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{"title"=>"A naturally occurring bovine tauopathy is geographically widespread in the UK", "type"=>"journal", "authors"=>[{"first_name"=>"Martin", "last_name"=>"Jeffrey", "scopus_author_id"=>"26643251800"}, {"first_name"=>"Pedro", "last_name"=>"Piccardo", "scopus_author_id"=>"7004382184"}, {"first_name"=>"Diane L.", "last_name"=>"Ritchie", "scopus_author_id"=>"7201711082"}, {"first_name"=>"James W.", "last_name"=>"Ironside", "scopus_author_id"=>"35445715400"}, {"first_name"=>"Alison J.E.", "last_name"=>"Green", "scopus_author_id"=>"7404025048"}, {"first_name"=>"Gillian", "last_name"=>"McGovern", "scopus_author_id"=>"6602822908"}], "year"=>2015, "source"=>"PLoS ONE", "identifiers"=>{"sgr"=>"84939223582", "pui"=>"605586092", "scopus"=>"2-s2.0-84939223582", "issn"=>"19326203", "doi"=>"10.1371/journal.pone.0129499", "pmid"=>"26091261"}, "id"=>"383b6ba0-8a24-3713-b1ee-ee6e92f7001a", "abstract"=>"Many human neurodegenerative diseases are associated with hyperphosphorylation and widespread intra-neuronal and glial associated aggregation of the microtubule associated protein tau. In contrast, animal tauopathies are not reported with only senescent animals showing inconspicuous tau labelling of fine processes albeit significant tau aggregation may occur in some experimental animal disease. Since 1986, an idiopathic neurological condition of adult cattle has been recognised in the UK as a sub-set of cattle slaughtered as suspect bovine spongiform encephalopathy cases. This disorder is characterised by brainstem neuronal chromatolysis and degeneration with variable hippocampal sclerosis and spongiform change. Selected cases of idiopathic brainstem neuronal chromatolysis (IBNC) were identified from archive material and characterised using antibodies specific to several tau hyperphosphorylation sites or different isoforms of the tau microtubule binding region. Labelling was also carried out for alpha synuclein, ubiquitin, TDP43, Aβ 1-42, Aβ 1-40. Widespread tau labelling was identified in all IBNC brains examined and with each of seven tau antibodies recognising different hyperphosphorylated sites. Labelling with each antibody was associated with dendrites, neuronal perikarya and glia. Thus IBNC is a sporadic, progressive neurological disease predominantly affecting aged cattle that occurs throughout the UK and is associated with hyperphosphorylation of tau, a rare example of a naturally-occurring tauopathy in a non-primate species. Secondary accumulation of alpha synuclein and ubiquitin was also present. The neuropathology does not precisely correspond with any human tauopathy. The cause of IBNC remains undetermined but environmental factors and exposure to agrochemicals needs to be considered in future aetiological investigations.", "link"=>"http://www.mendeley.com/research/naturally-occurring-bovine-tauopathy-geographically-widespread-uk", "reader_count"=>6, "reader_count_by_academic_status"=>{"Researcher"=>3, "Professor"=>3}, "reader_count_by_user_role"=>{"Researcher"=>3, "Professor"=>3}, "reader_count_by_subject_area"=>{"Biochemistry, Genetics and Molecular Biology"=>2, "Agricultural and Biological Sciences"=>1, "Medicine and Dentistry"=>1, "Neuroscience"=>1, "Veterinary Science and Veterinary Medicine"=>1}, "reader_count_by_subdiscipline"=>{"Medicine and Dentistry"=>{"Medicine and Dentistry"=>1}, "Neuroscience"=>{"Neuroscience"=>1}, "Agricultural and Biological Sciences"=>{"Agricultural and Biological Sciences"=>1}, "Biochemistry, Genetics and Molecular Biology"=>{"Biochemistry, Genetics and Molecular Biology"=>2}, "Veterinary Science and Veterinary Medicine"=>{"Veterinary Science and Veterinary Medicine"=>1}}, "reader_count_by_country"=>{"Italy"=>1}, "group_count"=>0}

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• http://doi.org/10.1590/0004-282x20180111
• http://doi.org/10.1016/j.molmed.2017.04.001
• http://doi.org/10.1016/j.jns.2017.10.040
• http://doi.org/10.1111/tbed.12884

