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1.

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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2.

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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3.

001-es BibID:BIBFORM082378
035-os BibID:(cikkazonosító)5 (WoS)000455320300001 (Scopus)85059798236
Első szerző:Ashton, Nicholas J.
Cím:Increased plasma neurofilament light chain concentration correlates with severity of post-mortem neurofibrillary tangle pathology and neurodegeneration / Nicholas J. Ashton, Antoine Leuzy, Yau Mun Lim, Claire Troakes, Tibor Hortobágyi, Kina Höglund, Dag Aarsland, Simon Lovestone, Michael Schöll, Kaj Blennow, Henrik Zetterberg, Abdul Hye
Dátum:2019
ISSN:2051-5960
Megjegyzések:Alzheimer's disease (AD) is pathologically characterized by the accumulation of amyloid- (A) plaques, neurofibrillary tangles and widespread neuronal loss in the brain. In recent years, blood biomarkers have emerged as a realistic prospect to highlight accumulating pathology for secondary prevention trials. Neurofilament light chain (NfL), a marker of axonal degeneration, is robustly elevated in the blood of many neurological and neurodegenerative conditions, including AD. A strong relationship with cerebrospinal fluid (CSF) NfL suggests that these biomarker modalities reflect the same pathological process. Yet, the connection between blood NfL and brain tissue pathology has not been directly compared. In this study, longitudinal plasma NfL from cognitively healthy controls (n=12) and AD participants (n=57) were quantified by the Simoa platform. On reaching post-mortem, neuropathological assessment was performed on all participants, with additional frozen and paraffin-embedded tissue acquired from 26 participants for further biochemical (A(1-42), A(1-40), tau) and histological (NfL) evaluation. Plasma NfL concentrations were significantly increased in AD and correlated with cognitive decline, independent of age. Retrospective stratification based on Braak staging revealed that baseline plasma NfL concentrations were associated with higher neurofibrillary tangle pathology at post-mortem. Longitudinal increases in plasma NfL were observed in all Braak groupings; a significant negative association, however, was found between plasma NfL at time point 1 and both its rate of change and annual percentage increase. Immunohistochemical evaluation of NfL in the medial temporal gyrus (MTG) demonstrated an inverse relationship between Braak stages and NfL staining. Importantly, a significant negative correlation was found between the plasma NfL measurement closest to death and the level of NfL staining in the MTG at post-mortem. For the first time, we demonstrate that plasma NfL associates with the severity of neurofibrillary tangle pathology and neurodegeneration in the post-mortem brain.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Acta Neuropathologica Communications. - 7 : 1 (2019), p. 1-11. -
További szerzők:Leuzy, Antoine Lim, Yau Mun Troakes, Claire Hortobágyi Tibor (1965-) (patológus) Höglund, Kina Aarsland, Dag Lovestone, Simon Schöll, Michael Blennow, Kaj Zetterberg, Henrik Hye, Abdul
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4.

001-es BibID:BIBFORM090909
035-os BibID:(WOS)000605104600001 (Scopus)85098720952
Első szerző:Attems, Johannes
Cím:Neuropathological consensus criteria for the evaluation of Lewy pathology in post-mortem brains : a multi-centre study / Attems Johannes, Toledo Jon B., Walker Lauren, Gelpi Ellen, Gentleman Steve, Halliday Glenda, Hortobagyi Tibor, Jellinger Kurt, Kovacs Gabor G., Lee Edward B., Love Seth, McAleese Kirsty E., Nelson Peter T., Neumann Manuela, Parkkinen Laura, Polvikoski Tuomo, Sikorska Beata, Smith Colin, Grinberg Lea Tenenholz, Thal Dietmar R., Trojanowski John Q., McKeith Ian G.
Dátum:2021
ISSN:0001-6322
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Acta Neuropathologica. - 141 (2021), p. 159-172. -
További szerzők:Toledo, Jon B. Walker, Lauren Gelpi, Ellen Gentleman, Steve Halliday, Glenda Hortobágyi Tibor (1965-) (patológus) Jellinger, Kurt Kovács Gábor Géza (1969-) (neurológus) Lee, Edward B. Love, Seth McAleese, Kirsty E. Nelson, Peter T. Neumann, Manuela Parkkinen, Laura Polvikoski, Tuomo Sikorska, Beata Smith, Colin Grinberg, Lea T. Thal, Dietmar R. Trojanowski, John Q. McKeith, Ian G.
Pályázati támogatás:2017-1.2.1-NKP-2017-00002
Egyéb
Egyéb
OTKA
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5.

