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1.

001-es BibID:BIBFORM083135
035-os BibID:(cikkazonosító)68 (scopus)85078993240 (wos)000519243400011
Első szerző:Bencze János (orvos)
Cím:Lemur tyrosine kinase 2 (LMTK2) level inversely correlates with phospho-tau in neuropathological stages of Alzheimer's disease / János Bencze, Máté Szarka, Viktor Bencs, Renáta Nóra Szabó, László V. Módis, Dag Aarsland, Tibor Hortobágyi
Dátum:2020
Megjegyzések:Alzheimer's disease (AD) is the most common neurodegenerative dementia. Mapping the pathomechanism and providing novel therapeutic options have paramount significance. Recent studies have proposed the role of LMTK2 in AD. However, its expression pattern and association with the pathognomonic neurofibrillary tangles (NFTs) in different brain regions and neuropathological stages of AD is not clear. We performed chromogenic (CHR) LMTK2 and fluorescent phospho-tau/LMTK2 double-labelling (FDL) immunohistochemistry (IHC) on 10-10 post-mortem middle frontal gyrus (MFG) and anterior hippocampus (aHPC) samples with early and late neuropathological Braak tau stages of AD. MFG in early stage was our ♭endogenous control' region as it is not affected by NFTs. Semi-quantitative CHR-IHC intensity scoring revealed significantly higher (p<0.001) LMTK2 values in this group compared to NFT-affected regions. FDL-IHC demonstrated LMTK2 predominance in the endogenous control region, while phospho-tau overburden and decreased LMTK2 immunolabelling were detected in NFT-affected groups (aHPC in early and both regions in late stage). Spearman's correlation coefficient showed strong negative correlation between phospho-tau/LMTK2 signals within each group. According to our results LMTK2 expression is inversely proportionate to the extent of NFT pathology, as well as decreased LMTK2 level is not a general feature in AD brain, rather it is characteristic to the NFT-affected regions.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Alzheimer's disease
LMTK2
neurodegeneration
tau
digital image analysis
Megjelenés:Brain Sciences. - 10 : 2 (2020), p. 1-14. -
További szerzők:Szarka Máté (1990-) Bencs Viktor (1995-) (orvos) Szabó Renáta Nóra Módis László V. (neurológus) Aarsland, Dag Hortobágyi Tibor (1965-) (patológus)
Pályázati támogatás:EFOP-3.6.3-VEKOP-16-2017-00009
EFOP
ÚNKP-19-3
Egyéb
NAP (2017-1.2.1-NKP-2017-00002)
Egyéb
GINOP-2.3.2-15-2016-00043
GINOP
ÚNKP-19-2
Egyéb
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2.

001-es BibID:BIBFORM072946
Első szerző:Bencze János (orvos)
Cím:Biological function of Lemur tyrosine kinase 2 (LMTK2) : implications in neurodegeneration / János Bencze, Gábor Miklós Mórotz, Woosung Seo, Viktor Bencs, János Kálmán, Christopher Charles John Miller, Tibor Hortobágyi
Dátum:2018
ISSN:1756-6606
Megjegyzések:Neurodegenerative disorders are frequent, incurable diseases characterised by abnormal protein accumulationand progressive neuronal loss. Despite their growing prevalence, the underlying pathomechanism remainsunclear. Lemur tyrosine kinase 2 (LMTK2) is a member of a transmembrane serine/threonine-protein kinase family.Although it was described more than a decade ago, our knowledge on LMTK2's biological functions is still insufficient.Recent evidence has suggested that LMTK2 is implicated in neurodegeneration. After reviewing the literature, weidentified three LMTK2-mediated mechanisms which may contribute to neurodegenerative processes: disrupted axonaltransport, tau hyperphosphorylation and enhanced apoptosis. Moreover, LMTK2 gene expression is decreased in anAlzheimer's disease mouse model. According to these features, LMTK2 might be a promising therapeutic target in nearfuture. However, further investigations are required to clarify the exact biological functions of this unique protein.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Alzheimer's disease
Axonal transport
LMTK2
Neurodegeneration
Tau
Megjelenés:Molecular Brain. - 11 : 20 (2018), p. 1-9. -
További szerzők:Mórotz Miklós Gábor Woosung Seo Bencs Viktor (1995-) (orvos) Kálmán János Miller, Christopher Charles John Hortobágyi Tibor (1965-) (patológus)
Pályázati támogatás:ÚNKP-17-3
ÚNKP
EFOP-3.6.3-VEKOP-16-2017-00009
EFOP
GINOP-2.3.2-15-2016-00043
GINOP
2017- 1.2.1-NKP-2017-00002
Egyéb
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3.

