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10.1212/NXI.0000000000000474 http://scihub22266oqcxt.onion/10.1212/NXI.0000000000000474 C6039209!6039209!29998156     free     free     free Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\29998156.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Neurol+Neuroimmunol+Neuroinflamm 2018 ; 5 (5): ä Nephropedia Template TP {{tp|p=29998156|t=2018. Autoimmune septin-5 cerebellar ataxia |pdf=|usr=}}{{29998156}} gab.com Text Autoimmune septin-5 cerebellar ataxia JO: Neurol Neuroimmunol Neuroinflamm http://www.kidney.de/pget.php?&tw=1&pmid=29998156 #FOAvip Objective: To report a form of autoimmune cerebellar ataxia in which antibodies target septin-5, a guanosine triphosphate (GTP)-binding neural protein involved in neurotransmitter exocytosis. Methods: Archived sera and CSF specimens with unclassified synaptic antibodies were re-evaluated by tissue-based indirect immunofluorescence assay. Autoantigens were identified by Western blot and mass spectrometry. Recombinant protein assays (Western blot, cell based, and protein screening array) confirmed antigen specificity. Results: Serum and CSF from 6 patients produced identical synaptic immunoglobulin G (IgG) staining patterns of synaptic regions (neuropil) of the mouse cerebrum and cerebellum. The molecular layer of the cerebellum and the thalamus demonstrated stronger immunoreactivity than the midbrain, hippocampus, cortex, and basal ganglia. The antigen revealed by mass spectrometry analysis of immunoprecipitated cerebellar proteins and confirmed by recombinant protein assays was septin-5. All 4 patients with records available had subacute onset of cerebellar ataxia with prominent eye movement symptoms (oscillopsia or vertigo). None had cancer detected. Improvements occurred after immunotherapies (2) or spontaneously (1). One patient died. Conclusion: Septin-5 IgG represents a biomarker for a potentially fatal but treatable autoimmune ataxia. Twit Text FOAVip Autoimmune septin-5 cerebellar ataxia ????Neurol Neuroimmunol Neuroinflamm http://www.kidney.de/pget.php?&tw=1&pmid=29998156 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29998156 #FOAvip English Wikipedia <ref>{{Cite pmid|29998156}}</ref> Autoimmune septin-5 cerebellar ataxia #MMPMID29998156 Honorat JA; Lopez-Chiriboga AS; Kryzer TJ; Fryer JP; Devine M; Flores A; Lennon VA; Pittock SJ; McKeon A Neurol Neuroimmunol Neuroinflamm 2018[Sep]; 5 (5): ä PMID29998156show ga Objective: To report a form of autoimmune cerebellar ataxia in which antibodies target septin-5, a guanosine triphosphate (GTP)-binding neural protein involved in neurotransmitter exocytosis. Methods: Archived sera and CSF specimens with unclassified synaptic antibodies were re-evaluated by tissue-based indirect immunofluorescence assay. Autoantigens were identified by Western blot and mass spectrometry. Recombinant protein assays (Western blot, cell based, and protein screening array) confirmed antigen specificity. Results: Serum and CSF from 6 patients produced identical synaptic immunoglobulin G (IgG) staining patterns of synaptic regions (neuropil) of the mouse cerebrum and cerebellum. The molecular layer of the cerebellum and the thalamus demonstrated stronger immunoreactivity than the midbrain, hippocampus, cortex, and basal ganglia. The antigen revealed by mass spectrometry analysis of immunoprecipitated cerebellar proteins and confirmed by recombinant protein assays was septin-5. All 4 patients with records available had subacute onset of cerebellar ataxia with prominent eye movement symptoms (oscillopsia or vertigo). None had cancer detected. Improvements occurred after immunotherapies (2) or spontaneously (1). One patient died. Conclusion: Septin-5 IgG represents a biomarker for a potentially fatal but treatable autoimmune ataxia. äAutoimmune septin-5 cerebellar ataxia (epmc).pdf DeepDyve Pubget Overpricing