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Disturbed sleep patterns are known to be associated with cognitive impairment and Alzheimer's disease. But it isn't entirely clear whether Alzheimer's disease is caused by sleep disturbances or the other way around. This popular press article: http://www.kurzweilai.net/sleep-disruptions-similar-to-jet-lag-linked-to-memory-and-learning-problems on a new study  in mice helps to shed some light on the issue. They disrupted the sleep of both normal mice and mice breed to exhibit a mice-model of Alzheimer's disease by altering the day/night pattern of light they were exposed to every three days to simulate jet lag. They found the cognition (Morris water maze performance) of both types of mice were impaired by the disturbed sleep schedule. The impairment to learning was more pronounced in the Alzheimer's mice, and that the degree of impairment was proportional to the reduction of the endogenous antioxidant glutathione (GSH) in the brains of the mice, with Alzheimer's mice showing a greater reduction in GSH than the normal mice. This would seem to emphasize the importance of maintaining good sleep patterns in order to avoid cognitive decline and Alzheimer's disease with aging. --Dean ---------  Journal of Alzheimer's Disease, vol. Preprint, no. Preprint, pp. 1-16, 2015; DOI: 10.3233/JAD-150026 Circadian Disruption Reveals a Correlation of an Oxidative GSH/GSSG Redox Shift with Learning and Impaired Memory in an Alzheimer’s Disease Mouse Model. LeVault, Kelsey, Tischkau, Shelley, Brewer, Gregory. It is unclear whether pre-symptomatic Alzheimer’s disease (AD) causes circadian disruption or whether circadian disruption accelerates AD pathogenesis. In order to examine the sensitivity of learning and memory to circadian disruption, we altered normal lighting phases by an 8 h shortening of the dark period every 3 days (jet lag) in the APPSwDI NOS2–/– model of AD (AD-Tg) at a young age (4-5 months), when memory is not yet affected compared to non-transgenic (non-Tg) mice. Analysis of activity in 12-12 h lighting or constant darkness showed only minor differences between AD-Tg and non-Tg mice. Jet lag greatly reduced activity in both genotypes during the normal dark time. Learning on the Morris water maze was significantly impaired only in the AD-Tg mice exposed to jet lag. However, memory 3 days after training was impaired in both genotypes. Jet lag caused a decrease of glutathione (GSH) levels that tended to be more pronounced in AD-Tg than in non-Tg brains and an associated increase in NADH levels in both genotypes. Lower brain GSH levels after jet lag correlated with poor performance on the maze. These data indicate that the combination of the environmental stress of circadian disruption together with latent stress of the mutant amyloid and NOS2 knockout contributes to cognitive deficits that correlate with lower GSH levels.
I've just read "Mitohormesis: Promoting Health and Lifespan by Increased Levels of Reactive Oxygen Species (ROS)" , and am starting to worry about all the supplements many of us take. I'd love to get others' views on this topic. Myself, I'd like to be as supplement-free as possible, but, obviously, many supplements wouldn't likely interfere with hormesis in a deleterious way. It would be great if there were a way to measure the effect of supplements on mtDNA function -- well, there are ways, but I mean: a way that's not hugely expensive and is accessible to the average CR'er. Brian  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4036400/