Healthy ageing has been found to be accompanied by changes in slow wave activity (SWA) and cognitive function. Furthermore, these changes have been seen predominantly in the prefrontal cortex (PFC) compared to other regions of the cortex. Current theories of cognitive ageing propose that this occurs due to a specified deterioration of neuronal substrates of the PFC, and as such, changes in SWA and cognitive function may decline at similar rates due to similar underlying aetiology. The main aim of the current thesis was to explore age-related differences in electroencephalographic (EEG) SWA during the first NREM period and cognitive performance that relies on the integrity of the PFC: executive function and social cognition. The extent to which executive function (reliant on dorsolateral PFC areas) and social cognitive function (reliant on ventromedial PFC regions) show similar age-related deterioration was investigated in Study 1. Here, 16 young (22.2 years) and 16 older (71.5 years) adults were administered with a cognitive testing battery including executive function measures: Verbal Fluency (VF) and Tower of London (TOL); as well as measures of social cognition: Go/No-go, Emotional Prosody and Ekman 60 Faces. Not all measures of PFC function were affected to the same extent. The older group performed significantly worse on the TOL, but not on the VF test. Additionally, simple aspects of social cognition did not display differences between the groups, but the older group performed significantly worse than the young group on more complex aspects of recognition of emotion from facial expression (Ekman 60 Faces) and Emotional Prosody. As most studies of cognitive ageing are cross-sectional and show large agerelated changes, the remainder of this thesis focused on age-related changes using a longitudinal design over a relatively small ageing period (mean = 6.29 years). The average age of participants at baseline was 67.1 years and the average age at follow-up was 73.4 years. In Study 2, in a sample of 11 participants, performance on executive function tests was measured (TOL, VF and Wisconsin Card Sorting Test: WCST). As found in the cross-sectional analyses reported in Study 1, the TOL task was found to be the most sensitive indicator of age-related changes, as this showed a decline with age; whereas, VF and WCST remained stable over time. Furthermore, in Study 3, localised SWA was recorded via EEG, and significant declines were found in low frequency delta (0.5 – 1 Hz), which was localised to the left frontal region.

<p>Several physical mechanisms concerning the impact of Rossby waves on ozone distribution and circulation in the stratosphere and troposphere are studied in the thesis.</p><p>Summertime total ozone variability over Middle Asia and Northern Scandinavia shows similar wave-like behaviour with typical periods of 10-20 days and amplitudes of 20-50 Dobson units. These variations are caused by eastward travelling Rossby waves in the lower stratosphere. The same mechanism plays the primary role in the formation of an intense low ozone episode over Scandinavia in August 2003. A strong anticyclone was formed in the troposphere over Europe as a part of a Rossby wave train. The anticyclone coincides with a displaced Artic pool of low-ozone air in the stratosphere aloft of the anticyclone. A combination of the two above-mentioned processes results in the total ozone minimum over Northern Europe for summer 2003.</p><p>Interannual variability of the atmospheric circulation and total ozone during winter is strongly controlled by the diabatic (Brewer-Dobson) circulation which is driven by upward propagating waves from the troposphere. In the Northern Hemisphere midlatitudes, wintertime total ozone shows antiphase behaviour with the Arctic Oscillation (AO) index on interannual and decadal time-scales. Weaker (stronger) wave activity leads to less (more) northward ozone transport and to a stronger (weaker) AO.</p><p>Rossby wave activity occurs as episodic wave events and this wave forcing is not uniform during winter. The November-December stratospheric eddy heat flux is strongly anticorrelated with the January-February eddy heat flux in the midlatitude stratosphere and troposphere. Weaker upward wave fluxes in early winter lead to stronger upward wave fluxes from the troposphere as well as to a stronger polar night jet during midwinter and vice versa. Hence upward wave activity fluxes in early winter define, to a considerable extent, the subsequent evolution of the midwinter circulation in the stratosphere and troposphere.</p>

Several physical mechanisms concerning the impact of Rossby waves on ozone distribution and circulation in the stratosphere and troposphere are studied in the thesis. Summertime total ozone variability over Middle Asia and Northern Scandinavia shows similar wave-like behaviour with typical periods of 10-20 days and amplitudes of 20-50 Dobson units. These variations are caused by eastward travelling Rossby waves in the lower stratosphere. The same mechanism plays the primary role in the formation of an intense low ozone episode over Scandinavia in August 2003. A strong anticyclone was formed in the troposphere over Europe as a part of a Rossby wave train. The anticyclone coincides with a displaced Artic pool of low-ozone air in the stratosphere aloft of the anticyclone. A combination of the two above-mentioned processes results in the total ozone minimum over Northern Europe for summer 2003. Interannual variability of the atmospheric circulation and total ozone during winter is strongly controlled by the diabatic (Brewer-Dobson) circulation which is driven by upward propagating waves from the troposphere. In the Northern Hemisphere midlatitudes, wintertime total ozone shows antiphase behaviour with the Arctic Oscillation (AO) index on interannual and decadal time-scales. Weaker (stronger) wave activity leads to less (more) northward ozone transport and to a stronger (weaker) AO. Rossby wave activity occurs as episodic wave events and this wave forcing is not uniform during winter. The November-December stratospheric eddy heat flux is strongly anticorrelated with the January-February eddy heat flux in the midlatitude stratosphere and troposphere. Weaker upward wave fluxes in early winter lead to stronger upward wave fluxes from the troposphere as well as to a stronger polar night jet during midwinter and vice versa. Hence upward wave activity fluxes in early winter define, to a considerable extent, the subsequent evolution of the midwinter circulation in the stratosphere and troposphere.

