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1.

001-es BibID:BIBFORM063502
Első szerző:Baek, Jean-Ha
Cím:Unfolded protein response is activated in Lewy body dementias / J.-H. Baek, D. Whitfield, D. Howlett, P. Francis, E. Bereczki, C. Ballard, T. Hortobágyi, J. Attems, D. Aarsland
Dátum:2016
ISSN:0305-1846
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Neuropathology And Applied Neurobiology 42 : 4 (2016), p. 352-365. -
További szerzők:Whitfield, David Howlett, David R. Francis, Paul T. Bereczki Erika Ballard, Clive G. Hortobágyi Tibor (1965-) (patológus) Attems, Johannes Aarsland, Dag
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2.

001-es BibID:BIBFORM063675
Első szerző:Berghoff, Anna S.
Cím:Atypical sporadic CJD-MM phenotype with white matter kuru plaques associated with intranuclear inclusion body and argyrophilic grain disease / Anna S. Berghoff, Anita Trummert, Ursula Unterberger, Thomas Ströbel, Tibor Hortobágyi, Gabor G. Kovacs
Dátum:2015
ISSN:0919-6544
Megjegyzések:We describe an atypical neuropathological phenotype ofsporadic Creutzfeldt-Jakob disease in a 76-year-old man.The clinical symptoms were characterized by progressivedementia, gait ataxia, rigidity and urinary incontinence.Thedisease duration was 6 weeks.MRI did not show prominentatrophy or hyperintensities in cortical areas, striatum orthalamus.Biomarker examination of the cerebrospinal fluiddeviated from that seen in pure Alzheimer's disease.Triphasic waves in the EEG were detected only later in thedisease course, while 14-3-3 assay was positive. PRNPgenotyping revealed methionine homozygosity (MM) atcodon 129. Neuropathology showed classical CJD changescorresponding to the MM type 1 cases. However, a strikingfeature was the presence of abundant kuru-type plaques inthe white matter. This rare morphology was associated withneuropathological signs of intranuclear inclusion bodydisease and advanced stage of argyrophilic grain disease.These alterations did not show correlation with each other,thus seemed to develop independently. This case furtherhighlights the complexity of neuropathological alterationsin the ageing brain.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
argyrophilic grain disease
Creutzfeldt-Jakob disease
intranuclear inclusion body disease
kuru plaque
prion
Megjelenés:Neuropathology. - 35 : 4 (2015), p. 336-342. -
További szerzők:Trummert, Anita Unterberger, Ursula Ströbel, Thomas Hortobágyi Tibor (1965-) (patológus) Kovács Gábor Géza (1969-) (neurológus)
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3.

