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10.1523/JNEUROSCI.1787-16.2017 http://scihub22266oqcxt.onion/10.1523/JNEUROSCI.1787-16.2017 C5637112!5637112!29021297     free     free     free       J+Neurosci 2017 ; 37 (41): 9799-807 Nephropedia Template TP {{tp|p=29021297|t=2017. Parkinson s Disease Is Not Simply a Prion Disorder |pdf=|usr=}}{{29021297}} gab.com Text Parkinson s Disease Is Not Simply a Prion Disorder JO: J Neurosci http://www.kidney.de/pget.php?&tw=1&pmid=29021297 #FOAvip The notion that prion-like spreading of misfolded ?-synuclein (?-SYN) causes Parkinson's disease (PD) has received a great deal of attention. Although attractive in its simplicity, the hypothesis is difficult to reconcile with postmortem analysis of human brains and connectome-mapping studies. An alternative hypothesis is that PD pathology is governed by regional or cell-autonomous factors. Although these factors provide an explanation for the pattern of neuronal loss in PD, they do not readily explain the apparently staged distribution of Lewy pathology in many PD brains, the feature of the disease that initially motivated the spreading hypothesis by Braak and colleagues. While each hypothesis alone has its shortcomings, a synthesis of the two can explain much of what we know about the etiopathology of PD.Dual Perspectives Companion Paper:Prying into the Prion Hypothesis for Parkinson's Disease, by Patrik Brundin and Ronald Melki Twit Text FOAVip Parkinson s Disease Is Not Simply a Prion Disorder ????J Neurosci http://www.kidney.de/pget.php?&tw=1&pmid=29021297 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29021297 #FOAvip English Wikipedia <ref>{{Cite pmid|29021297}}</ref> Parkinson s Disease Is Not Simply a Prion Disorder #MMPMID29021297 Surmeier DJ; Obeso JA; Halliday GM J Neurosci 2017[Oct]; 37 (41): 9799-807 PMID29021297show ga The notion that prion-like spreading of misfolded ?-synuclein (?-SYN) causes Parkinson's disease (PD) has received a great deal of attention. Although attractive in its simplicity, the hypothesis is difficult to reconcile with postmortem analysis of human brains and connectome-mapping studies. An alternative hypothesis is that PD pathology is governed by regional or cell-autonomous factors. Although these factors provide an explanation for the pattern of neuronal loss in PD, they do not readily explain the apparently staged distribution of Lewy pathology in many PD brains, the feature of the disease that initially motivated the spreading hypothesis by Braak and colleagues. While each hypothesis alone has its shortcomings, a synthesis of the two can explain much of what we know about the etiopathology of PD.Dual Perspectives Companion Paper:Prying into the Prion Hypothesis for Parkinson's Disease, by Patrik Brundin and Ronald Melki äParkinson s Disease Is Not Simply a Prion Disorder (epmc).pdf DeepDyve Pubget Overpricing