001-es BibID:BIBFORM020090
Első szerző:Benyó Zoltán
Cím:Functional importance of neuronal nitric oxide synthase in the endothelium of rat basilar arteries / Zoltán Benyó, Zsombor Lacza, Tibor Hortobágyi, Christoph Görlach, Michael Wahl
Dátum:2000
ISSN:0006-8993
Megjegyzések:The function of the neuronal isoform of nitric oxide synthase (nNOS) was studied by comparing the effects of the specific nNOS blocker 7-nitro indazole monosodium salt (7-NINA) with that of the general NOS inhibitor N(G)-nitro-L-arginine (L-NA) in isolated rat basilar arteries (BAs). 7-NINA had no significant effect on the resting tone of the vessels, while both L-NA and 1H-[1,2,4]oxadiazolo[4, 3-a]quinoxalin-1-one (ODQ), a selective inhibitor of the soluble guanylyl cyclase, induced contraction. The relaxant effect of bradykinin was attenuated in the presence of L-NA but was not changed by 7-NINA. In contrast, 7-NINA markedly reduced the acetylcholine-induced, endothelium-dependent relaxation. These results demonstrate that nNOS contributes significantly to the relaxant effect of acetylcholine, indicating the functional importance of this isoenzyme in the cerebrovascular endothelium.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Brain Research. - 877 : 1 (2000), p. 79-84. -
További szerzők:Lacza Zsombor Hortobágyi Tibor (1965-) (patológus) Görlach, Christoph Wahl, Michael
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4.

001-es BibID:BIBFORM071437
Első szerző:Bereczki Erika
Cím:Synaptic markers of cognitive decline in neurodegenerative diseases : a proteomic approach / Erika Bereczki, Rui M. Branca, Paul T. Francis, Joana B. Pereira, Jean-Ha Baek, Tibor Hortobágyi, Bengt Winblad, Clive Ballard, Janne Lehtiö, Dag Aarsland
Dátum:2017
ISSN:0006-8950
Megjegyzések:See Attems and Jellinger (doi:10.1093/brain/awx360) for a scientific commentary on this article.Cognitive changes occurring throughout the pathogenesis of neurodegenerative diseases are directly linked to synaptic loss. We used in-depth proteomics to compare 32 post-mortem human brains in the prefrontal cortex of prospectively followed patients with Alzheimer's disease, Parkinson's disease with dementia, dementia with Lewy bodies and older adults without dementia. In total, we identified 10 325 proteins, 851 of which were synaptic proteins. Levels of 25 synaptic proteins were significantly altered in the various dementia groups. Significant loss of SNAP47, GAP43, SYBU (syntabulin), LRFN2, SV2C, SYT2 (synaptotagmin 2), GRIA3 and GRIA4 were further validated on a larger cohort comprised of 92 brain samples using ELISA or western blot. Cognitive impairment before death and rate of cognitive decline significantly correlated with loss of SNAP47, SYBU, LRFN2, SV2C and GRIA3 proteins. Besides differentiating Parkinson's disease dementia, dementia with Lewy bodies, and Alzheimer's disease from controls with high sensitivity and specificity, synaptic proteins also reliably discriminated Parkinson's disease dementia from Alzheimer's disease patients. Our results suggest that these particular synaptic proteins have an important predictive and discriminative molecular fingerprint in neurodegenerative diseases and could be a potential target for early disease intervention.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Brain 141 : 2 (2018), p. 582-595. -
További szerzők:Branca, Rui M. Francis, Paul T. Pereira, Joana B. Baek, Jean-Ha Hortobágyi Tibor (1965-) (patológus) Winblad, Bengt Ballard, Clive G. Lehtiö, Janne Aarsland, Dag
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5.

001-es BibID:BIBFORM020046
Első szerző:Bódi István (neuropatológus)
Cím:A 72-year-old woman with right frontal extra-axial mass / Istvan Bodi, Tibor Hortobágyi, Stefan Buk
Dátum:2008
ISSN:1015-6305
Megjegyzések:We present a case of plasma cell predominant lymphoplasmacyte-rich meningioma with numerous crystalline inclusions. A 72-year-old woman presented with 1-year history of memory disturbance and an MRI revealing a right frontal extra-axial mass. Histology showed a benign meningioma with multifocal accumulation of numerous large cells with abundant eosinophilic cytoplasm, filled with lamellar inclusions and bipyramidal crystals. In addition, some classic plasma cells, mastocytes and lymphocytes were also detected. The crystal-containing cells were positive by CD79a and PGM1 and expressed polyclonal light chains, with kappa predominance. Electron microscopy showed crystals with needle or rectangular shape in plasma cells. Plasma cell inclusions have been reported occasionally in reactive inflammatory lesions but more frequently in plasma cell tumors and lymphoplasmacytic lymphoma, maybe associated with crystal-storing histiocytosis. Although plasma cell predominant lymphoplasmacyte-rich meningioma is not uncommon, to our knowledge, similar crystalline inclusions in plasma cells have not been reported previously in meningioma.
Tárgyszavak:Orvostudományok Klinikai orvostudományok esettanulmány
Megjelenés:Brain Pathology. - 18 : 2 (2008), p. 279-282. -
További szerzők:Hortobágyi Tibor (1965-) (patológus) Buk, Stefan
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6.

