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10.1186/s40478-017-0435-7 http://scihub22266oqcxt.onion/10.1186/s40478-017-0435-7 28420443/?report=reader!5395835!28420443     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Acta+Neuropathol+Commun 2017 ; 5 (1): 30 Nephropedia Template TP {{tp|p=28420443|t=2017. Tau phosphorylation induced by severe closed head traumatic brain injury is linked to the cellular prion protein |pdf=|usr=}}{{28420443}} gab.com Text Tau phosphorylation induced by severe closed head traumatic brain injury is linked to the cellular prion protein JO: Acta Neuropathol Commun http://www.kidney.de/pget.php?&tw=1&pmid=28420443 #FOAvip Studies in vivo and in vitro have suggested that the mechanism underlying Alzheimer's disease (AD) neuropathogenesis is initiated by an interaction between the cellular prion protein (PrP(C)) and amyloid-beta oligomers (Abetao). This PrP(C)-Abetao complex activates Fyn kinase which, in turn, hyperphosphorylates tau (P-Tau) resulting in synaptic dysfunction, neuronal loss and cognitive deficits. AD transgenic mice lacking PrP(C) accumulate Abeta, but show normal survival and no loss of spatial learning and memory suggesting that PrP(C) functions downstream of Abetao production but upstream of intracellular toxicity within neurons. Since AD and traumatic brain injury (TBI)-linked chronic traumatic encephalopathy are tauopathies, we examined whether similar mechanistic pathways are responsible for both AD and TBI pathophysiologies. Using transgenic mice expressing different levels of PrP(C), our studies investigated the influence and necessity of PrP(C) on biomarker (total-tau [T-Tau], P-Tau, GFAP) levels in brain and blood as measured biochemically following severe TBI in the form of severe closed head injury (sCHI). We found that following sCHI, increasing levels of T-Tau and P-Tau in the brain were associated with the PrP(C) expression levels. A similar relationship between PrP(C) expression and P-Tau levels following sCHI were found in blood in the absence of significant T-Tau changes. This effect was not seen with GFAP which increased within 24 h following sCHI and progressively decreased by the 7 day time point regardless of the PrP(C) expression levels. Changes in the levels of all biomarkers were independent of gender. We further enhanced and expanded the quantitation of brain biomarkers with correlative studies using immunohisochemistry. We also demonstrate that a TBI-induced calpain hyperactivation is not required for the generation of P-Tau. A relationship was demonstrated between the presence/absence of PrP(C), the levels of P-Tau and cognitive dysfunction. Our studies suggest that PrP(C) is important in mediating TBI related pathology. Twit Text FOAVip Tau phosphorylation induced by severe closed head traumatic brain injury is linked to the cellular prion protein ????Acta Neuropathol Commun http://www.kidney.de/pget.php?&tw=1&pmid=28420443 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28420443 #FOAvip English Wikipedia <ref>{{Cite pmid|28420443}}</ref> Tau phosphorylation induced by severe closed head traumatic brain injury is linked to the cellular prion protein #MMPMID28420443 Rubenstein R; Chang B; Grinkina N; Drummond E; Davies P; Ruditzky M; Sharma D; Wang K; Wisniewski T Acta Neuropathol Commun 2017[Apr]; 5 (1): 30 PMID28420443show ga Studies in vivo and in vitro have suggested that the mechanism underlying Alzheimer's disease (AD) neuropathogenesis is initiated by an interaction between the cellular prion protein (PrP(C)) and amyloid-beta oligomers (Abetao). This PrP(C)-Abetao complex activates Fyn kinase which, in turn, hyperphosphorylates tau (P-Tau) resulting in synaptic dysfunction, neuronal loss and cognitive deficits. AD transgenic mice lacking PrP(C) accumulate Abeta, but show normal survival and no loss of spatial learning and memory suggesting that PrP(C) functions downstream of Abetao production but upstream of intracellular toxicity within neurons. Since AD and traumatic brain injury (TBI)-linked chronic traumatic encephalopathy are tauopathies, we examined whether similar mechanistic pathways are responsible for both AD and TBI pathophysiologies. Using transgenic mice expressing different levels of PrP(C), our studies investigated the influence and necessity of PrP(C) on biomarker (total-tau [T-Tau], P-Tau, GFAP) levels in brain and blood as measured biochemically following severe TBI in the form of severe closed head injury (sCHI). We found that following sCHI, increasing levels of T-Tau and P-Tau in the brain were associated with the PrP(C) expression levels. A similar relationship between PrP(C) expression and P-Tau levels following sCHI were found in blood in the absence of significant T-Tau changes. This effect was not seen with GFAP which increased within 24 h following sCHI and progressively decreased by the 7 day time point regardless of the PrP(C) expression levels. Changes in the levels of all biomarkers were independent of gender. We further enhanced and expanded the quantitation of brain biomarkers with correlative studies using immunohisochemistry. We also demonstrate that a TBI-induced calpain hyperactivation is not required for the generation of P-Tau. A relationship was demonstrated between the presence/absence of PrP(C), the levels of P-Tau and cognitive dysfunction. Our studies suggest that PrP(C) is important in mediating TBI related pathology. |Animals[MESH] |Biomarkers/metabolism[MESH] |Brain Injuries, Traumatic/*metabolism/pathology/psychology[MESH] |Brain/drug effects/*metabolism/pathology[MESH] |Calpain/antagonists & inhibitors/metabolism[MESH] |Cognition/physiology[MESH] |Disease Models, Animal[MESH] |Disease Progression[MESH] |Female[MESH] |Glial Fibrillary Acidic Protein/metabolism[MESH] |Male[MESH] |Mice, 129 Strain[MESH] |Mice, Inbred C57BL[MESH] |Mice, Transgenic[MESH] |Phosphorylation[MESH] |PrPC Proteins/*metabolism[MESH] |Sex Characteristics[MESH]Tau phosphorylation induced by severe closed head traumatic brain inju(epmc).pdf DeepDyve Pubget Overpricing