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10.1371/journal.pgen.1006593 http://scihub22266oqcxt.onion/10.1371/journal.pgen.1006593 C5333801!5333801!28253260     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       PLoS+Genet 2017 ; 13 (3): ä Nephropedia Template TP {{tp|p=28253260|t=2017. Direct Keap1-Nrf2 disruption as a potential therapeutic target for Alzheimer?s disease |pdf=|usr=}}{{28253260}} gab.com Text Direct Keap1-Nrf2 disruption as a potential therapeutic target for Alzheimer s disease JO: PLoS Genet http://www.kidney.de/pget.php?&tw=1&pmid=28253260 #FOAvip Nrf2, a transcriptional activator of cell protection genes, is an attractive therapeutic target for the prevention of neurodegenerative diseases, including Alzheimer?s disease (AD). Current Nrf2 activators, however, may exert toxicity and pathway over-activation can induce detrimental effects. An understanding of the mechanisms mediating Nrf2 inhibition in neurodegenerative conditions may therefore direct the design of drugs targeted for the prevention of these diseases with minimal side-effects. Our study provides the first in vivo evidence that specific inhibition of Keap1, a negative regulator of Nrf2, can prevent neuronal toxicity in response to the AD-initiating A?42 peptide, in correlation with Nrf2 activation. Comparatively, lithium, an inhibitor of the Nrf2 suppressor GSK-3, prevented A?42 toxicity by mechanisms independent of Nrf2. A new direct inhibitor of the Keap1-Nrf2 binding domain also prevented synaptotoxicity mediated by naturally-derived A? oligomers in mouse cortical neurons. Overall, our findings highlight Keap1 specifically as an efficient target for the re-activation of Nrf2 in AD, and support the further investigation of direct Keap1 inhibitors for the prevention of neurodegeneration in vivo. Twit Text FOAVip Direct Keap1-Nrf2 disruption as a potential therapeutic target for Alzheimer s disease ????PLoS Genet http://www.kidney.de/pget.php?&tw=1&pmid=28253260 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28253260 #FOAvip English Wikipedia <ref>{{Cite pmid|28253260}}</ref> Direct Keap1-Nrf2 disruption as a potential therapeutic target for Alzheimer?s disease #MMPMID28253260 Kerr F; Sofola-Adesakin O; Ivanov DK; Gatliff J; Gomez Perez-Nievas B; Bertrand HC; Martinez P; Callard R; Snoeren I; Cochemé HM; Adcott J; Khericha M; Castillo-Quan JI; Wells G; Noble W; Thornton J; Partridge L PLoS Genet 2017[Mar]; 13 (3): ä PMID28253260show ga Nrf2, a transcriptional activator of cell protection genes, is an attractive therapeutic target for the prevention of neurodegenerative diseases, including Alzheimer?s disease (AD). Current Nrf2 activators, however, may exert toxicity and pathway over-activation can induce detrimental effects. An understanding of the mechanisms mediating Nrf2 inhibition in neurodegenerative conditions may therefore direct the design of drugs targeted for the prevention of these diseases with minimal side-effects. Our study provides the first in vivo evidence that specific inhibition of Keap1, a negative regulator of Nrf2, can prevent neuronal toxicity in response to the AD-initiating A?42 peptide, in correlation with Nrf2 activation. Comparatively, lithium, an inhibitor of the Nrf2 suppressor GSK-3, prevented A?42 toxicity by mechanisms independent of Nrf2. A new direct inhibitor of the Keap1-Nrf2 binding domain also prevented synaptotoxicity mediated by naturally-derived A? oligomers in mouse cortical neurons. Overall, our findings highlight Keap1 specifically as an efficient target for the re-activation of Nrf2 in AD, and support the further investigation of direct Keap1 inhibitors for the prevention of neurodegeneration in vivo. äDirect Keap1-Nrf2 disruption as a potential therapeutic target for Alz(epmc).pdf DeepDyve Pubget Overpricing