001-es BibID:BIBFORM063696
Első szerző:Bondulich, Marie K.
Cím:Tauopathy induced by low level expression of a human brain-derived tau fragment in mice is rescued by phenylbutyrate / Marie K. Bondulich, Tong Guo, Christopher Meehan, John Manion, Teresa Rodriguez Martin, Jacqueline C. Mitchell, Tibor Hortobagyi, Natalia Yankova, Virginie Stygelbout, Jean-Pierre Brion, Wendy Noble, Diane P. Hanger
Dátum:2016
ISSN:0006-8950
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Brain 139 : 8 (2016), p. 2290-2306. -
További szerzők:Guo, Tong Meehan, Christopher Manion, John Rodriguez-Martin, Teresa Mitchell, Jacqueline C. Hortobágyi Tibor (1965-) (patológus) Yankova, Natalia Stygelbout, Virginie Brion, Jean-Pierre Noble, Wendy Hanger, Diane P.
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7.

001-es BibID:BIBFORM020023
Első szerző:Elliott, Mark S. J.
Cím:Increased binding to 5-HT1A and 5-HT2A receptors is associated with large vessel infarction and relative preservation of cognition / Marc S. J. Elliott, Clive G. Ballard, Rajesh N. Kalaria, Robert Perry, Tibor Hortobágyi, Paul T. Francis
Dátum:2009
ISSN:0006-8950
Megjegyzések:Vascular dementia accounts for approximately 15-20% of all dementias. In addition, a significant subset of people with Alzheimer's disease have concurrent cerebrovascular disease. Vascular dementia is caused by different cerebrovascular morphological abnormalities including large artery territory infarction (multi-infarct vascular dementia) and sub-cortical ischaemic vascular dementia. Despite this distinction, there is a lack of studies examining the neurochemistry of individual vascular dementia subtypes. Serotonin is believed to play an important role in cognition, and serotonin receptors may provide a novel target for future anti-dementia therapeutics. This study aimed to determine levels of two serotonin receptors in subtypes of vascular dementia and relate any changes to cognition. We have determined, using saturation radioligand binding, the binding parameters (affinity and maximal binding) of ((3)H)-WAY 100635 binding to 5-HT(1A) receptors and ((3)H)-ketanserin binding to 5-HT(2A) receptors in post-mortem tissue from the frontal and temporal cortices of patients with either multi-infarct vascular dementia, sub-cortical ischaemic vascular dementia, mixed Alzheimer's disease/vascular dementia or stroke no dementia (SND). 5-HT(1A) and 5-HT(2A) receptor binding was significantly increased in the temporal cortex of patients with either multi-infarct vascular dementia or SND, compared to age-matched controls. 5-HT(1A) receptor maximal binding in the temporal cortex was also positively correlated with cognition as determined by Mini-Mental State Examination (MMSE) and Cambridge Assessment of Mental Health for the Elderly scores (CAMCOG). These results reveal an important distinction between the neurochemistry of multi-infarct vascular dementia/SND and sub-cortical ischaemic vascular dementia, suggesting that pharmacological manipulation of serotonin offers the possibility to develop novel therapies for stroke and multi-infarct vascular dementia patients. The results also highlight the importance of the cortical 5-HT(1A) receptor in mediating cognition.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Brain. - 132 : 7 (2009), p. 1858-1865. -
További szerzők:Ballard, Clive G. Kalaria, Rajesh N. Perry, Robert Hortobágyi Tibor (1965-) (patológus) Francis, Paul T.
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8.