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• {"type"=>"COMMENT", "annotationUri"=>"info:doi/10.1371/annotation/5adef4ac-a7e4-46a4-8806-c8533d5c862c", "title"=>"IBNC Tauopathy or TSE Prion disease, it appears, no one is sure", "body"=>"Greetings Plos et al, \n\nin reference to; \n\n‘’A Naturally Occurring Bovine Tauopathy Is Geographically Widespread in the UK’’\n\nI kindly wish to comment please, as follows.\n\nI was stunned by this report. \n\nThis Research Report should have been titled ;\n\n‘’It Appears A Naturally Occurring Bovine Tauopathy Is Geographically Widespread in the UK’’\n\n>>>Thus IBNC _appears_ to be the first naturally occurring and geographically widespread tauopathy in a species other than humans.<<< \n\n>>>IBNC _appear_ to lack intracellular neurofibrillary tangles,<<<\n\n>>>Thus IBNC _appears_ to be the first naturally occurring and geographically widespread tauopathy in a species other than humans<<<\n\n>>>IBNC appears to be a complex proteinopathy with evidence for additional secondary accumulation of alpha synuclein, ubiquitin, and possibly PrP [5]. <<<\n\n>>>however, it appears to represent a naturally-occurring predominantly 3R tauopathy in a non-primate species.<<<\n\n>>>In the absence of any specific aetiological cause of IBNC yet identified, and based on the existing epidemiology and presence of P-tau we have considered the possibility that IBNC might also have a significant environmental component. Epidemiological investigations to explore usage of herbicides, insecticides, parasiticides and other chemicals used in agriculture would be helpful in future investigations of IBNC and might provide further insight into some causes of neurodegeneration in man.<<< \n\nThis is supposition at best in my opinion, and at worse, I will refrain from comment.\n\nToo many _appears_ , appears this, appears that. \n\nToo many _In the absence of any specific aetiological cause of IBNC yet identified_\n\nis this what science has come to?\n\nhas science become some entwined with corporate special interest, do we change science now?\n\nI believe that is far too early to rule out IBNC as a Transmissible Spongiform Encephalopathy TSE prion disease, either of typical or typical strain.\n\nit can be argued that there is potential for Alzheimer’s to be a low dose TSE Prion disease ;\n\nhttp://www.plosone.org/annotation/listThread.action?root=82860 \n\nwhat about horizontal and or vertical transmission of an atypical strain of the BSE TSE prion disease into a low dose that is not detectible with TSE Prion testing to date?\n\nwhat about a completely different strain, another atypical, of the TSE prion disease, to low to detect to date, and I stress to date? \n\nto abandon the TSE prion and IBNC link there from would be foolish in my opinion. \n\nSEAC, FatPride, BSE Inquiry, have never found a link to pesticides, or OP’s, or metals, as a _cause_, to any TSE prion disease. \n\nI have also followed the metals, pesticide debate as a cause for the TSE prion disease. to date, this has proven to be fruitless for any _cause_ of the TSE prion disease. not to say the potential for these factors for one to be more susceptible to a TSE prion from surrounding environmental factors i.e. surrounding TSE prion exposures from the various routes and sources of the TSE prion disease (see metals and pesticide i.e. FatePride towards the bottom). from Mark Purdey and his research, to a farmer with BSE that treated his kids with OP’s for head lice, and nothing scientific to date has confirmed a link to the TSE prion disease as a _cause_. \n\nWe MUST not abandon transmission studies, and or any link to the TSE prion disease. \n\nIT appears, in the absence of any scientific link to any specific herbicides, insecticides, parasiticides and other chemicals to date to IBNC, to just explore other options instead of the transmission studies to prove one way or the other whether or not the IBNC or BBD or whatever you want to call this, while ignoring