La dynamique de la stratosphère au printemps et en été reste à ce jour largement inexplorée. Or dans les contextes actuels du recouvrement de la couche d’ozone et de l’augmentation des émissions de gaz à effet de serre, une amélioration de la compréhension des processus dynamiques contrôlant la stratosphère s’avère nécessaire, afin de mieux appréhender l’évolution du climat dans le futur. Des observations satellitaires récentes du printemps/été arctique ont montré l’existence de phénomènes de transport irréversibles depuis les régions tropicales vers la région arctique. Cependant, les mécanismes associés à ces évènements restent mal connus. Ce travail de thèse consiste en l’analyse dynamique et climatologique de ces phénomènes, afin d’évaluer les mécanismes responsables de leur développement et de leur fréquence d’apparition. Une attention particulière est donnée aux rares évènements, où la signature de l’intrusion persiste dans une anomalie anticyclonique jusqu’en été, soit plusieurs mois après son établissement en région polaire. Les données des instruments satellitaires MLS/Aura et MIPAS/ENVISAT, de l’instrument ballon SPIRALE, et le modèle d’advection MIMOSA ont permis d’identifier, caractériser et quantifier ces évènements. L’analyse des conditions dynamiques a été faite à partir des données météorologiques réanalysées de L’ECMWF. Enfin, le développement d’un algorithme de détection systématique de ces intrusions a permis d’en établir une climatologie entre les années 1980 et 2011. Parmi les résultats majeurs de cette étude, il apparaît que la fréquence de ces évènements, contrôlés par l’activité ondulatoire, a fortement augmenté depuis les années 2000. Nous montrons aussi que leur développement au printemps est fortement lié à l’évolution dynamique de la stratosphère durant l’hiver et au régime de circulation intertropicale. / The stratosphere dynamics remains largely unexplored in summer and spring. In the context of the ozone layer recovery and the increasing of greenhouse gases emissions, efforts must be provided to improve our knowledge of the dynamical processes driving the stratosphere. Such improvements would lead to better future climate trends estimates. Recently, spring and summer satellites observations revealed occurrences of irreversible air masses transport from the tropics to the Arctic region. However, the associated mechanisms are poorly understood. The present work consists of dynamical and climatological analyses of these events in order to identify their causes and their occurrence frequency. In particular, we focused on the sporadic events, where the intrusion signal persists several months in the polar region, trapped within an anticyclonic anomaly before disappearing in summer. We used MLS/Aura and MIPAS/ENVISAT satellites data, the SPIRALE balloon borne data and the results of the advection model MIMOSA to identify, characterize and quantify these events. Stratospheric dynamical conditions are investigated using the reanalyses data of the ECMWF. Finally, a systematic algorithm to detect low-latitude intrusions has been developed and applied on MIMOSA results to perform a climatology between 1980 and 2011 The results suggest that the frequency of these events, driven by the planetary wave activity, is increasing since the 21st century. Furthermore, their occurrence in spring appears to depend on the stratospheric dynamical evolution during winter and on the tropical region dynamical regime.

