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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:BIBFORM019968
Első szerző:Engmann, Olivia
Cím:Cyclin-dependent kinase 5 activator p25 is generated during memory formation and is reduced at an early stage in Alzheimer's disease / Olivia Engmann, Tibor Hortobágyi, Andrew J. Thompson, Jennifer Guadagno, Claire Troakes, Salvador Soriano, Safa Al-Sarraj, Yong Kim, Karl Peter Giese
Dátum:2011
ISSN:0006-3223
Megjegyzések:BACKGROUND: The cyclin-dependent kinase 5 activator p35 can be cleaved into p25. Formation of p25 has been suggested to contribute to neurodegeneration in Alzheimer's disease (AD). However, overexpression of low levels of p25 in mice enhances memory formation. Therefore, it has been suggested that p25 formation might be an event early in AD to compensate for impairments in synaptic plasticity. Ongoing p25 formation has been hypothesized to contribute to neurodegeneration at the later stages of AD. METHODS: Here, we tested the early compensation hypothesis by analyzing the levels of p25 and its precursor p35 in AD postmortem samples from different brain regions at different stages of tau pathology, using quantitative Western blots. Furthermore, we studied p35 and p25 during spatial memory formation. By employing quantitative mass spectrometry, we identified proteins downstream of p25, which were then studied in AD samples. RESULTS: We found that p25 is generated during spatial memory formation. Furthermore, we demonstrate that overexpression of p25 in the physiological range increases the expression of two proteins implicated in spine formation, septin 7 and optic atrophy 1. We show that the expression of p35 and p25 is reduced as an early event in AD. Moreover, expression of the p25-regulated protein optic atrophy 1 was reduced in a time course similar to p25 expression. CONCLUSIONS: Our findings suggest that p25 generation is a mechanism underlying hippocampal memory formation that is impaired in the early stages of AD. Our findings argue against the previously raised early compensation hypothesis and they propose that p25-mediated neurotoxicity does not occur in AD.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Biological Psychiatry. - 70 : 2 (2011), p. 159-168. -
További szerzők:Hortobágyi Tibor (1965-) (patológus) Thompson, Andrew J. Guadagno, Jennifer Troakes, Claire Soriano, Salvador Al-Sarraj, Safa Kim, Yong Giese, Karl Peter
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6.

001-es BibID:BIBFORM020095
Első szerző:Hortobágyi Tibor (patológus)
Cím:Desmoplastic ganglioglioma with meningiomatous and myofibroblastic components presenting with epilepsy / T. Hortobágyi, M. Honavar, R. Selway, S. Al-Sarraj
Dátum:2008
Tárgyszavak:Orvostudományok Klinikai orvostudományok esettanulmány
Megjelenés:Neuropathology and Applied Neurobiology. - 34 : 1 (2008), p. 118-123. -
További szerzők:Honavar, M. Selway, R. Al-Sarraj, Safa
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7.

001-es BibID:BIBFORM020293
Első szerző:Hortobágyi Tibor (patológus)
Cím:The significance of diffuse axonal injury : how to diagnose it and what does it tell us? / Tibor Hortobágyi, Safa Al-Sarraj
Dátum:2008
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Advances in clinical neuroscience & rehabilitation. - 8 : 2 (2008), p. 16-18. -
További szerzők:Al-Sarraj, Safa
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8.

001-es BibID:BIBFORM020059
Első szerző:Hortobágyi Tibor (patológus)
Cím:Traumatic axonal damage in the brain can be detected using β-APP immunohistochemistry within 35 min after head injury to human adults / T. Hortobágyi, S. Wise, N. Hunt, N. Cary, V. Djurovic, A. Fegan-Earl, K. Shorrock, D. Rouse, S. Al-Sarraj
Dátum:2007
ISSN:0305-1846
Megjegyzések:Immunohistochemistry staining for beta-amyloid precursor protein (beta-APP) is a sensitive method to detect early axonal damage in traumatic brain injury, which was previously estimated to be of minimum 60-90 min after head injury. We present seven cases of well-documented posttraumatic survival of 35-60 min where beta-APP detects early axonal damage. Cases were selected from routine work where documentation about survival is judged to be accurate. These are divided into three groups: group 1: severe head injury (n = 7) with documented survival between 35 and 60 min. Group 2: severe head injury (n = 4) with documented survival of less than 30 min. Group 3: cases (n = 4) where death was not due to head injury but survival is documented between 45 and 109 min. The brains were fixed in formalin for 4 weeks and six regions (frontal lobe with anterior corpus callosum, parietal lobe with deep white matter, basal ganglia with posterior limb of internal capsule, cerebellum with white matter and middle cerebellar peduncle and pons with basis pontis and superior cerebellar peduncle) were sampled. All blocks were stained for haematoxylin and eosin and beta-APP and selected ones for CD68, using antigen retrieval method. In group 1 sections revealed beta-APP immunoreactivity in forms of small globules and granules and occasionally as thin and short filaments. These were detected in the pons, corpus callosum, internal capsule and cerebral white matter, with some variation in localization and intensity. In groups 2 and 3 all the sections were negative for beta-APP staining. None of the cases showed evidence of severe brain swelling, increased intracranial pressure, ischaemia or infection. Using the antigen retrieval method, beta-APP immunohistochemistry can detect axonal damage within 35 min after severe head injury. These results may have an implication in the consideration of minimal survival time after traumatic head injury in medico-legal practice.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Neuropathology and Applied Neurobiology. - 33 : 2 (2007), p. 226-237. -
További szerzők:Wise, S. Hunt, N. Cary, N. Djurovic, Vesna Fegan-Earl, A. Shorrock, K. Rouse, D. Al-Sarraj, Safa
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9.

001-es BibID:BIBFORM020019
Első szerző:Hortobágyi Tibor (patológus)
Cím:Cysticercosis of the fourth ventricle causing sudden death : a case report and review of the literature / Tibor Hortobágyi, Ali Alhakim, Olaf Biedrzycki, Vesna Djurovic, Jeewan Rawal, Safa Al-Sarraj
Dátum:2008
ISSN:1219-4956
Megjegyzések:A 15 years old girl of African origin was admitted with a history of headaches and a generalised tonic seizure. Her clinical examination including fundoscopy was normal. She claimed she had been assaulted. Within a few hours of her admission she was found dead in her bed during the ward round. Cardiopulmonary resuscitation was unsuccessful. At post-mortem, the major organs showed no pathological changes and neck dissection showed no abnormality. Neuropathological examination after formalin fixation revealed a cystic lesion in the fourth ventricle, ependymitis and acute hydrocephalus. Histology showed parts of the parasite Taenia solium and the diagnosis was neurocysticercosis. This case highlights the need for forensic and general pathologists as well as forensic medical examiners and paediatricians to be aware of neurocysticercosis as a possible cause of sudden death in the presence of normal clinical findings and negative autopsy, especially in patients from Asian, African or South American countries. As cysticercosis is the commonest cause of seizures in the developing world, neurocysticercosis needs to be considered as a cause of sudden and unexpected death in any patient with a history of headaches and/or seizures.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Pathology and Oncology Research. - 15 : 1 (2008), p. 143-146. -
További szerzők:Alhakim, Ali Biedrzycki, Olaf Djurovic, Vesna Rawal, Jeewan Al-Sarraj, Safa
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10.

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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11.

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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12.

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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