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1.

001-es BibID:BIBFORM063334
Első szerző:Alafuzoff, Irina
Cím:Neuropathological assessments of the pathology in frontotemporal lobar degeneration with TDP43-positive inclusions : an inter-laboratory study by the BrainNet Europe consortium / Irina Alafuzoff, Maria Pikkarainen, Manuela Neumann, Thomas Arzberger, Safa Al-Sarraj, Istvan Bodi, Nenad Bogdanovic, Orso Bugiani, Isidro Ferrer, Ellen Gelpi, Stephen Gentleman, Giorgio Giaccone, Manuel B. Graeber, Tibor Hortobagyi, Paul G. Ince, James W. Ironside, Nikolaos Kavantzas, Andrew King, Penelope Korkolopoulou, Gábor G. Kovács, David Meyronet, Camelia Monoranu, Tatjana Nilsson, Piero Parchi, Efstratios Patsouris, Tamas Revesz, Wolfgang Roggendorf, Annemieke Rozemuller, Danielle Seilhean, Nathalie Streichenberger, Dietmar R. Thal, Stephen B. Wharton, Hans Kretzschmar
Dátum:2015
ISSN:0300-9564
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal Of Neural Transmission. - 122 : 7 (2015), p. 957-972. -
További szerzők:Pikkarainen, Maria Neumann, Manuela Arzberger, Thomas Al-Sarraj, Safa Bódi István (1967-) (neuropatológus) Bogdanovic, Nenad Bugiani, Orso Ferrer, Isidro Gelpi, Ellen Gentleman, Stephen Giaccone, Giorgio Graeber, Manuel Hortobágyi Tibor (1965-) (patológus) Ince, Paul Ironside, James W. Kavantzas, Nikolaos King, Andrew Korkolopoulou, Penelope Kovács Gábor Géza (1969-) (neurológus) Meyronet, David Monoranu, Camelia Nilsson, Tatjana Parchi, Piero Patsouris, Efstratios Révész Tamás Roggendorf, Wolfgang Rozemuller, Annemieke Seilhean, Danielle Streichenberger, Nathalie Thal, Dietmar R. Wharton, Stephen B. Kretzschmar, Hans
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2.

001-es BibID:BIBFORM042976
Első szerző:Alafuzoff, Irina
Cím:The need to unify neuropathological assessments of vascular alterations in the ageing brain : multicentre survey by the BrainNet Europe consortium / Irina Alafuzoff, Ellen Gelpi, Safa Al-Sarraj, Thomas Arzberger, Johannes Attems, Istvan Bodi, Nenad Bogdanovic, Herbert Budka, Orso Bugiani, Elisabet Englund, Isidro Ferrer, Stephen Gentleman, Giorgio Giaccone, Manuel B. Graeber, Tibor Hortobagyi, Romana Höftberger, James W. Ironside, Kurt Jellinger, Nikolaos Kavantzas, Andrew King, Penelope Korkolopoulou, Gábor G. Kovács, David Meyronet, Camelia Monoranu, Piero Parchi, Efstratios Patsouris, Wolfgang Roggendorf, Annemieke Rozemuller, Danielle Seilhean, Nathalie Streichenberger, Dietmar R. Thal, Stephen B. Wharton, Hans Kretzschmar
Dátum:2012
ISSN:0531-5565
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Experimental Gerontology. - 47 : 11 (2012), p. 825-833. -
További szerzők:Gelpi, Ellen Al-Sarraj, Safa Arzberger, Thomas Attems, Johannes Bódi István (1967-) (neuropatológus) Bogdanovic, Nenad Budka, Herbert Bugiani, Orso Englund, Elisabet Ferrer, Isidro Gentleman, Stephen Giaccone, Giorgio Graeber, Manuel Hortobágyi Tibor (1965-) (patológus) Höftberger, Romana Ironside, James W. Jellinger, Kurt Kavantzas, Nikolaos King, Andrew Korkolopoulou, Penelope Kovács Gábor Géza (1969-) (neurológus) Meyronet, David Monoranu, Camelia Parchi, Piero Patsouris, Efstratios Roggendorf, Wolfgang Rozemuller, Annemieke Seilhean, Danielle Streichenberger, Nathalie Thal, Dietmar R. Wharton, Stephen B. Kretzschmar, Hans
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3.