the existing epidemiology and knowledge of the TSE prion disease with the primitive TSE prion testing to date, it appears all this would be foolish, it appears this would be very questionable, in my opinion. ... \n\nTerry S. Singeltary Sr. \n\nREFERENCES \n\n1992 NEW BRAIN DISORDER 3. WHAT ABOUT REPORTS OF NEW FORM OF BSE ? http://collections.europarchive.org/tna/20090114131343/http://www.bseinquiry.gov.uk/files/yb/1992/10/26001001.pdf \n\n''THE LINE TO TAKE'' ON IBNC $$$ 1995 $$$ 1995 page 9 of 14 ; *** 31. Mr. Bradley informed the Committee that the CVO had informed the CMO about the IBNC results and the transmission from retina and he, like the Committee was satisfied that the controls already in place or proposed were adequate. ... http://web.archive.org/web/20030327015011/http://www.bseinquiry.gov.uk/files/yb/1995/06/21005001.pdf\n\nIN CONFIDENCE *** BSE ATYPICAL LESION DISTRIBUTION http://web.archive.org/web/20041226015813/http://www.bseinquiry.gov.uk/files/yb/1993/03/14001001.pdf \n\nBSE: BRAIN STEM NEURONAL CHROMATOLYSIS – ‘’BOVINE BRAIN DISORDER’’ http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1992/10/23002001.pdf \n\nzinc link to cows speculative http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1992/10/27002001.pdf\n\nDRAFT IN CONFIDENCE IDIOPATHIC BRAIN STEM NEURONAL CHROMATOLYSIS AND HIPPOCAMPAL SCLEROSIS (Vet. Rec. 1992, M Jeffrey, J W Wilemsith p359-362 http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1992/10/20003001.pdf \n\nBSE: DISCLOSURE OF INFORMATION AND FORECAST http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1992/10/12002001.pdf \n\nSEAC idiopathic brainstem neuronal chromatolysis IBNC 2009 http://webarchive.nationalarchives.gov.uk/20091010132922/http://www.seac.gov.uk/papers/102-2.pdf http://webarchive.nationalarchives.gov.uk/20091010132922/http://www.seac.gov.uk/minutes/draft102.pdf \n\nNEW RESULTS ON IDIOPATHIC BRAINSTEM NEURONAL CHROMATOLYSIS \"All of the 15 cattle tested showed that the brains had abnormally accumulated PrP\" http://webarchive.nationalarchives.gov.uk/20091010132922/http://www.seac.gov.uk/papers/102-2.pdf \n\nAtypical prion proteins and IBNC in cattle DEFRA project code SE1796 FOIA Final report These findings together might suggest an additional family of neurodegenerative diseases where the infectious form of PrP is not readily detected by our current diagnostic tests. IBNC is likely to represent a subset of this group of cattle. Based on these data, our overall conclusion is that a second type of BSE is unlikely to have co-existed at a high prevalence with the classical form in the cattle population during the UK epidemic. http://randd.defra.gov.uk/Document.aspx?Document=SE1796_8548_FIN.doc\n\nProject Documents • Final Report - Annex : Atypical prion proteins in cattle (10064k) • Final Report - SID5 : Atypical prion proteins in cattle (201k) http://randd.defra.gov.uk/Default.aspx?Menu=Menu&Module=More&Location=None&ProjectID=14257&FromSearch=Y&Publisher=1&SearchText=SE1796&SortString=ProjectCode&SortOrder=Asc&Paging=10#Description if links above do not work, see ; http://bse-atypical.blogspot.com/2010/07/atypical-prion-proteins-and-ibnc-in.html \n\nITEM 6 FATEPRIDE (SEAC 97/4) 35. ***However, there was no evidence that environmental factors, including manganese, cause disease. http://www.seac.gov.uk/papers/draft98-1.pdf http://webarchive.nationalarchives.gov.uk/20080726154405/http://www.seac.gov.uk/papers/draft98-1.pdf\n\nFATEPriDE KEY FINDINGS ORGANOPHOSPHATE NO RELATIONSHIP TO CAUSE TSE http://webarchive.nationalarchives.gov.uk/20080726154822/http://www.seac.gov.uk/papers/97-4.pdf\n\nOP'S MEETING WITH PURDEY http://web.archive.org/web/20010614051238/http://www.bseinquiry.gov.uk/files/yb/1994/02/09001001.pdf \n\nCopper deficiency in the young bovine results in dramatic decreases in brain copper concentration ***but does not alter brain prion protein biology L. R. Legleiter, J. W. Spears and H. C. Liu Department of Animal Science and Interdepartmental