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10.1186/s40035-017-0077-5 http://scihub22266oqcxt.onion/10.1186/s40035-017-0077-5 C5348787!5348787!28293421     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Transl+Neurodegener 2017 ; 6 (ä): ä Nephropedia Template TP {{tp|p=28293421|t=2017. Protein misfolding in neurodegenerative diseases: implications and strategies |pdf=|usr=}}{{28293421}} gab.com Text Protein misfolding in neurodegenerative diseases: implications and strategies JO: Transl Neurodegener http://www.kidney.de/pget.php?&tw=1&pmid=28293421 #FOAvip A hallmark of neurodegenerative proteinopathies is the formation of misfolded protein aggregates that cause cellular toxicity and contribute to cellular proteostatic collapse. Therapeutic options are currently being explored that target different steps in the production and processing of proteins implicated in neurodegenerative disease, including synthesis, chaperone-assisted folding and trafficking, and degradation via the proteasome and autophagy pathways. Other therapies, like mTOR inhibitors and activators of the heat shock response, can rebalance the entire proteostatic network. However, there are major challenges that impact the development of novel therapies, including incomplete knowledge of druggable disease targets and their mechanism of action as well as a lack of biomarkers to monitor disease progression and therapeutic response. A notable development is the creation of collaborative ecosystems that include patients, clinicians, basic and translational researchers, foundations and regulatory agencies to promote scientific rigor and clinical data to accelerate the development of therapies that prevent, reverse or delay the progression of neurodegenerative proteinopathies. Twit Text FOAVip Protein misfolding in neurodegenerative diseases: implications and strategies ????Transl Neurodegener http://www.kidney.de/pget.php?&tw=1&pmid=28293421 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28293421 #FOAvip English Wikipedia <ref>{{Cite pmid|28293421}}</ref> Protein misfolding in neurodegenerative diseases: implications and strategies #MMPMID28293421 Sweeney P; Park H; Baumann M; Dunlop J; Frydman J; Kopito R; McCampbell A; Leblanc G; Venkateswaran A; Nurmi A; Hodgson R Transl Neurodegener 2017[]; 6 (ä): ä PMID28293421show ga A hallmark of neurodegenerative proteinopathies is the formation of misfolded protein aggregates that cause cellular toxicity and contribute to cellular proteostatic collapse. Therapeutic options are currently being explored that target different steps in the production and processing of proteins implicated in neurodegenerative disease, including synthesis, chaperone-assisted folding and trafficking, and degradation via the proteasome and autophagy pathways. Other therapies, like mTOR inhibitors and activators of the heat shock response, can rebalance the entire proteostatic network. However, there are major challenges that impact the development of novel therapies, including incomplete knowledge of druggable disease targets and their mechanism of action as well as a lack of biomarkers to monitor disease progression and therapeutic response. A notable development is the creation of collaborative ecosystems that include patients, clinicians, basic and translational researchers, foundations and regulatory agencies to promote scientific rigor and clinical data to accelerate the development of therapies that prevent, reverse or delay the progression of neurodegenerative proteinopathies. äProtein misfolding in neurodegenerative diseases: implications and str(epmc).pdf DeepDyve Pubget Overpricing