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10.1007/s00401-013-1123-8 http://scihub22266oqcxt.onion/10.1007/s00401-013-1123-8 23666556/?report=reader!3690181!23666556     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 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       Acta+Neuropathol 2013 ; 126 (1): 39-50 Nephropedia Template TP {{tp|p=23666556|t=2013. Robust cytoplasmic accumulation of phosphorylated TDP-43 in transgenic models of tauopathy |pdf=|usr=}}{{23666556}} gab.com Text Robust cytoplasmic accumulation of phosphorylated TDP-43 in transgenic models of tauopathy JO: Acta Neuropathol http://www.kidney.de/pget.php?&tw=1&pmid=23666556 #FOAvip Frontotemporal lobar degeneration (FTLD) has been subdivided based on the main pathology found in the brains of affected individuals. When the primary pathology is aggregated, hyperphosphorylated tau, the pathological diagnosis is FTLD-tau. When the primary pathology is cytoplasmic and/or nuclear aggregates of phosphorylated TAR-DNA-binding protein (TDP-43), the pathological diagnosis is FTLD-TDP. Notably, TDP-43 pathology can also occur in conjunction with a number of neurodegenerative disorders; however, unknown environmental and genetic factors may regulate this TDP-43 pathology. Using transgenic mouse models of several diseases of the central nervous system, we explored whether a primary proteinopathy might secondarily drive TDP-43 proteinopathy. We found abnormal, cytoplasmic accumulation of phosphorylated TDP-43 specifically in two tau transgenic models, but TDP-43 pathology was absent in mouse models of Abeta deposition, alpha-synucleinopathy or Huntington's disease. Though tau pathology showed considerable overlap with cytoplasmic, phosphorylated TDP-43, tau pathology generally preceded TDP-43 pathology. Biochemical analysis confirmed the presence of TDP-43 abnormalities in the tau mice, which showed increased levels of high molecular weight, soluble TDP-43 and insoluble full-length and ~35 kD TDP-43. These data demonstrate that the neurodegenerative cascade associated with a primary tauopathy in tau transgenic mice can also promote TDP-43 abnormalities. These findings provide the first in vivo models to understand how TDP-43 pathology may arise as a secondary consequence of a primary proteinopathy. Twit Text FOAVip Robust cytoplasmic accumulation of phosphorylated TDP-43 in transgenic models of tauopathy ????Acta Neuropathol http://www.kidney.de/pget.php?&tw=1&pmid=23666556 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=23666556 #FOAvip English Wikipedia <ref>{{Cite pmid|23666556}}</ref> Robust cytoplasmic accumulation of phosphorylated TDP-43 in transgenic models of tauopathy #MMPMID23666556 Clippinger AK; D'Alton S; Lin WL; Gendron TF; Howard J; Borchelt DR; Cannon A; Carlomagno Y; Chakrabarty P; Cook C; Golde TE; Levites Y; Ranum L; Schultheis PJ; Xu G; Petrucelli L; Sahara N; Dickson DW; Giasson B; Lewis J Acta Neuropathol 2013[Jul]; 126 (1): 39-50 PMID23666556show ga Frontotemporal lobar degeneration (FTLD) has been subdivided based on the main pathology found in the brains of affected individuals. When the primary pathology is aggregated, hyperphosphorylated tau, the pathological diagnosis is FTLD-tau. When the primary pathology is cytoplasmic and/or nuclear aggregates of phosphorylated TAR-DNA-binding protein (TDP-43), the pathological diagnosis is FTLD-TDP. Notably, TDP-43 pathology can also occur in conjunction with a number of neurodegenerative disorders; however, unknown environmental and genetic factors may regulate this TDP-43 pathology. Using transgenic mouse models of several diseases of the central nervous system, we explored whether a primary proteinopathy might secondarily drive TDP-43 proteinopathy. We found abnormal, cytoplasmic accumulation of phosphorylated TDP-43 specifically in two tau transgenic models, but TDP-43 pathology was absent in mouse models of Abeta deposition, alpha-synucleinopathy or Huntington's disease. Though tau pathology showed considerable overlap with cytoplasmic, phosphorylated TDP-43, tau pathology generally preceded TDP-43 pathology. Biochemical analysis confirmed the presence of TDP-43 abnormalities in the tau mice, which showed increased levels of high molecular weight, soluble TDP-43 and insoluble full-length and ~35 kD TDP-43. These data demonstrate that the neurodegenerative cascade associated with a primary tauopathy in tau transgenic mice can also promote TDP-43 abnormalities. These findings provide the first in vivo models to understand how TDP-43 pathology may arise as a secondary consequence of a primary proteinopathy. |Amyloid beta-Protein Precursor/genetics[MESH] |Animals[MESH] |Brain/metabolism/*pathology[MESH] |Cytoplasm/*metabolism/pathology/ultrastructure[MESH] |DNA-Binding Proteins/*metabolism/ultrastructure[MESH] |Disease Models, Animal[MESH] |Gene Expression Regulation/genetics[MESH] |Humans[MESH] |Mice[MESH] |Mice, Transgenic[MESH] |Microscopy, Immunoelectron[MESH] |Mutation/genetics[MESH] |Neurons/*pathology/ultrastructure[MESH] |Phosphorylation/genetics[MESH] |Polycomb-Group Proteins[MESH] |Presenilin-1/genetics[MESH] |Tauopathies/genetics/*pathology[MESH] |Transcription Factors/metabolism[MESH]Robust cytoplasmic accumulation of phosphorylated TDP-43 in transgenic(epmc).pdf DeepDyve Pubget Overpricing