Nutrition Program, North Carolina State University, Raleigh, NC http://www.ncbi.nlm.nih.gov/pubmed/18599661 \n\nSEAC 103/1 SPONGIFORM ENCEPHALOPATHY ADVISORY COMMITTEE Draft minutes of the 102nd meeting held on 4th March 2009 Nobel House, 17 Smith Square, London SW1P 3JR\n\nhttp://webarchive.nationalarchives.gov.uk/20110205132946/http://www.seac.gov.uk/minutes/minutes102.pdf\n\nhttp://webarchive.nationalarchives.gov.uk/20110205132946/http://www.seac.gov.uk/minutes/minutes103.pdf\n\n\nFrom: Terry S. Singeltary Sr. \n\nSent: Tuesday, August 13, 2013 3:58 PM \n\nTo: Science.Advisory.Council@defra.gsi.gov.uk \n\nSubject: Idiopathic Brainstem Neuronal Chromatolysis (IBNC): a novel prion protein related disorder of cattle?\n\nGreetings Honorable Science Advisory Council et al @ DEFRA, \n\nI wish to ask a question about something I have seen no updates on, that concerns me. \n\nIDIOPATHIC BRAINSTEM NEURONAL CHROMATOLYSIS IBNC or what I some times call, IBNC BSE. \n\nI have seen nothing in the scientific literature updated on this in years, since around 2008, then it was like it fell off the face of the earth ?\n\ncan you please give me some sort of update on the IBNC BSE science to date ?\n\nhow many cases of IBNC BSE have been detected ?\n\nis there an ongoing surveillance for this the IBNC BSE, and are the BSE test even capable of detecting it ? \n\ncould the USA and or North America even detect, if they were even looking for it ? \n\nlatest studies, if any more since \"All of the 15 cattle tested showed that the brains had abnormally accumulated PrP\" ?\n\nthank you,\n\nkind regards, terry \n\nResearch article Idiopathic Brainstem Neuronal Chromatolysis (IBNC): a novel prion protein related disorder of cattle? Martin Jeffrey1*, Belinda Baquero Perez2, Stuart Martin1, Linda Terry2 and Lorenzo González1 \n\nhttp://www.biomedcentral.com/1746-6148/4/38 \n\n2015\n\nPRION 2015 ORAL AND POSTER CONGRESSIONAL ABSTRACTS\n\nO.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations \n\nEmmanuel Comoy, Jacqueline Mikol, Val\u0002erie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France \n\n***thus questioning the origin of human sporadic cases. We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.\n\n===============\n\nO.08: H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism: Clinical and pathologic features in wild-type and E211K cattle following intracranial inoculation \n\nS Jo Moore, M Heather West Greenlee, Jodi Smith, Eric Nicholson, Cathy Vrentas, and Justin Greenlee United States Department of Agriculture; Ames, IA USA \n\n***This study demonstrates that the phenotype of E211K H-type BSE remains stable when transmitted to cattle without the E211K polymorphism, and exhibits a number of features that differ from classical BSE in both wild-type and E211K cattle. \n\n==============\n\nP.108: Successful oral challenge of adult cattle with classical BSE\n\nSandor Dudas1,*, Kristina Santiago-Mateo1, Tammy Pickles1, Catherine Graham2, and Stefanie Czub1 1Canadian Food Inspection Agency; NCAD Lethbridge; Lethbridge, Alberta, Canada; 2Nova Scotia Department of Agriculture; Pathology Laboratory; Truro, Nova Scotia, Canada\n\n***Our study demonstrates susceptibility of adult cattle to oral transmission of classical BSE. We are further examining explanations for the unusual disease presentation in the third challenged animal.\n\n========================\n\nP.86: Estimating the risk of transmission of BSE and scrapie to ruminants and humans by protein misfolding cyclic amplification\n\nMorikazu Imamura, Naoko Tabeta, Yoshifumi Iwamaru, and Yuichi Murayama National Institute of Animal Health; Tsukuba, Japan\n\nAlthough these results were not compatible with the previous reports describing the lack of transmissibility of H-type BSE to ovine and human transgenic mice, ***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.