001-es BibID:BIBFORM072390
035-os BibID:(cikkazonosító)6 (WoS)000423680100001 (Scopus)85041407397
Első szerző:Datki Zsolt
Cím:Exceptional in vivo catabolism of neurodegeneration-related aggregates / Datki Zsolt, Olah Zita, Hortobagyi Tibor, Macsai Lilla, Zsuga Katalin, Fulop Livia, Bozso Zsolt, Galik Bence, Acs Eva, Foldi Angela, Szarvas Amanda, Kalman Janos
Dátum:2018
ISSN:2051-5960
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Acta Neuropathologica Communications. - 6 : 1 (2018), p. 1-12. -
További szerzők:Oláh Zita Hortobágyi Tibor (1965-) (patológus) Mácsai Lilla Zsuga Katalin Fülöp Lívia (Szeged) Bozsó Zsolt Galik Bence Ács Éva Földi Angéla Szarvas Amanda Kálmán János
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6.

001-es BibID:BIBFORM075028
035-os BibID:(WoS)000441903500008 (Scopus)85050314318
Első szerző:Fekete Rebeka
Cím:Microglia control the spread of neurotropic virus infection via P2Y12 signalling and recruit monocytes through P2Y12-independent mechanisms / Rebeka Fekete, Csaba Cserép, Nikolett Lénárt, Krisztina Tóth, Barbara Orsolits, Bernadett Martinecz, Előd Méhes, Bálint Szabó, Valéria Németh, Balázs Gönci, Beáta Sperlágh, Zsolt Boldogkői, Ágnes Kittel, Mária Baranyi, Szilamér Ferenczi, Krisztina Kovács, Gergely Szalay, Balázs Rózsa, Connor Webb, Gabor G. Kovacs, Tibor Hortobágyi, Brian L. West, Zsuzsanna Környei, Ádám Dénes
Dátum:2018
ISSN:0001-6322
Megjegyzések:Neurotropic herpesviruses can establish lifelong infection in humans and contribute to severe diseases including encephalitis and neurodegeneration. However, the mechanisms through which the brain's immune system recognizes and controls viral infections propagating across synaptically linked neuronal circuits have remained unclear. Using a well-established model of alphaherpesvirus infection that reaches the brain exclusively via retrograde transsynaptic spread from the periphery, and in vivo two-photon imaging combined with high resolution microscopy, we show that microglia are recruited to and isolate infected neurons within hours. Selective elimination of microglia results in a marked increase in the spread of infection and egress of viral particles into the brain parenchyma, which are associated with diverse neurological symptoms. Microglia recruitment and clearance of infected cells require cell-autonomous P2Y12 signalling in microglia, triggered by nucleotides released from affected neurons. In turn, we identify microglia as key contributors to monocyte recruitment into the inflamed brain, which process is largely independent of P2Y12. P2Y12-positive microglia are also recruited to infected neurons in the human brain during viral encephalitis and both microglial responses and leukocyte numbers correlate with the severity of infection. Thus, our data identify a key role for microglial P2Y12 in defence against neurotropic viruses, whilst P2Y12-independent actions of microglia may contribute to neuroinflammation by facilitating monocyte recruitment to the sites of infection.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Microglia
P2Y12
Neurotropic virus
Transsynaptic spread
Neuroinflammation
Megjelenés:Acta Neuropathologica. - 136 : 3 (2018), p. 461-482. -
További szerzők:Cserép Csaba Lénárt Nikolett Tóth Krisztina Orsolits Barbara Martinecz Bernadett Méhes Előd Szabó Bálint Németh Valéria Gönci Balázs Sperlágh Beáta Boldogkői Zsolt Kittel Ágnes Baranyi Mária Ferenczi Szilamér (1977-) (biológus) Kovács Krisztina Szalay Gergely Rózsa Balázs Webb, Connor Kovács Gábor Géza (1969-) (neurológus) Hortobágyi Tibor (1965-) (patológus) West, Brian L. Környei Zsuzsanna Dénes Ádám
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7.

