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Gloria, Y.

Publications and source records attributed to Gloria, Y..

2 recordsLinked to original sources

iSleep: Continuous, binocular pupil tracking in sleep and reduced consciousness for physiological monitoring, predictions and interventions

Monitoring pupil dynamics is a key tool in understanding arousal. Pupil size can serve as a biomarker for the autonomic nervous system balance as well as for identifying brain states. While internal states can also be self-reported when awake, automated detection and non-invasive monitoring is crucial during sleep and reduced consciousness. Here, we introduce iSleep, an innovative pupil tracking and analysis framework for sleep in humans. It features comfortable, humidified eye-tracking goggles and a platform for integrated analysis and prediction capabilities. We show that iSleep allows safe and continuous access to binocular pupil size and ocular dynamics during sleep and anesthesia. iSleep reveals that pupillary fluctuations correlate tightly with brain activity, heartbeat, and breathing, and can reliably predict brain states. Pupil constrictions reflect parasympathetic drive and likely serve a protective function for deep sleep stability; while dilations indicate arousals. Unexpectedly, we observed a decoupling of binocular movements during periods of sleep, indicating alterations in reflexes which usually govern voluntary eye movements. Finally, iSleep was tested in surgery patients under general anesthesia, revealing dynamic pupil changes to noxious stimuli, suggesting the potential for nociception monitoring during surgeries. In summary, iSleep offers an easy-to-use, robust alternative to read out brain states during sleep and anesthesia, opening new avenues in monitoring, diagnostics, and treatments, previously obscured by closed eyelids.

neuroscience↗

Impairment of hippocampal astrocyte-mediated striatal dopamine release and locomotion in Alzheimer's disease

Clinical and translational research has identified deficits in the dopaminergic neurotransmission in the striatum in Alzheimers disease (AD) and this could be related to the pathophysiology of psychiatric symptoms appearing even at early stages of the pathology. We hypothesized that AD pathology in the hippocampus may influence dopaminergic neurotransmission even in the absence of AD-related lesion in the mesostriatal circuit. We thus chemogenetically manipulated the activity of hippocampal neurons and astrocytes in wild-type and hemizygous TgF344-AD (Tg) rats, an animal model of AD pathology. We assessed the brain-wide functional output of this manipulation using in vivo Single Photon Emission Computed Tomography to measure cerebral blood flow and D2/3 receptor binding. We also assessed the effects of the chemogenetic manipulations on astrocytic and microglial capacity to surround and phagocytize A{beta} both locally and in the striatum. Our results show that acute and chronic neuronal and astrocytic stimulation induces widespread effects on the brain regional activation pattern, notably with an inhibition of striatal activation. In the TgF344-AD rats, both these effects were blunted. Chemogenetic stimulation in the hippocampus increased microglial density and its capacity to limit AD pathology, whereas these effects were absent in the striatum perhaps as a consequence of the altered connectivity between the hippocampus and the striatum. Our work suggests that hippocampal AD pathology may alter mesostriatal signalling and induce widespread alterations of brain activity. Neuronal and astrocytic activation may induce a protective, A{beta}-limiting phenotype of microglia, which surrounds A{beta} plaques and limits A{beta} concentration more efficiently.

neuroscience↗