\n\n================ \n\nP.136: Mother to offspring transmission of CWD—Detection in fawn tissues using the QuIC assay \n\nAmy Nalls, Erin McNulty, Clare Hoover, Jeanette Hayes-Klug, Kelly Anderson, Edward Hoover, and Candace Mathiason Colorado State University; Fort Collins, CO USA \n\n***Our findings demonstrate that transmission of prions from mother to offspring can occur, and *** may be underestimated for all prion diseases. \n\n=============== \n\nhttps://prion2015.files.wordpress.com/2015/05/programguide1.pdf \n\nALSO, PLEASE SEE ;\n\n31 Jan 2015 at 20:14 GMT \n\n*** Ruminant feed ban for cervids in the United States? ***\n\n31 Jan 2015 at 20:14 GMT \n\nhttp://www.plosone.org/annotation/listThread.action?root=85351 \n\nSaturday, May 30, 2015 PRION 2015 ORAL AND POSTER CONGRESSIONAL ABSTRACTS https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf \n\nWednesday, June 10, 2015 Zoonotic Potential of CWD Prions LATE-BREAKING ABSTRACTS https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf https://prion2015.files.wordpress.com/2015/05/programguide1.pdf\n\nNo documents available. Attachments View All (1) Docket No. APHIS-2014-0107 Bovine Spongiform Encephalopathy; Importation of Animals and Animal Products Singeltary Submission View Attachment: http://www.regulations.gov/#!documentDetail;D=APHIS-2014-0107-0003 \n\nPrion-like transmission and spreading of tau pathology Florence Clavaguera1, Jürgen Hench1, Michel Goedert2 and Markus Tolnay1,* DOI: 10.1111/nan.12197 http://onlinelibrary.wiley.com/doi/10.1111/nan.12197/abstract?campaign=wolacceptedarticle \n\nSaturday, October 19, 2013 A comparative study of modified confirmatory techniques and additional immuno-based methods for non-conclusive autolytic Bovine spongiform encephalopathy cases http://www.biomedcentral.com/content/pdf/1746-6148-9-212.pdf \n\nspontaneous atypical BSE ??? As of December 2011, around 60 atypical BSE cases have currently been reported in 13 countries, *** with over one third in France. http://www.biomedcentral.com/1746-6148/8/74 \n\nThursday, July 24, 2014 *** Protocol for further laboratory investigations into the distribution of infectivity of Atypical BSE SCIENTIFIC REPORT OF EFSA New protocol for Atypical BSE investigations http://bse-atypical.blogspot.com/2014/07/protocol-for-further-laboratory.html \n\nP.66: Transport of CWD prions in Alberta soils Alsu Kuznetsova1, Debbie McKenzie2, Tariq Siddique1, and Judd Aiken2 1University of Alberta; Department of Renewable Resources; Edmonton, Canada; 2University of Alberta; Centre for Prions and Protein Folding Diseases; Edmonton, Canada\n\nP.161: Prion soil binding may explain efficient horizontal CWD transmission Nathaniel Denkers1, Davin Henderson1, Shannon Bartelt-Hunt2, Jason Bartz3, and Edward Hoover1 1Colorado State University; Fort Collins, Colorado USA; 2University of Nebraska-Lincoln; Omaha, Nebraska USA; 3Creighton University; Omaha, Nebraska USA Conclusion. Silty clay loam exhibits highly efficient prion binding, inferring a durable environmental reservoir, and an efficient mechanism for indirect horizontal CWD transmission. https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf \n\nTuesday, June 23, 2015 Report on the monitoring and testing of ruminants for the presence of transmissible spongiform encephalopathies (TSEs) in the EU in 2013 Final version 18 May 2015 http://transmissiblespongiformencephalopathy.blogspot.com/2015/06/report-on-monitoring-and-testing-of.html \n\nend...TSS ", "isRemoved"=>false, "created"=>"2015-07-03T16:53:14Z", "lastModified"=>"2015-07-03T16:53:14Z", "creator"=>{"userId"=>"118765"}, "highlightedText"=>"", "competingInterestStatement"=>{"creatorWasPrompted"=>true, "hasCompetingInterests"=>false}, "parentArticle"=>{"doi"=>"info:doi/10.1371/journal.pone.0129499", "state"=>"published", "journals"=>{"PLoSONE"=>{"journalKey"=>"PLoSONE", "eIssn"=>"1932-6203", "title"=>"PLOS ONE"}}}, "replyTreeSize"=>0, "mostRecentActivity"=>"2015-07-03T16:53:14Z", "replies"=>[]}

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• {"month"=>"6", "year"=>"2018", "pdf_views"=>"5", "xml_views"=>"0", "html_views"=>"8"}
