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10.1016/j.tins.2016.05.002 http://scihub22266oqcxt.onion/10.1016/j.tins.2016.05.002 C4967375!4967375 !27325209     free     free     free       Trends+Neurosci 2016 ; 39 (8 ): 552-566 Nephropedia Template TP {{tp|p=27325209 |t=2016. Sleep: A Novel Mechanistic Pathway, Biomarker, and Treatment Target in the Pathology of Alzheimer s Disease? |pdf=|usr=}}{{27325209 }} gab.com Text Sleep: A Novel Mechanistic Pathway, Biomarker, and Treatment Target in the Pathology of Alzheimer s Disease JO: Trends Neurosci http://www.kidney.de/pget.php?&tw=1&pmid=27325209 #FOAvip Sleep disruption appears to be a core component of Alzheimer's disease (AD) and its pathophysiology. Signature abnormalities of sleep emerge before clinical onset of AD. Moreover, insufficient sleep facilitates accumulation of amyloid-? (A?), potentially triggering earlier cognitive decline and conversion to AD. Building on such findings, this review has four goals: evaluating (i) associations and plausible mechanisms linking non-rapid-eye-movement (NREM) sleep disruption, A?, and AD; (ii) a role for NREM sleep disruption as a novel factor linking cortical A? to impaired hippocampus-dependent memory consolidation; (iii) the potential diagnostic utility of NREM sleep disruption as a new biomarker of AD; and (iv) the possibility of sleep as a new treatment target in aging, affording preventative and therapeutic benefits. Twit Text FOAVip Sleep: A Novel Mechanistic Pathway, Biomarker, and Treatment Target in the Pathology of Alzheimer s Disease ????Trends Neurosci http://www.kidney.de/pget.php?&tw=1&pmid=27325209 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27325209 #FOAvip English Wikipedia <ref>{{Cite pmid|27325209 }}</ref> Sleep: A Novel Mechanistic Pathway, Biomarker, and Treatment Target in the Pathology of Alzheimer s Disease? #MMPMID27325209 Mander BA ; Winer JR ; Jagust WJ ; Walker MP Trends Neurosci 2016[Aug]; 39 (8 ): 552-566 PMID27325209 show ga Sleep disruption appears to be a core component of Alzheimer's disease (AD) and its pathophysiology. Signature abnormalities of sleep emerge before clinical onset of AD. Moreover, insufficient sleep facilitates accumulation of amyloid-? (A?), potentially triggering earlier cognitive decline and conversion to AD. Building on such findings, this review has four goals: evaluating (i) associations and plausible mechanisms linking non-rapid-eye-movement (NREM) sleep disruption, A?, and AD; (ii) a role for NREM sleep disruption as a novel factor linking cortical A? to impaired hippocampus-dependent memory consolidation; (iii) the potential diagnostic utility of NREM sleep disruption as a new biomarker of AD; and (iv) the possibility of sleep as a new treatment target in aging, affording preventative and therapeutic benefits. |Aging/*physiology [MESH] |Alzheimer Disease/diagnosis/*physiopathology/*therapy [MESH] |Animals [MESH] |Humans [MESH]Sleep: A Novel Mechanistic Pathway, Biomarker, and Treatment Target in(epmc).pdf DeepDyve Pubget Overpricing