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10.1093/emph/eow035 http://scihub22266oqcxt.onion/10.1093/emph/eow035 C5381352!5381352!28096295     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Evol+Med+Public+Health 2017 ; 2017 (1): 39-46 Nephropedia Template TP {{tp|p=28096295|t=2017. Does selection for short sleep duration explain human vulnerability to Alzheimer?s disease?|pdf=|usr=}}{{28096295}} gab.com Text Does selection for short sleep duration explain human vulnerability to Alzheimer s disease JO: Evol Med Public Health http://www.kidney.de/pget.php?&tw=1&pmid=28096295 #FOAvip Compared with other primates, humans sleep less and have a much higher prevalence of Alzheimer ?s disease (AD) pathology. This article reviews evidence relevant to the hypothesis that natural selection for shorter sleep time in humans has compromised the efficacy of physiological mechanisms that protect against AD during sleep. In particular, the glymphatic system drains interstitial fluid from the brain, removing extra-cellular amyloid beta (eA?) twice as fast during sleep. In addition, melatonin?a peptide hormone that increases markedly during sleep?is an effective antioxidant that inhibits the polymerization of soluble eA? into insoluble amyloid fibrils that are associated with AD. Sleep deprivation increases plaque formation and AD, which itself disrupts sleep, potentially creating a positive feedback cycle. These and other physiological benefits of sleep may be compromised by short sleep durations. Our hypothesis highlights possible long-term side effects of medications that reduce sleep, and may lead to potential new strategies for preventing and treating AD. Twit Text FOAVip Does selection for short sleep duration explain human vulnerability to Alzheimer s disease ????Evol Med Public Health http://www.kidney.de/pget.php?&tw=1&pmid=28096295 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28096295 #FOAvip English Wikipedia <ref>{{Cite pmid|28096295}}</ref> Does selection for short sleep duration explain human vulnerability to Alzheimer?s disease? #MMPMID28096295 Nesse RM; Finch CE; Nunn CL Evol Med Public Health 2017[]; 2017 (1): 39-46 PMID28096295show ga Compared with other primates, humans sleep less and have a much higher prevalence of Alzheimer ?s disease (AD) pathology. This article reviews evidence relevant to the hypothesis that natural selection for shorter sleep time in humans has compromised the efficacy of physiological mechanisms that protect against AD during sleep. In particular, the glymphatic system drains interstitial fluid from the brain, removing extra-cellular amyloid beta (eA?) twice as fast during sleep. In addition, melatonin?a peptide hormone that increases markedly during sleep?is an effective antioxidant that inhibits the polymerization of soluble eA? into insoluble amyloid fibrils that are associated with AD. Sleep deprivation increases plaque formation and AD, which itself disrupts sleep, potentially creating a positive feedback cycle. These and other physiological benefits of sleep may be compromised by short sleep durations. Our hypothesis highlights possible long-term side effects of medications that reduce sleep, and may lead to potential new strategies for preventing and treating AD. äDoes selection for short sleep duration explain human vulnerability to(epmc).pdf DeepDyve Pubget Overpricing