• {"month"=>"7", "year"=>"2018", "pdf_views"=>"2", "xml_views"=>"3", "html_views"=>"9"}
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Figshare

• {"files"=>["https://ndownloader.figshare.com/files/2126795"], "description"=>"<p>(a) Parallel punctuate labelling along dendrites (arrows) and around the perikarya of two neurons in the hypoglossal nucleus. (b) Punctuate neuronal perikaryonal land dendritic labelling in the thalamus. Note vacuolation of some affected neurons. (c) No ubiquitin labelling of neurons or neuropil in the thalamus of a control cow brain. Bars: a = 20μm; b = 100μm; c = 50 μm.</p>", "links"=>[], "tags"=>["tau antibodies recognising", "future aetiological investigations", "uk", "antibody", "spongiform encephalopathy cases", "tau labelling", "tdp", "tau microtubule binding region", "Occurring Bovine Tauopathy", "tau hyperphosphorylation sites", "IBNC"], "article_id"=>1454882, "categories"=>["Biological Sciences"], "users"=>["Martin Jeffrey", "Pedro Piccardo", "Diane L. Ritchie", "James W. Ironside", "Alison J. E. Green", "Gillian McGovern"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0129499.g005", "stats"=>{"downloads"=>1, "page_views"=>11, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Ubiquitin_immunohistochemistry_/1454882", "title"=>"Ubiquitin immunohistochemistry.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2015-06-19 03:06:20"}
• {"files"=>["https://ndownloader.figshare.com/files/2126797"], "description"=>"<p>Western blot analysis of tau isoforms within the thalamus (Th), cerebellum (Cb) and hippocampus (H) from a single case of IBNC. Tau isoforms in the brains of animals in which no P-tau was detected (control A and control B) following immunohistochemistry are shown on the blot for comparison.</p>", "links"=>[], "tags"=>["tau antibodies recognising", "future aetiological investigations", "uk", "antibody", "spongiform encephalopathy cases", "tau labelling", "tdp", "tau microtubule binding region", "Occurring Bovine Tauopathy", "tau hyperphosphorylation sites", "IBNC"], "article_id"=>1454884, "categories"=>["Biological Sciences"], "users"=>["Martin Jeffrey", "Pedro Piccardo", "Diane L. Ritchie", "James W. Ironside", "Alison J. E. Green", "Gillian McGovern"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0129499.g006", "stats"=>{"downloads"=>1, "page_views"=>21, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Western_Blot_for_tau_on_IBNC_brains_and_controls_/1454884", "title"=>"Western Blot for tau on IBNC brains and controls.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2015-06-19 03:06:20"}
• {"files"=>["https://ndownloader.figshare.com/files/2126799"], "description"=>"<p>* data from Defra website</p><p>** data from personal hand–written notes</p><p>*** peak of the UK BSE epidemic</p><p>NA data not available.</p><p>Table showing annual frequency of IBNC cases relative to negative subset and confirmed cases of BSE in Scotland.</p>", "links"=>[], "tags"=>["tau antibodies recognising", "future aetiological investigations", "uk", "antibody", "spongiform encephalopathy cases", "tau labelling", "tdp", "tau microtubule binding region", "Occurring Bovine Tauopathy", "tau hyperphosphorylation sites", "IBNC"], "article_id"=>1454886, "categories"=>["Biological Sciences"], "users"=>["Martin Jeffrey", "Pedro Piccardo", "Diane L. Ritchie", "James W. Ironside", "Alison J. E. Green", "Gillian McGovern"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0129499.t001", "stats"=>{"downloads"=>6, "page_views"=>9, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Table_showing_annual_frequency_of_IBNC_cases_relative_to_negative_subset_and_confirmed_cases_of_BSE_in_Scotland_/1454886", "title"=>"Table showing annual frequency of IBNC cases relative to negative subset and confirmed cases of BSE in Scotland.", "pos_in_sequence"=>0, "defined_type"=>3, "published_date"=>"2015-06-19 03:06:20"}