001-es BibID:BIBFORM020015
Első szerző:Alafuzoff, Irina
Cím:Assessment of beta-amyloid deposits in human brain : a study of the BrainNet Europe Consortium / Irina Alafuzoff, Dietmar R. Thal, Thomas Arzberger, Nenad Bogdanovic, Safa Al-Sarraj, Istvan Bodi, Susan Boluda, Orso Bugiani, Charles Duyckaerts, Ellen Gelpi, Stephen Gentleman, Giorgio Giaccone, Manuel Graeber, Tibor Hortobagyi, Romana Höftberger, Paul Ince, James W. Ironside, Nikolaos Kavantzas, Andrew King, Penelope Korkolopoulou, Gábor G. Kovács, David Meyronet, Camelia Monoranu, Tatjana Nilsson, Piero Parchi, Efstratios Patsouris, Maria Pikkarainen, Tamas Revesz, Annemieke Rozemuller, Danielle Seilhean, Walter Schulz-Schaeffer, Nathalie Streichenberger, Stephen B. Wharton, Hans Kretzschmar
Dátum:2009
ISSN:0001-6322
Megjegyzések:Beta-Amyloid (A-beta) related pathology shows a range of lesions which differ both qualitatively and quantitatively. Pathologists, to date, mainly focused on the assessment of both of these aspects but attempts to correlate the findings with clinical phenotypes are not convincing. It has been recently proposed in the same way as iota and alpha synuclein related lesions, also A-beta related pathology may follow a temporal evolution, i.e. distinct phases, characterized by a step-wise involvement of different brain-regions. Twenty-six independent observers reached an 81% absolute agreement while assessing the phase of A-beta, i.e. phase 1 = deposition of A-beta exclusively in neocortex, phase 2 = additionally in allocortex, phase 3 = additionally in diencephalon, phase 4 = additionally in brainstem, and phase 5 = additionally in cerebellum. These high agreement rates were reached when at least six brain regions were evaluated. Likewise, a high agreement (93%) was reached while assessing the absence/presence of cerebral amyloid angiopathy (CAA) and the type of CAA (74%) while examining the six brain regions. Of note, most of observers failed to detect capillary CAA when it was only mild and focal and thus instead of type 1, type 2 CAA was diagnosed. In conclusion, a reliable assessment of A-beta phase and presence/absence of CAA was achieved by a total of 26 observers who examined a standardized set of blocks taken from only six anatomical regions, applying commercially available reagents and by assessing them as instructed. Thus, one may consider rating of A-beta-phases as a diagnostic tool while analyzing subjects with suspected Alzheimer's disease (AD). Because most of these blocks are currently routinely sampled by the majority of laboratories, assessment of the A-beta phase in AD is feasible even in large scale retrospective studies.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Acta Neuropathologica. - 117 : 3 (2009), p. 309-320. -
További szerzők:Thal, Dietmar R. Arzberger, Thomas Bogdanovic, Nenad Al-Sarraj, Safa Bódi István (1967-) (neuropatológus) Boluda, Susan Bugiani, Orso Duyckaerts, Charles Gelpi, Ellen Gentleman, Stephen Giaccone, Giorgio Graeber, Manuel Hortobágyi Tibor (1965-) (patológus) Höftberger, Romana Ince, Paul Ironside, James W. Kavantzas, Nikolaos King, Andrew Korkolopoulou, Penelope Kovács Gábor Géza (1969-) (neurológus) Meyronet, David Monoranu, Camelia Nilsson, Tatjana Parchi, Piero Patsouris, Efstratios Pikkarainen, Maria Révész Tamás Rozemuller, Annemieke Seilhean, Danielle Schulz-Schaeffer, Walter Streichenberger, Nathalie Wharton, Stephen B. Kretzschmar, Hans
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4.