001-es BibID:BIBFORM104870
035-os BibID:(scopus)85137215998 (wos)000847625400001
Első szerző:Gilvesy, Abris
Cím:Spatiotemporal characterization of cellular tau pathology in the human locus coeruleus-pericoerulear complex by three-dimensional imaging / Gilvesy Abris, Husen Evelina, Magloczky Zsofia, Mihaly Orsolya, Hortobágyi Tibor, Kanatani Shigeaki, Heinsen Helmut, Renier Nicolas, Hökfelt Tomas, Mulder Jan, Uhlen Mathias, Kovacs Gabor G., Adori Csaba
Dátum:2022
ISSN:0001-6322
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Acta Neuropathologica. - 144 : 4 (2022), p. 651-676. -
További szerzők:Husen, Evelina Maglóczky Zsófia Mihály Orsolya Hortobágyi Tibor (1965-) (patológus) Kanatani, Shigeaki Heinsen, Helmut Renier, Nicolas Hökfelt, Tomas Mulder, Jan Uhlén, Mathias Kovács Gábor Géza (1969-) (neurológus) Adori Csaba
Pályázati támogatás:NAP, KTIA_13_NAP-A-II/7
Egyéb
NKFIH_SNN_132999
Egyéb
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8.

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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9.

001-es BibID:BIBFORM063323
Első szerző:Kovács Gábor Géza (neurológus)
Cím:Aging-related tau astrogliopathy (ARTAG) : harmonized evaluation strategy / Gabor G. Kovacs, Isidro Ferrer, Lea T. Grinberg, Irina Alafuzoff, Johannes Attems, Herbert Budka, Nigel J. Cairns, John F. Crary, Charles Duyckaerts, Bernardino Ghetti, Glenda M. Halliday, James W. Ironside, Seth Love, Ian R. Mackenzie, David G. Munoz, Melissa E. Murray, Peter T. Nelson, Hitoshi Takahashi, John Q. Trojanowski, Olaf Ansorge, Thomas Arzberger, Atik Baborie, Thomas G. Beach, Kevin F. Bieniek, Eileen H. Bigio, Istvan Bodi, Brittany N. Dugger, Mel Feany, Ellen Gelpi, Stephen M. Gentleman, Giorgio Giaccone, Kimmo J. Hatanpaa, Richard Heale, Patrick R. Hof, Monika Hofer, Tibor Hortobágyi, Kurt Jellinger, Gregory A. Jicha, Paul Ince, Julia Kofler, Enikö Kövari, Jillian J. Kril, David M. Mann, Radoslav Matej, Ann C. McKee, Catriona McLean, Ivan Milenkovic, Thomas J. Montine, Shigeo Murayama, Edward B. Lee, Jasmin Rahimi, Roberta D. Rodriguez, Annemieke Rozemüller, Julie A. Schneider, Christian Schultz, William Seeley, Danielle Seilhean, Colin Smith, Fabrizio Tagliavini, Masaki Takao, Dietmar Rudolf Thal, Jon B. Toledo, Markus Tolnay, Juan C. Troncoso, Harry V. Vinters, Serge Weis, Stephen B. Wharton, Charles L. White III, Thomas Wisniewski, John M. Woulfe, Masahito Yamada, Dennis W. Dickson
Dátum:2016
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Acta neuropathologica 131 : 1 (2016), p. 87-102. -
További szerzők:Ferrer, Isidro Grinberg, Lea T. Alafuzoff, Irina Attems, Johannes Budka, Herbert Cairns, Nigel J. Crary, John F. Duyckaerts, Charles Ghetti, Bernardino Halliday, Glenda Ironside, James W. Love, Seth Mackenzie, Ian R. Munoz, David G. Murray, Melissa E. Nelson, Peter T. Takahashi, Hitoshi Trojanowski, John Q. Ansorge, Olaf Arzberger, Thomas Baborie, Atik Beach, Thomas G. Bieniek, Kevin F. Bigio, Eileen H. Bódi István (1967-) (neuropatológus) Dugger, Brittany N. Feany, Mel Gelpi, Ellen Gentleman, Stephen Giaccone, Giorgio Hatanpaa, Kimmo J. Heale, Richard Hof, Patrick R. Hofer, Monika Hortobágyi Tibor (1965-) (patológus) Jellinger, Kurt Jicha, Gregory A. Ince, Paul Kofler, Julia Kővári Enikő Kril, Jillian J. Mann, David M. Matej, Radoslav McKee, Ann C. McLean, Catriona Milenkovic, Ivan Montine, Thomas J. Murayama, Shigeo Lee, Edward B. Rahimi, Jasmin Rodriguez, Roberta D. Rozemuller, Annemieke Schneider, Julie A. Schultz, Christian Seeley, William Seilhean, Danielle Smith, Colin Tagliavini, Fabrizio Takao, Masaki Thal, Dietmar R. Toledo, Jon B. Tolnay, Markus Troncoso, Juan C. Vinters, Harry V. Weis, Serge Wharton, Stephen B. White III, Charles L. Wisniewski, Thomas Woulfe, John M. Yamada, Masahito Dickson, Dennis W.
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10.