• {"files"=>["https://ndownloader.figshare.com/files/2126800"], "description"=>"<p>*variable Western blot immune-phenotypes are reported in Argyrophilic grain disease [<a href=\"http://www.plosone.org/article/info:doi/10.1371/journal.pone.0129499#pone.0129499.ref028\" target=\"_blank\">28</a>].</p><p>Table showing characteristics of some human tauopathies compared with IBNC.</p>", "links"=>[], "tags"=>["tau antibodies recognising", "future aetiological investigations", "uk", "antibody", "spongiform encephalopathy cases", "tau labelling", "tdp", "tau microtubule binding region", "Occurring Bovine Tauopathy", "tau hyperphosphorylation sites", "IBNC"], "article_id"=>1454887, "categories"=>["Biological Sciences"], "users"=>["Martin Jeffrey", "Pedro Piccardo", "Diane L. Ritchie", "James W. Ironside", "Alison J. E. Green", "Gillian McGovern"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0129499.t002", "stats"=>{"downloads"=>5, "page_views"=>12, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Table_showing_characteristics_of_some_human_tauopathies_compared_with_IBNC_/1454887", "title"=>"Table showing characteristics of some human tauopathies compared with IBNC.", "pos_in_sequence"=>0, "defined_type"=>3, "published_date"=>"2015-06-19 03:06:20"}
• {"files"=>["https://ndownloader.figshare.com/files/2126773"], "description"=>"<p>Presence or absence of labelling of dendrites of the CA1 sector of hippocampus from a single case of IBNC following labelling with multiple tau specific antibodies. Panels show labelling with antibodies specific to hyperphosphorylated threonine or serine residues: a, threonine 205; b, threonine 212; c, serine 214; d, threonine 231; e, serine 396; f, serine 404. Labelling is also shown for antibodies specific to 3 repeat (g) or 4 repeat (h) isoforms. Bars = 100μm.</p>", "links"=>[], "tags"=>["tau antibodies recognising", "future aetiological investigations", "uk", "antibody", "spongiform encephalopathy cases", "tau labelling", "tdp", "tau microtubule binding region", "Occurring Bovine Tauopathy", "tau hyperphosphorylation sites", "IBNC"], "article_id"=>1454864, "categories"=>["Biological Sciences"], "users"=>["Martin Jeffrey", "Pedro Piccardo", "Diane L. Ritchie", "James W. Ironside", "Alison J. E. Green", "Gillian McGovern"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0129499.g001", "stats"=>{"downloads"=>0, "page_views"=>9, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Hippocampal_tau_and_P_tau_labelling_with_8_antibodies_/1454864", "title"=>"Hippocampal tau and P-tau labelling with 8 antibodies.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2015-06-19 03:06:20"}
• {"files"=>["https://ndownloader.figshare.com/files/2126778"], "description"=>"<p>Glial associated patterns of immunohistochemical labelling with AT8 antibody. (a) Striatum showing white and grey matter labelling of glial cells. (b) Detail of glial cells in hippocampus showing stellate morphology. (c) Further detail of glia labelling showing stellate pattern and loss of glial cytoplasm with maintained peripheral rim of labelling. (d) Control cow brain with encephalic listeriosis. No labelling for P-tau is present. Bars: a = 200μm; b = 100μm; c = 20μm; d = 200μm.</p>", "links"=>[], "tags"=>["tau antibodies recognising", "future aetiological investigations", "uk", "antibody", "spongiform encephalopathy cases", "tau labelling", "tdp", "tau microtubule binding region", "Occurring Bovine Tauopathy", "tau hyperphosphorylation sites", "IBNC"], "article_id"=>1454868, "categories"=>["Biological Sciences"], "users"=>["Martin Jeffrey", "Pedro Piccardo", "Diane L. Ritchie", "James W. Ironside", "Alison J. E. Green", "Gillian McGovern"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0129499.g002", "stats"=>{"downloads"=>3, "page_views"=>11, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Glial_P_tau_labelling_/1454868", "title"=>"Glial P-tau labelling.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2015-06-19 03:06:20"}
