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10.1007/s00401-016-1649-7 http://scihub22266oqcxt.onion/10.1007/s00401-016-1649-7 C5325841!5325841 !27885490     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\27885490 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Acta+Neuropathol 2017 ; 133 (3 ): 353-366 Nephropedia Template TP {{tp|p=27885490 |t=2017. Localized cortical chronic traumatic encephalopathy pathology after single, severe axonal injury in human brain |pdf=|usr=}}{{27885490 }} gab.com Text Localized cortical chronic traumatic encephalopathy pathology after single, severe axonal injury in human brain JO: Acta Neuropathol http://www.kidney.de/pget.php?&tw=1&pmid=27885490 #FOAvip Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease associated with repetitive mild impact traumatic brain injury from contact sports. Recently, a consensus panel defined the pathognomonic lesion for CTE as accumulations of abnormally hyperphosphorylated tau (p-tau) in neurons (neurofibrillary tangles), astrocytes and cell processes distributed around small blood vessels at sulcal depths in irregular patterns within the cortex. The pathophysiological mechanism for this lesion is unknown. Moreover, a subset of CTE cases harbors cortical ?-amyloid plaques. In this study, we analyzed postmortem brain tissues from five institutionalized patients with schizophrenia and history of surgical leucotomy with subsequent survival of at least another 40 years. Because leucotomy involves severing axons bilaterally in prefrontal cortex, this surgical procedure represents a human model of single traumatic brain injury with severe axonal damage and no external impact. We examined cortical tissues at the leucotomy site and at both prefrontal cortex rostral and frontal cortex caudal to the leucotomy site. For comparison, we analyzed brain tissues at equivalent neuroanatomical sites from non-leucotomized patients with schizophrenia, matched in age and gender. All five leucotomy cases revealed severe white matter damage with dense astrogliosis at the axotomy site and also neurofibrillary tangles and p-tau immunoreactive neurites in the overlying gray matter. Four cases displayed p-tau immunoreactivity in neurons, astrocytes and cell processes encompassing blood vessels at cortical sulcal depths in irregular patterns, similar to CTE. The three cases with apolipoprotein E ?4 haplotype showed scattered ?-amyloid plaques in the overlying gray matter, but not the two cases with apolipoprotein E ?3/3 genotype. Brain tissue samples from prefrontal cortex rostral and frontal cortex caudal to the leucotomy site, and all cortical samples from the non-leucotomized patients, showed minimal p-tau and ?-amyloid pathology. These findings suggest that chronic axonal damage contributes to the unique pathology of CTE over time. Twit Text FOAVip Localized cortical chronic traumatic encephalopathy pathology after single, severe axonal injury in human brain ????Acta Neuropathol http://www.kidney.de/pget.php?&tw=1&pmid=27885490 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27885490 #FOAvip English Wikipedia <ref>{{Cite pmid|27885490 }}</ref> Localized cortical chronic traumatic encephalopathy pathology after single, severe axonal injury in human brain #MMPMID27885490 Shively SB ; Edgerton SL ; Iacono D ; Purohit DP ; Qu BX ; Haroutunian V ; Davis KL ; Diaz-Arrastia R ; Perl DP Acta Neuropathol 2017[Mar]; 133 (3 ): 353-366 PMID27885490 show ga Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease associated with repetitive mild impact traumatic brain injury from contact sports. Recently, a consensus panel defined the pathognomonic lesion for CTE as accumulations of abnormally hyperphosphorylated tau (p-tau) in neurons (neurofibrillary tangles), astrocytes and cell processes distributed around small blood vessels at sulcal depths in irregular patterns within the cortex. The pathophysiological mechanism for this lesion is unknown. Moreover, a subset of CTE cases harbors cortical ?-amyloid plaques. In this study, we analyzed postmortem brain tissues from five institutionalized patients with schizophrenia and history of surgical leucotomy with subsequent survival of at least another 40 years. Because leucotomy involves severing axons bilaterally in prefrontal cortex, this surgical procedure represents a human model of single traumatic brain injury with severe axonal damage and no external impact. We examined cortical tissues at the leucotomy site and at both prefrontal cortex rostral and frontal cortex caudal to the leucotomy site. For comparison, we analyzed brain tissues at equivalent neuroanatomical sites from non-leucotomized patients with schizophrenia, matched in age and gender. All five leucotomy cases revealed severe white matter damage with dense astrogliosis at the axotomy site and also neurofibrillary tangles and p-tau immunoreactive neurites in the overlying gray matter. Four cases displayed p-tau immunoreactivity in neurons, astrocytes and cell processes encompassing blood vessels at cortical sulcal depths in irregular patterns, similar to CTE. The three cases with apolipoprotein E ?4 haplotype showed scattered ?-amyloid plaques in the overlying gray matter, but not the two cases with apolipoprotein E ?3/3 genotype. Brain tissue samples from prefrontal cortex rostral and frontal cortex caudal to the leucotomy site, and all cortical samples from the non-leucotomized patients, showed minimal p-tau and ?-amyloid pathology. These findings suggest that chronic axonal damage contributes to the unique pathology of CTE over time. |Aged [MESH] |Aged, 80 and over [MESH] |Antigens, CD/metabolism [MESH] |Antigens, Differentiation, Myelomonocytic/metabolism [MESH] |Apolipoproteins E/genetics [MESH] |Cerebral Cortex/*pathology [MESH] |Chronic Traumatic Encephalopathy/*pathology [MESH] |Female [MESH] |Glial Fibrillary Acidic Protein/metabolism [MESH] |Humans [MESH] |Male [MESH] |Neurofibrillary Tangles/*pathology [MESH] |Neurons/metabolism/pathology [MESH] |Plaque, Amyloid/*pathology [MESH] |Psychosurgery [MESH] |Schizophrenia/complications/pathology [MESH]Localized cortical chronic traumatic encephalopathy pathology after si(epmc).pdf DeepDyve Pubget Overpricing