Le somnambulisme est une parasomnie commune, caractérisée par des éveils incomplets lors des stades de sommeil lent, au cours desquels les individus atteints présentent des comportements moteurs d’une complexité variable accompagnés de confusion et d’un jugement altéré. La littérature actuelle suggère que ce trouble serait associé à des particularités de l’activité en ondes lentes et des oscillations lentes, deux indices de l’intégrité du processus homéostatique et de la profondeur du sommeil. Toutefois, en raison de certaines lacunes méthodologiques dans les études existantes, le rôle de ces marqueurs électroencéphalographiques dans la pathophysiologie du somnambulisme reste à éclaircir. Notre premier article a donc investigué d’éventuelles anomalies de l’activité en ondes lentes et des oscillations lentes chez les somnambules, en comparant leur sommeil au cours de la nuit entière à celui de participants contrôles. De plus, comme les somnambules semblent réagir différemment (en termes de fragmentation du sommeil notamment) des dormeurs normaux à une pression homéostatique accrue, nous avons comparé l’activité en ondes lentes et les oscillations lentes en nuit de base et suite à une privation de sommeil de 38 heures. Les résultats de nos enregistrements électroencéphalographiques chez 10 somnambules adultes et neuf participants contrôles montrent une élévation de la puissance spectrale de l’activité en ondes lentes et de la densité des oscillations lentes en nuit de récupération par rapport à la nuit de base pour nos deux groupes. Toutefois, contrairement à plusieurs études précédentes, nous ne n’observons pas de différence entre somnambules et dormeurs normaux quant à l’activité en ondes lentes et aux oscillations lentes pour aucune des deux nuits. Au-delà ce certaines considérations méthodologiques ayant pu contribuer à ce résultat inattendu, nous croyons qu’il justifie un questionnement sur l’hétérogénéité des somnambules comme population. Notre deuxième article s’est penché sur les facteurs électroencéphalographiques transitoires susceptibles d’être associés au déclenchement des épisodes de somnambulisme. Nous avons comparé les fluctuations d’activité en ondes lentes et des oscillations lentes dans les minutes avant des épisodes de somnambulisme spontanés (c.a.d.: non associés à un stimulus identifiable) à celles survenant avant des éveils normaux comparables chez 12 somnambules adultes. Nous montrons que, comparativement aux éveils normaux, les épisodes de somnambulisme sont précédés d’un sommeil plus profond, tel qu’indiqué par une plus grande densité spectrale de l’activité en ondes lentes et une plus grande densité des oscillations lentes. Cet approfondissement du sommeil, spécifique aux épisodes de somnambulisme, semble survenir sur un laps de temps relativement long (>3 minutes), et non abruptement au cours des secondes précédant l’épisode. Ces données ouvrent un questionnement quant aux mécanismes en jeu dans la survenue des épisodes de somnambulisme spontanés. Globalement, cette thèse suggère que des phénomènes liés à l’activité en ondes lentes et aux oscillations lentes seraient liés au déclenchement des épisodes de somnambulisme, mais que des études supplémentaires devront être menées afin de délimiter le rôle précis que ces marqueurs jouent dans la pathophysiologie du somnambulisme. / Sleepwalking is a common parasomnia characterized by sudden but incomplete arousals out of non-rapid eye movement sleep during which predisposed individuals display motor behaviours of various complexity, accompanied by mental confusion and altered judgement. A growing body of evidence suggests that this condition could be associated with atypical patterns in slow wave activity and slow oscillations, both markers of the integrity of the homeostasis process and of sleep intensity. However, due to methodological limitations in past studies, the role of these electroencephalographic markers in the pathophysiology of sleepwalking remains unclear. Our first article aimed at describing slow wave activity and slow oscillations abnormalities in sleepwalkers by comparing whole night sleep in 10 adult sleepwalkers and 9 control participants. In addition, since past studies have shown that increased homeostatic pressure has differential effects on sleepwalkers versus normal controls (e.g., in terms of sleep fragmentation), we compared slow wave activity and slow oscillations during baseline sleep and recovery sleep after 38 hours of sleep deprivation in patients and controls. Results show that sleep deprivation increases slow wave activity power density and slow oscillations density in both groups. However, contrary to our predictions, no group differences were noted on any of the two nights on slow wave activity or slow oscillations. Beyond methodological considerations which may partially account for this unexpected result, this study opens questions as to the homogeneity of sleepwalkers as a clinical population. Our second study focused on transient electroencephalographic fluctuations that may be associated with the onset of sleepwalking episodes. We compared slow wave activity and slow oscillations fluctuations in the moments leading up to spontaneous (that is, occurring without an identifiable internal or external stimuli) somnambulistic episodes recorded in the sleep laboratory in 12 adult sleepwalkers and comparing these patterns to those observed prior to non-behavioural awakenings observed in the same patients. We showed that when compared to non-behavioural awakenings from the same sleep stage and sleep period, somnambulistic episodes were preceded by deeper sleep, as indicated by higher slow wave activity power density and slow oscillations density. This deepening of sleepwalkers’ sleep occurs over a relatively long period of time (>3 minutes) before the episode, rather than abruptly in the seconds preceding episode onset. These findings raise key questions about fundamental mechanisms involved in the occurrence of spontaneously recorded somnambulistic episodes. Taken as a whole, the results from the work presented in this thesis show that electrophysiological processes related to slow wave activity and slow oscillations play a role in the occurrence of somnambulistic episodes. However, the functional significance of these electroencephalographic markers in the pathophysiology of sleepwalking remains to be clarified.