001-es BibID:BIBFORM029484
Első szerző:Al-Sarraj, Safa
Cím:p62 positive, TDP-43 negative, neuronal cytoplasmic and intranuclear inclusions in the cerebellum and hippocampus define the pathology of C9orf72-linked FTLD and MND/ALS / Safa Al-Sarraj, Andrew King, Claire Troakes, Bradley Smith, Satomi Maekawa, Istvan Bodi, Boris Rogelj, Ammar Al-Chalabi, Tibor Hortobágyi, Christopher E. Shaw
Dátum:2011
ISSN:0001-6322
Megjegyzések:Neuronal cytoplasmic inclusions (NCIs) containing phosphorylated TDP-43 (p-TDP-43) are the pathological hallmarks of motor neuron disease/amyotrophic lateral sclerosis (MND/ALS) and FTLD-TDP. The vast majority of NCIs in the brain and spinal cord also label for ubiquitin and p62, however, we have previously reported a subset of TDP-43 proteinopathy patients who have unusual and abundant p62 positive, TDP-43 negative inclusions in the cerebellum and hippocampus. Here we sought to determine whether these cases carry the hexanucleotide repeat expansion in C9orf72. Repeat primer PCR was performed in 36 MND/ALS, FTLD-MND/ALS and FTLD-TDP cases and four controls. Fourteen individuals with the repeat expansion were detected. In all the 14 expansion mutation cases there were abundant globular and star-shaped p62 positive NCIs in the pyramidal cell layer of the hippocampus, the vast majority of which were p-TDP-43 negative. p62 positive NCIs were also abundant in the cerebellar granular and molecular layers in all cases and in Purkinje cells in 12/14 cases but they were only positive for p-TDP-43 in the granular layer of one case. Abundant p62 positive, p-TDP-43 negative neuronal intranuclear inclusions (NIIs) were seen in 12/14 cases in the pyramidal cell layer of the hippocampus and in 6/14 cases in the cerebellar granular layer. This unusual combination of inclusions appears pathognomonic for C9orf72 repeat expansion positive MND/ALS and FTLD-TDP which we believe form a pathologically distinct subset of TDP-43 proteinopathies. Our results suggest that proteins other than TDP-43 are binding p62 and aggregating in response to the mutation which may play a mechanistic role in neurodegeneration.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Acta Neuropathologica. - 122 : 6 (2011), p. 691-702. -
További szerzők:King, Andrew Troakes, Claire Smith, Bradley Maekawa, Satomi Bódi István (1967-) (neuropatológus) Rogelj, Boris Al-Chalabi, Ammar Shaw, Christopher E. Hortobágyi Tibor (1965-) (patológus)
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5.

001-es BibID:BIBFORM020043
Első szerző:Hortobágyi Tibor (patológus)
Cím:71-year-old man with multiple metastases to the brain / Tibor Hortobágyi, Nick W. Thomas, Andrew King
Dátum:2008
ISSN:0919-6544
Tárgyszavak:Orvostudományok Klinikai orvostudományok esettanulmány
Megjelenés:Neuropathology. - 28 : 1 (2008), p. 103-105. -
További szerzők:Thomas, Nick W. King, Andrew
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6.