001-es BibID:BIBFORM069028
Első szerző:Kovács G. Gábor
Cím:Multisite Assessment of Aging-Related Tau Astrogliopathy (ARTAG) / Gabor G. Kovacs, Sharon X. Xie, Edward B. Lee, John L. Robinson, Carrie Caswell, David J. Irwin, Jon B. Toledo, Victoria E. Johnson, Douglas H. Smith, Irina Alafuzoff, Johannes Attems, Janos Bencze, Kevin F. Bieniek, Eileen H. Bigio, Istvan Bodi, Herbert Budka, Dennis W. Dickson, Brittany N. Dugger, Charles Duyckaerts, Isidro Ferrer, Shelley L. Forrest, Ellen Gelpi, Stephen M. Gentleman, Giorgio Giaccone, Lea T. Grinberg, Glenda M. Halliday, Kimmo J. Hatanpaa, Patrick R. Hof, Monika Hofer, Tibor Hortobágyi, James W. Ironside, Andrew King, Julia Kofler, Enikö Kövari, Jillian J. Kril, Seth Love, Ian R. Mackenzie, Qinwen Mao, Radoslav Matej, Catriona McLean, David G. Munoz, Melissa E. Murray, Janna Neltner, Peter T. Nelson, Diane Ritchie, Roberta D. Rodriguez, Zdenek Rohan, Annemieke Rozemuller, Kenji Sakai, Christian Schultz, Danielle Seilhean, Vanessa Smith, Pawel Tacik, Hitoshi Takahashi, Masaki Takao, Dietmar Rudolf Thal, Serge Weis, Stephen B. Wharton, Charles L. White III, John M. Woulfe, Masahito Yamada, John Q. Trojanowski
Dátum:2017
Megjegyzések:Aging-related tau astrogliopathy (ARTAG) is a recently introduced terminology. To facilitate the consistent identification of ARTAG and to distinguish ARTAG from other main types of astroglial tau pathologies related to primary frontotemporal lobar degeneration-related tauopathies we evaluated how consistently neuropathologists recognize i) different astroglial tau immunoreactivities including those of ARTAG and those associated with primary tauopathies (study 1); ii) ARTAG subtypes (study 2A); and iii) the severity of ARTAG (study 2B). Microphotographs and scanned sections immunostained for AT8 tau were made available for download and preview. Percentage (%) of agreement and kappa values with 95% confidence interval (CI) were calculated for each evaluation. The overall agreement for study 1 was > 60% with a kappa value of 0.54 (95% CI 0.433-0.645). Moderate agreement (> 90%, kappa: 0.48, 95% CI 0.457-0.900) was reached in study 2A for the identification of ARTAG pathology for each ARTAG subtype (kappa: 0.37-0.71), whereas fair agreement (kappa: 0.39, 95% CI 0.341-0.445) was reached for the evaluation of ARTAG severity. The overall assessment of ARTAG showed moderate agreement (kappa: 0.59, 95% CI 0.534-0.653) between raters. Our study supports the application of the current harmonized evaluation strategy of ARTAG with a slight modification of the evaluation of its severity.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
aging
ARTAG
tau-astrogliopathy
digital pathology
interrater agreement
tau
neuropathology
Megjelenés:Journal of Neuropathology & Experimental Neurology 76 : 7 (2017), p. 605-619. -
További szerzők:Xie, Sharon X. Lee, Edward B. Robinson, John L. Caswell, Carrie Irwin, David J. Toledo, Jon B. Johnson, Victoria E. Smith, Douglas H. Alafuzoff, Irina Attems, Johannes Bencze János (1991-) (orvos) Bieniek, Kevin F. Bigio, Eileen H. Bódi István (1967-) (neuropatológus) Budka, Herbert Dickson, Dennis W. Dugger, Brittany N. Duyckaerts, Charles Ferrer, Isidro Forrest, Shelley L. Gelpi, Ellen Gentleman, Stephen Giaccone, Giorgio Grinberg, Lea T. Halliday, Glenda Hatanpaa, Kimmo J. Hof, Patrick R. Hofer, Monika Hortobágyi Tibor (1965-) (patológus) Ironside, James W. King, Andrew Kofler, Julia Kővári Enikő Kril, Jillian J. Love, Seth Mackenzie, Ian R. Mao, Qinwen Matej, Radoslav McLean, Catriona Munoz, David G. Murray, Melissa E. Neltner, Janna Nelson, Peter T. Ritchie, Diane Rodriguez, Roberta D. Rohan, Zdenek Rozemuller, Annemieke Sakai, Kenji Schultz, Christian Seilhean, Danielle Smith, Vanessa Tacik, Pawel Takahashi, Hitoshi Takao, Masaki Thal, Dietmar R. Weis, Serge Wharton, Stephen B. White III, Charles L. Woulfe, John M. Yamada, Masahito Trojanowski, John Q.
Pályázati támogatás:NAP_KTIA_13_NAP-A-II/7
MTA
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4.

