Welcome to the WCN 2021 Interactive Program
The congress will officially run on Central European Time (CET) - Rome Time
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Please note that all sessions will run at their scheduled time and be followed by a LIVE Q&A/Discussion at the end
The viewing of sessions, cannot be accessed from this conference calendar. All sessions are accessible via the Virtual Platform
- JAMES C. STEVENS (United States of America)
2021 UPDATE ON THE EVALUATION AND MANAGEMENT OF NARCOLEPSY
- Claudio L. Bassetti (Switzerland)
SLEEP: THE PRICE WE PAY FOR HIGHER ORDER COGNITION
- Logan D. Schneider (United States of America)
Abstract
Abstract Body
Sleep-wake neurocircuitry has demonstrated a number of changes associated with the aging process. For example, reductions in noradrenergic tone result in diminished monoamine-mediated wakefulness. There is also evidence of breakdown of the circadian rhythm due, in part, to conditions such as cataracts or macular degeneration, but also to age-related changes in the suprachiasmatic nucleus, the location of the body’s “master clock” housed in the hypothalamus. The consequence of reduced circadian amplitude is less-consistent periods of sleeping/waking across the 24-hour day, with resultant increased nighttime and decreased daytime activity. However, in healthy elder populations there appears to be more day-to-day consistency in sleep-wake patterns, despite the diminished strength of the circadian rhythmicity.
Sleep–wake and circadian disturbances in neurodegenerative disease are secondary to pathological degeneration of primary brain regions important for regulating the sleep–wake and circadian cycles. Common proteins associated with neurodegenerative processes – amyloid β, tau, and α-synuclein – accumulate as a consequence of normal neuronal activity, but unhealthy sleep patterns may also contribute to neurodegeneration through sleep’s role in the clearance of the toxic consequences of neuronal activity during sleep. With the recent description of the brain’s extensive perivascular glymphatic system, facilitating clearance of such metabolic byproducts most effectively in slow wave sleep, the connection between sleep and neural/glial health is beginning to crystalize. As such, the finding that clearance of potentially neurotoxic substances (such as amyloid β and tau) is hindered by sleep deprivation and/or disruption has implications for human neurodegenerative disease pathogenesis.
SLEEP AND CEREBROVASCULAR DISEASE
- JAMES C. STEVENS (United States of America)
Abstract
Abstract Body
SLEEP and CEREBROVASCULAR DISEASE
Review of the current knowledge base concerning the complex interaction between sleep, sleep disorders and cerebrovascular disease. Through reviewing the literature, recommendations will be provided concerning primary and secondary prevention of stroke through addressing the diagnosis and treatment of sleep-related conditions.