001-es BibID:BIBFORM019976
Első szerző:Hortobágyi Tibor (patológus)
Cím:Optineurin inclusions occur in a minority of TDP-43 positive ALS and FTLD-TDP cases and are rarely observed in other neurodegenerative disorders / Tibor Hortobágyi, Claire Troakes, Agnes L. Nishimura, Caroline Vance, John C. van Swieten, Harro Seelaar, Andrew King, Safa Al-Sarraj, Boris Rogelj, Christopher E. Shaw
Dátum:2011
ISSN:0001-6322
Megjegyzések:Optineurin (OPTN) is a multifunctional protein involved in vesicular trafficking, signal transduction and gene expression. OPTN mutations were described in eight Japanese patients with familial and sporadic amyotrophic lateral sclerosis (FALS, SALS). OPTN-positive inclusions co-localising with TDP-43 were described in SALS and in FALS with SOD-1 mutations, potentially linking two pathologically distinct pathways of motor neuron degeneration. We have explored the abundance of OPTN inclusions using a range of antibodies in postmortem tissues from 138 cases and controls including sporadic and familial ALS, frontotemporal lobar degeneration (FTLD) and a wide range of neurodegenerative proteinopathies. OPTN-positive inclusions were uncommon and detected in only 11/32 (34%) of TDP-43-positive SALS spinal cord and 5/15 (33%) of FTLD-TDP. Western blot of lysates from FTLD-TDP frontal cortex and TDP-43-positive SALS spinal cord revealed decreased levels of OPTN protein compared to controls (p < 0.05), however, this correlated with decreased neuronal numbers in the brain. Large OPTN inclusions were not detected in FALS with SOD-1 and FUS mutation, respectively, or in FTLD-FUS cases. OPTN-positive inclusions were identified in a few Alzheimer's disease (AD) cases but did not co-localise with tau and TDP-43. Occasional striatal neurons contained granular cytoplasmic OPTN immunopositivity in Huntington's disease (HD) but were absent in spinocerebellar ataxia type 3. No OPTN inclusions were detected in FTLD-tau and α-synucleinopathy. We conclude that OPTN inclusions are relatively rare and largely restricted to a minority of TDP-43 positive ALS and FTLD-TDP cases. Our results do not support the proposition that OPTN inclusions play a central role in the pathogenesis of ALS, FTLD or any other neurodegenerative disorder.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Acta Neuropathologica. - 121 : 4 (2011), p. 519-527. -
További szerzők:Troakes, Claire Nishimura, Agnes Lumi Vance, Caroline Swieten, John C. van Seelaar, Harro King, Andrew Al-Sarraj, Safa Rogelj, Boris Shaw, Christopher E.
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7.

001-es BibID:BIBFORM082383
035-os BibID:(cikkazonosító)551
Első szerző:Kattuah, Wejdan
Cím:Heterogeneous Nuclear Ribonucleoprotein E2 (hnRNP E2) Is a Component of TDP-43 Aggregates Specifically in the A and C Pathological Subtypes of Frontotemporal Lobar Degeneration / Wejdan Kattuah, Boris Rogelj, Andrew King, Christopher E. Shaw, Tibor Hortobágyi, Claire Troakes
Dátum:2019
ISSN:1662-453X
Megjegyzések:TAR DNA-binding protein 43 (TDP-43) is the major component of the ubiquitin-positive protein aggregates seen in the majority of frontotemporal lobar degeneration and amyotrophic lateral sclerosis cases. TDP-43 belongs to the heterogeneous nuclear ribonucleoprotein (hnRNP) family that is involved in the regulation of RNA transcription, splicing, transport and translation. There are a great many hnRNPs, which often have overlapping functions and act cooperatively in RNA processing. Here we demonstrate that another hnRNP family member, hnRNP E2, shows a striking accumulation within dystrophic neurites and cytoplasmic inclusions in the frontal cortex and hippocampus of a subset of FTLD-TDP cases belonging to pathological subtypes A and C, where hnRNP E2 was found to co-localize with 87% of TDP-43 immunopositive inclusions. hnRNP E2-positive inclusions were not seen in FTLD-TDP cases with the C9orf72 expansion or in any other neurodegenerative disorders examined. This interaction with TDP-43 in specific FTLD subtypes suggests different underlying neurodegenerative pathways.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Frontiers in Neuroscience. - 13 (2019), p. 1-11. -
További szerzők:Rogelj, Boris King, Andrew Shaw, Christopher E. Hortobágyi Tibor (1965-) (patológus) Troakes, Claire
Pályázati támogatás:2017-1.2.1-NKP-2017-00002
Egyéb
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8.

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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9.

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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10.