001-es BibID:BIBFORM051639
035-os BibID:PMID: 22471883
Első szerző:Kovács G. Gábor
Cím:Neuropathology of the hippocampus in FTLD-Tau with Pick bodies : a study of the BrainNet Europe Consortium / G. G. Kovacs, A. J. M. Rozemuller, J. C. van Swieten, E. Gelpi, K. Majtenyi, S. Al-Sarraj, C. Troakes, I. Bódi, A. King, T. Hortobágyi, M. M. Esiri, O. Ansorge, G. Giaccone, I. Ferrer, T. Arzberger, N. Bogdanovic, T. Nilsson, I. Leisser, I. Alafuzoff, J. W. Ironside, H. Kretzschmar, H. Budka
Dátum:2013
ISSN:0305-1846
Megjegyzések:Aims: Frontotemporal lobar degeneration with Pick bodies (Pick's disease) is characterized by the presence of tau immunoreactive spherical structures in the cytoplasm of neurons. In view of confusion about the molecular pathology of Pick's disease, we aimed to evaluate the spectrum of tau pathology and concomitant neurodegeneration-associated protein depositions in the characteristically affected hippocampus. Methods: We evaluated immunoreactivity for tau (AT8, 3R, 4R), α-synuclein, TDP43, p62, and ubiquitin in the hippocampus, entorhinal and temporal cortex in 66 archival cases diagnosed neuropathologically as Pick's disease. Results: Mean age at death was 68.2 years (range 49 to 96). Fifty-two (79%) brains showed 3R immunoreactive spherical inclusions in the granule cells of the dentate gyrus. These typical cases presented mainly with the behavioural variant of FTD, followed by progressive aphasia, mixed syndromes or early memory disturbance. α-Synuclein immunoreactivity was seen only in occasional spherical tau-positive inclusions, TDP-43 IR was absent, and 4R IR was present only as neurofibrillary tangles in pyramidal neurons. Aβ immunoreactivity was observed in 16 cases; however, the overall level of Alzheimer's disease-related alterations was mainly low or intermediate (n = 3). Furthermore, we identified six cases with unclassifiable tauopathy. Conclusions: 1) Pick's disease may occur also in elderly patients and is characterized by a relatively uniform pathology with 3R tau inclusions particularly in the granule cells of dentate gyrus; 2) even minor deviation from these morphological criteria suggests a different disorder; and 3) immunohistological revision of archival cases expands the spectrum of tauopathies that require further classification. © 2012 The Authors. Neuropathology and Applied Neurobiology © 2012 British Neuropathological Society.
Tárgyszavak:Orvostudományok Klinikai orvostudományok magyar nyelvű folyóiratközlemény hazai lapban
Megjelenés:Neuropathology and Applied Neurobiology. - 39 : 2 (2013), p. 166-178. -
További szerzők:Rozemuller, A. J. M. Swieten, John C. van Gelpi, Ellen Majtényi Katalin Al-Sarraj, Safa Troakes, Claire Bódi István (1967-) (neuropatológus) King, Andrew Hortobágyi Tibor (1965-) (patológus) Esiri, M. M. Ansorge, Olaf Giaccone, Giorgio Ferrer, Isidro Arzberger, Thomas Bogdanovic, Nenad Nilsson, Tatjana Leisser, I. Alafuzoff, Irina Ironside, James W. Kretzschmar, Hans Budka, Herbert
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5.

001-es BibID:BIBFORM051599
035-os BibID:PMID: 22934812
Első szerző:Troakes, Claire
Cím:Transportin 1 colocalization with Fused in Sarcoma (FUS) inclusions is not characteristic for amyotrophic lateral sclerosis-FUS confirming disrupted nuclear import of mutant FUS and distinguishing it from frontotemporal lobar degeneration with FUS inclusions / C. Troakes, T. Hortobágyi, C. Vance, S. Al-Sarraj, B. Rogelj, C. E. Shaw
Dátum:2013
ISSN:0305-1846
Megjegyzések:AIMS: Transportin 1 (TNPO 1) is an abundant component of the Fused in Sarcoma (FUS)-immunopositive inclusions seen in a subgroup of frontotemporal lobar degeneration (FTLD-FUS). TNPO 1 has been shown to bind to the C-terminal nuclear localizing signal (NLS) of FUS and mediate its nuclear import. Amyotrophic lateral sclerosis (ALS)-linked C-terminal mutants disrupt TNPO 1 binding to the NLS and impair nuclear import in cell culture. If this held true for human ALS then we predicted that FUS inclusions in patients with C-terminal FUS mutations would not colocalize with TNPO 1. METHODS: Expression of TNPO 1 and colocalization with FUS was studied in the frontal cortex of FTLD-FUS (n = 3) and brain and spinal cord of ALS-FUS (n = 3), ALS-C9orf72 (n = 3), sporadic ALS (n = 7) and controls (n = 7). Expression levels and detergent solubility of TNPO 1 was measured by Western blot. RESULTS: Aggregates of TNPO 1 were abundant and colocalized with FUS inclusions in the cortex of all FTLD-FUS cases. In contrast, no TNPO 1-positive aggregates or FUS colocalization was evident in two-thirds, ALS-FUS cases and was rare in one ALS-FUS case. Nor were they present in C9orf72 or sporadic ALS. No increase in the levels of TNPO 1 was seen in Western blots of spinal cord tissues from all ALS cases compared with controls. CONCLUSIONS: These findings confirm that C-terminal FUS mutations prevent TNPO 1 binding to the NLS, inhibiting nuclear import and promoting cytoplasmic aggregation. The presence of TNPO 1 in wild-type FUS aggregates in FTLD-FUS distinguishes the two pathologies and implicates different disease mechanisms.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Neuropathology and Applied Neurobiology. - 39 : 5 (2013), p. 553-561. -
További szerzők:Hortobágyi Tibor (1965-) (patológus) Vance, Caroline Al-Sarraj, Safa Rogelj, Boris Shaw, Christopher E.
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