Aging and Alzheimer’s disease (AD), are associated with disabling sleep and cognitive deficits. Specifically, aging and Alzheimer’s disease is associated with reduced quantity and quality of the deepest stage of sleep, called slow-wave-sleep (SWS). Interestingly, SWS has been implicated in hippocampus-dependent memory in mice. More importantly, sleep deprivation, aging, and AD are all associated with deficits in memory. Therefore, I hypothesize that, in aging and AD, the sleep deficits are, at least in part, responsible for memory impairments and increasing the quantity and quality of SWS will reverse these memory deficits. I first developed mouse models of SWS enhancement in aging and AD. Chemogenetic activation of the parafacial zone GABAergic neurons enhances SWS in aged mice as previously described in adult mice. Similarly, in AD mice, SWS enhancement is as effective as in littermate wild-type controls. Then, I used these mouse models to characterize the role of SWS in memory using novel gain-of-sleep experiments. I found that acute SWS enhancement: 1) reduce spatial memory in adult mice and 2) failed to improve spatial memory in aged mice. In a preliminary study, acute SWS enhancement seems to improve contextual memory in AD mice. Collectively, my work provides a novel mouse model of SWS enhancement in aging and AD, offering a pivotal tool to study the role of SWS in physiological functions and neurodegenerative diseases. Furthermore, my results suggest that acute SWS enhancement does not benefit the behavioral manifestation of memory consolidation in adult mice and aged mice.

Diverses études se sont penchées sur les paramètres EEG du sommeil en ondes lentes, y compris l’activité en ondes lentes en lien avec le somnambulisme, mais les résultats se révèlent inconsistants et contradictoires. Le premier objectif de la présente étude était d’analyser quantitativement l’EEG en sommeil en mesurant les fluctuations de puissance spectrale en delta (1-4 Hz) et delta lent (0.5-1 Hz) avant des épisodes de somnambulisme. Le second était de détecter les oscillations lentes (> 75 μV, fréquence d'environ 0.7-0.8 Hz) et très lentes (> 140 μV, fréquence d'environ 0.7-0.8 Hz) afin d'examiner leur changement d'amplitude et de densité avant de tels épisodes. Suite à une privation de sommeil de 25 heures, les enregistrements polysomnographiques de 22 adultes atteints de somnambulisme ont été scrutés. L’analyse des 200 secondes avant les épisodes révèle que ceux-ci ne sont pas précédés d’une augmentation graduelle de puissance spectrale en delta ni en delta lent, tant sur les dérivations frontale, centrale que pariétale. Toutefois, une hausse statistiquement significative de la densité des oscillations lentes et des oscillations très lentes a été observée au cours des 20 sec immédiatement avant le début des épisodes. Reste à déterminer le rôle exact de ces paramètres de l’EEG en sommeil par rapport à la manifestation et au diagnostic des parasomnies en sommeil lent. / Several studies have investigated slow-wave sleep EEG parameters, including slow-wave activity (SWA) in relation to somnambulism, but results have been both inconsistent and contradictory. The first goal of the present study was to conduct a quantitative analysis of sleepwalkers’ sleep EEG by studying fluctuations in spectral power for delta (1-4 Hz) and slow delta (0.5-1 Hz) before the onset of somnambulistic episodes. A secondary aim was to detect slow wave oscillations to examine their changes in amplitude and density prior to behavioral episodes of somnambulism. Twenty-two adult sleepwalkers were investigated polysomnographically following 25 h of sleep deprivation. Analysis of patients’ sleep EEG over the 200 sec prior to the episodes’ onset revealed that the episodes were not preceded by a gradual increase in spectral power for either delta or slow delta over frontal, central, or parietal leads. However, time course comparisons revealed significant changes in the density of slow and very slow wave oscillations, with significant increases occurring during the final 20 sec immediately preceding episode onset. The specificity of these sleep EEG parameters for the occurrence and diagnosis of NREM parasomnias remains to be determined.