas social defeat at ZT1–3 did not have any significant effect on PER2 rhythm and expression.3
This truly indicates that a GC signal evoked by stressor exposure can be sensed by and perturb core clock components in the SCN, but only at certain times of the day. The time-dependent stress signal is likely perceived via intermediary GR-containing brain areas like the PVN, dorsomedial hypothalamic nucleus, or the raphe nuclei.27

Stress and Depressive-Like Behavior Might be Linked to the Circadian Clock

Regardless of the predictability level of the stressor and the effect on protein expression and oscillation amplitude of core clock components, alterations of the molecular clockwork within the SCN were often correlated with depressive-like behavior. The more pronounced effects of stressor exposure at ZT13–15 on the SCN molecular clock were also correlated with more severe effects on behavior, such as reduced activity at the beginning of the active phase and lack of social preference, indicating depressive-like behavior. Moreover, effects of immune system functions were significantly more severe following stressor exposure at early night (ZT13–15) compared to early day (ZT1–3).2
A link between circadian rhythm disturbances and mood disorders is beyond doubt. Virtually all of the successful treatments for mood disorders seem to affect circadian rhythms and it is assumed that stabilization and/or resetting of these rhythms by treatments are crucial for therapeutic efficacy (for review see Ref. 28). For instance, the effects of seasonal affective disorder, a mood disorder that correlates with the extremely shortened daily light period during the winter season, can be alleviated by bright light therapy. Patients suffering from seasonal affective disorder have abnormal levels of the dark phase hormone melatonin and exhibit a delayed chronobiological cycle.49 Since clock genes, especially Per1 and Per2, are inducible by light in the SCN, early morning light can phase-advance behavioral and endocrine rhythms, thus alleviating depressive-like symptoms.25


Findings presented in this chapter highlight the complexity of the multilevel interaction of the circadian and the stress system, as summarized in Fig. 38.3. The circadian clock controls the activity of the HPA axis through multisynaptic contacts between the SCN and the PVN which provides the basis for the activity-related circadian GC release. In addition, the central clock alters the sensitivity of the adrenal gland to the incoming ACTH message, thereby influencing the secretion of GC.
Vice versa, stress affects core clock components such as PER2 and CLOCK/BMAL1 within the central oscillator, which is often correlated with depressive-like behavior.
In addition, rotating shift-work and frequent jet lag are provoked by our modern-life habits. Individuals who are exposed to these lifestyles have a greater risk of developing both somatic and affective disorders. Human epidemiological studies have shown that rotating shift nurses exhibit a higher risk to suffer from breast cancer compared to day shift nurses.38 Likewise, shift-work experience is associated with a higher incidence of major depressive disorder.6
Given the interrelated influence of these bodily control systems, a proper functioning of the systems is critical for a healthy body and mind. It becomes clear that the balance between the two systems is crucial for the maintenance of proper circadian rhythms such as the GC rhythms that exert widespread function within our bodies.
Further studies are required to understand the exact molecular interactions between these two systems and their interplay in the development of human pathology to resolve the outstanding issues.

This Article was published in an Elsevier book.


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About me

I am a neuroscientist specialized in research on circadian rhythms, or so called "chronobiology", which is a research field that describes how daily fluctuations in sleep-wakefulness, social behavior, hormonal release, immune system mechanims and other bodily functions are controlled by a "body clock".

Curriculum vitae

  • Feb 2015
    Scientific coordinator, Max Planck Institute for Biology of Ageing, Cologne, Germany
  • Aug 2014
    Associate professor (habilitation), Department of Neuroscience, Karolinska Institutet, Stockholm
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