001-es BibID:BIBFORM020036
Első szerző:Maekawa, Satomi
Cím:TDP-43 is consistently co-localized with ubiquitinated inclusions in sporadic and Guam amyotrophic lateral sclerosis but not in familial amyotrophic lateral sclerosis with and without SOD1 mutations / Satomi Maekawa, P. Nigel Leigh, Andrew King, Edith Jones, John C. Steele, Istvan Bodi, Christopher E. Shaw, Tibor Hortobagyi, Safa Al-Sarraj
Dátum:2009
ISSN:0919-6544
Megjegyzések:The transactive response (TAR) DNA binding protein 43 (TDP-43) has been recently implicated as a major component of ubiquitinated inclusions in amyotrophic lateral sclerosis (ALS, motor neuron disease: MND) and ALS-related disorders. In this study, we examined abnormal TDP-43 pathology in 13 sporadic ALS (SALS), six familial ALS (FALS) with and without Cu/Zn superoxide dismutase (SOD1) mutations (SOD1-FALS and non-SOD1-FALS), Guam ALS, two frontotemporal lobar degeneration with MND/ALS (FTLD-MND/ALS), one FTLD with ubiquitin-only-immunoreactive inclusions (FTLD-U) and two progressive supranuclear palsy (PSP). Sections from the spinal cord were processed for immunohistochemistry using antibodies against TDP-43, ubiquitin, p62, cystatin C, phosphorylated tau protein (P-tau; AT8), alpha-synuclein and phosphorylated neurofilament protein (P-NF). In 12 out of 13 SALS and both Guam ALS cases ubiquitin and p62-immunoreactive (IR) neuronal inclusions co-localized with TDP-43. In three out of four SOD1-FALS and one of two non-SOD1-FALS cases, TDP-43-IR inclusions were absent despite the presence of p62 and/or ubiquitin-IR inclusions. However, a single TDP-43-IR neuronal inclusion co-localized with p62 and ubiquitin in one SOD1-FALS (His48Gln) case. Except for one neuron in a Guam case, all TDP-43-IR neuronal inclusions were negative for P-tau (AT8). TDP-43-IR glial inclusions and neurites were also demonstrated. The TDP-43 is a consistent component of the ubiquitinated inclusions in SALS and Guam ALS, but TDP-43-IR inclusions are absent or scarce in SOD1-FALS.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Neuropathology. - 29 : 6 (2009), p. 672-683. -
További szerzők:Leigh, P. Nigel King, Andrew Jones, Edith Steele, John C. Bódi István (1967-) (neuropatológus) Shaw, Christopher E. Hortobágyi Tibor (1965-) (patológus) Al-Sarraj, Safa
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11.

001-es BibID:BIBFORM067303
Első szerző:Skrobot, Olivia A.
Cím:Reply: Atherosclerosis and vascular cognitive impairment neuropathological guideline / Olivia A. Skrobot, Johannes Attems, Margaret Esiri, Tibor Hortobágyi, James W. Ironside, Rajesh N. Kalaria, Andrew King, G. A. Lammie, David Mann, James Neal, Yoav Ben-Shlomo, P. G. Kehoe, Seth Love
Dátum:2017
ISSN:0006-8950
Tárgyszavak:Orvostudományok Klinikai orvostudományok levél
Megjelenés:Brain. - 140 : 2 (2017), p. e13. -
További szerzők:Attems, Johannes Esiri, M. M. Hortobágyi Tibor (1965-) (patológus) Ironside, James W. Kalaria, Rajesh N. King, Andrew Lammie, George A. Mann, David J. Neal, James Ben-Shlomo, Yoav Kehoe, Patrick G. Love, Seth
Internet cím:DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

12.

001-es BibID:BIBFORM065465
Első szerző:Skrobot, Olivia A.
Cím:Vascular cognitive impairment neuropathology guidelines (VCING) : the contribution of cerebrovascular pathology to cognitive impairment / Olivia A. Skrobot, Johannes Attems, Margaret Esiri, Tibor Hortobágyi, James W. Ironside, Rajesh N. Kalaria, Andrew King, George A. Lammie, David Mann, James Neal, Yoav Ben-Shlomo, Patrick G. Kehoe, Seth Love
Dátum:2016
ISSN:0006-8950
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Brain 139 : 11 (2016), p. 2957-2969. -
További szerzők:Attems, Johannes Esiri, M. M. Hortobágyi Tibor (1965-) (patológus) Ironside, James W. Kalaria, Rajesh N. King, Andrew Lammie, George A. Mann, David J. Neal, James Ben-Shlomo, Yoav Kehoe, Patrick G. Love, Seth
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:
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