• {"files"=>["https://ndownloader.figshare.com/files/2126783"], "description"=>"<p>Dendrite and peri-neuronal tau immunohistochemical labelling patterns with AT8 antibody. (a) Detail of dendritic labelling of CA1 dendrites in hippocampus. Parallel rows of puncta suggest labelling is at or adjacent to the plasma-membrane. (b) Labelling around the perikarya and processes of neurons in the thalamus. (c) Some dendrites that are labelled with AT8 also appear to be the origins of loculated vacuoles. Bars: 100μm.</p>", "links"=>[], "tags"=>["tau antibodies recognising", "future aetiological investigations", "uk", "antibody", "spongiform encephalopathy cases", "tau labelling", "tdp", "tau microtubule binding region", "Occurring Bovine Tauopathy", "tau hyperphosphorylation sites", "IBNC"], "article_id"=>1454873, "categories"=>["Biological Sciences"], "users"=>["Martin Jeffrey", "Pedro Piccardo", "Diane L. Ritchie", "James W. Ironside", "Alison J. E. Green", "Gillian McGovern"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0129499.g003", "stats"=>{"downloads"=>3, "page_views"=>25, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Neuronal_and_dendritic_P_tau_labelling_/1454873", "title"=>"Neuronal and dendritic P-tau labelling.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2015-06-19 03:06:20"}
• {"files"=>["https://ndownloader.figshare.com/files/2126789"], "description"=>"<p>(a) Generalised punctuate pattern of neuropil labelling in the dorso-lateral geniculate nucleus of the midbrain sparing neuronal perikarya. (b) Punctuate pattern labelling of dendrites in the substantia nigra. (c) Punctuate labelling of neuropil associated with dentate gyrus of hippocampus. (d) No labelling for alpha synuclein in the dentate gyrus of a control cow. Bars: 100μm.</p>", "links"=>[], "tags"=>["tau antibodies recognising", "future aetiological investigations", "uk", "antibody", "spongiform encephalopathy cases", "tau labelling", "tdp", "tau microtubule binding region", "Occurring Bovine Tauopathy", "tau hyperphosphorylation sites", "IBNC"], "article_id"=>1454879, "categories"=>["Biological Sciences"], "users"=>["Martin Jeffrey", "Pedro Piccardo", "Diane L. Ritchie", "James W. Ironside", "Alison J. E. Green", "Gillian McGovern"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0129499.g004", "stats"=>{"downloads"=>2, "page_views"=>22, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Alpha_synuclein_immunohistochemistry_/1454879", "title"=>"Alpha synuclein immunohistochemistry.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2015-06-19 03:06:20"}

PMC Usage Stats | Further Information

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• {"unique-ip"=>"4", "full-text"=>"5", "pdf"=>"1", "scanned-summary"=>"0", "scanned-page-browse"=>"0", "figure"=>"0", "supp-data"=>"0", "cited-by"=>"0", "year"=>"2018", "month"=>"10"}
• {"unique-ip"=>"3", "full-text"=>"1", "pdf"=>"1", "scanned-summary"=>"0", "scanned-page-browse"=>"0", "figure"=>"4", "supp-data"=>"0", "cited-by"=>"0", "year"=>"2018", "month"=>"11"}
• {"unique-ip"=>"5", "full-text"=>"6", "pdf"=>"1", "scanned-summary"=>"0", "scanned-page-browse"=>"0", "figure"=>"0", "supp-data"=>"0", "cited-by"=>"0", "year"=>"2018", "month"=>"9"}
• {"unique-ip"=>"1", "full-text"=>"0", "pdf"=>"2", "scanned-summary"=>"0", "scanned-page-browse"=>"0", "figure"=>"0", "supp-data"=>"0", "cited-by"=>"0", "year"=>"2019", "month"=>"2"}
• {"unique-ip"=>"9", "full-text"=>"7", "pdf"=>"3", "scanned-summary"=>"0", "scanned-page-browse"=>"0", "figure"=>"0", "supp-data"=>"0", "cited-by"=>"0", "year"=>"2019", "month"=>"3"}
• {"unique-ip"=>"5", "full-text"=>"2", "pdf"=>"2", "scanned-summary"=>"0", "scanned-page-browse"=>"0", "figure"=>"2", "supp-data"=>"0", "cited-by"=>"0", "year"=>"2019", "month"=>"4"}
• {"unique-ip"=>"8", "full-text"=>"8", "pdf"=>"1", "scanned-summary"=>"0", "scanned-page-browse"=>"0", "figure"=>"0", "supp-data"=>"0", "cited-by"=>"0", "year"=>"2019", "month"=>"5"}

Relative Metric

{"start_date"=>"2015-01-01T00:00:00Z", "end_date"=>"2015-12-31T00:00:00Z", "subject_areas"=>[]}

F1000Prime