001-es BibID:BIBFORM063335
Első szerző:Mitchell, Jacqueline C.
Cím:Wild type human TDP-43 potentiates ALS-linked mutant TDP-43 driven progressive motor and cortical neuron degeneration with pathological features of ALS / Jacqueline C. Mitchell, Remy Constable, Eva So, Caroline Vance, Emma Scotter, Leanne Glover, Tibor Hortobagyi, Eveline S. Arnold, Shuo-Chien Ling, Melissa McAlonis, Sandrine Da Cruz, Magda Polymenidou, Lino Tessarolo, Don W. Cleveland, Christopher E. Shaw
Dátum:2015
ISSN:2051-5960
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Acta Neuropathologica Communications. - 3 : 1 (2015), p. 1-16. -
További szerzők:Constable, Remy So, Eva Vance, Caroline Scotter, Emma L. Glover, Leanne Hortobágyi Tibor (1965-) (patológus) Arnold, Eveline S. Ling, Shuo-Chien McAlonis, Melissa Da Cruz, Sandrine Polymenidou, Magda Tessarolo, Lino Cleveland, Don W. Shaw, Christopher E.
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11.

001-es BibID:BIBFORM042979
Első szerző:Mitchell, Jacqueline C.
Cím:Overexpression of human wild-type FUS causes progressive motor neuron degeneration in an age- and dose-dependent fashion / Jacqueline C. Mitchell, Philip McGoldrick, Caroline Vance, Tibor Hortobagyi, Jemeen Sreedharan, Boris Rogelj, Elizabeth L. Tudor, Bradley N. Smith, Christian Klasen, Christopher C. J. Miller, Jonathan D. Cooper, Linda Greensmith, Christopher E. Shaw
Dátum:2013
ISSN:0001-6322
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Acta Neuropathologica. - 125 : 2 (2013), p. 273-288. -
További szerzők:McGoldrick, Philip Vance, Caroline Hortobágyi Tibor (1965-) (patológus) Sreedharan, Jemeen Rogelj, Boris Tudor, Elizabeth L. Smith, Bradley Klasen, Christian Miller, Christopher Charles John Cooper, Jonathan D. Greensmith, Linda Shaw, Christopher E.
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