001-es BibID:BIBFORM019979
Első szerző:Engmann, Olivia
Cím:Schizophrenia is associated with dysregulation of a Cdk5 activator that regulates synaptic protein expression and cognition / Olivia Engmann, Tibor Hortobágyi, Ruth Pidsley, Claire Troakes, Hans-Gert Bernstein, Michael R. Kreutz, Jonathan Mill, Margareta Nikolic, Karl Peter Giese
Dátum:2011
ISSN:0006-8950
Megjegyzések:Cyclin-dependent kinase 5 is activated by small subunits, of which p35 is the most abundant. The functions of cyclin-dependent kinase 5 signalling in cognition and cognitive disorders remains unclear. Here, we show that in schizophrenia, a disorder associated with impaired cognition, p35 expression is reduced in relevant brain regions. Additionally, the expression of septin 7 and OPA1, proteins downstream of truncated p35, is decreased in schizophrenia. Mimicking a reduction of p35 in heterozygous knockout mice is associated with cognitive endophenotypes. Furthermore, a reduction of p35 in mice results in protein changes similar to schizophrenia post-mortem brain. Hence, heterozygous p35 knockout mice model both cognitive endophenotypes and molecular changes reminiscent of schizophrenia. These changes correlate with reduced acetylation of the histone deacetylase 1 target site H3K18 in mice. This site has previously been shown to be affected by truncated p35. By restoring H3K18 acetylation with the clinically used specific histone deacetylase 1 inhibitor MS-275 both cognitive and molecular endophenotypes of schizophrenia can be rescued in p35 heterozygous knockout mice. In summary, we suggest that reduced p35 expression in schizophrenia has an impact on synaptic protein expression and cognition and that these deficits can be rescued, at least in part, by the inhibition of histone deacetylase 1.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Brain. - 134 : 8 (2011), p. 2408-2421. -
További szerzők:Hortobágyi Tibor (1965-) (patológus) Pidsley, Ruth Troakes, Claire Bernstein, Hans-Gert Kreutz, Michael R. Mill, Jonathan Nikolic, Margareta Giese, Karl Peter
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9.

001-es BibID:BIBFORM043340
Első szerző:Farkas Szabolcs (orvos)
Cím:Signal transduction pathway activity compensates dopamine D2/D3 receptor density changes in Parkinson's disease : a preliminary comparative human brain receptor autoradiography study with [3H]raclopride and [35S]GTPgammaS / Farkas Szabolcs, Nagy Katalin, Jia Zhisheng, Hortobágyi Tibor, Varrone Andrea, Halldin Christer, Csiba László, Gulyás Balázs
Dátum:2012
ISSN:0006-8993
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Brain Research. - 1453 (2012), p. 56-63. -
További szerzők:Nagy Katalin (1960-) (orvosdiagnosztikai laboratóriumi analitikus) Jia, Zhisheng Hortobágyi Tibor (1965-) (patológus) Varrone, Andrea Halldin, Christer Csiba László (1952-) (neurológus, pszichiáter) Gulyás Balázs
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10.

001-es BibID:BIBFORM020093
Első szerző:Hortobágyi Tibor (patológus)
Cím:Neurotrophin-mediated neuroprotection by solid fetal telencephalic graft in middle cerebral artery occlusion : a preventive approach / T. Hortobágyi, T. Harkany, R. Reisch, R. Urbanics, M. Kálmán, C. Nyakas, Z. Nagy
Dátum:1998
ISSN:0361-9230
Megjegyzések:In the present study, embryonic rat neocortex was implanted into the parietal subcortical area of adult naive animals. On the 7th day, the middle cerebral artery was permanently occluded ipsilateral to the graft. Twenty-four hours after middle cerebral artery occlusion, the extent of infarct was visualized by means of 2,3,5-triphenyltetrazolium chloride histochemistry and quantified in four different standardized coronal plains. Subsequently, the effects of fetal tissue grafting and those of transplantation were identified by using glial fibrillary acidic protein and nerve growth factor immunocytochemistry. The grafts integrated well into their new environment and significantly reduced the size of infarct in middle cerebral artery-occluded animals compared with both sham-operated and control rats 24 h postoperation. The underlying mechanism of this phenomenon might be an increased neurotrophic, particularly nerve growth factor, release by the grafted fetal tissue. Moreover, reactive astroglial cells may also trigger the neuroprotection by additional ischemia-induced nerve growth factor release. The present data demonstrate the potential neurotrophin-mediated protective effects of fetal brain tissue implanted into the adult rat brain before unilateral middle cerebral artery occlusion and the beneficial effects of astrocyte activation.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Brain Research Bulletin. - 47 : 2 (1998), p. 185-191. -
További szerzők:Harkány Tibor Reisch, R. Urbanics R. Kálmán M. Nyakas Csaba Nagy Zoltán (1942-) (neurológus)
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11.

001-es BibID:BIBFORM063676
Első szerző:Howlett, David R.
Cím:Regional Multiple Pathology Scores Are Associated with Cognitive Decline in Lewy Body Dementias / David R. Howlett, David Whitfield, Mary Johnson, Johannes Attems, John T. O'Brien, Dag Aarsland, Mitchell K.P. Lai, Jasinda H. Lee, Christopher Chen, Clive Ballard, Tibor Hortobágyi, Paul T. Francis
Dátum:2015
ISSN:1015-6305
Megjegyzések:Dementia with Lewy bodies (DLB) and Parkinson's disease dementia (PDD) are characterizedby the presence of ?-synuclein-containing Lewy bodies and Lewy neurites.However, both dementias also show variable degrees of Alzheimer's disease (AD) pathology(senile plaques and neurofibrillary tangles), particularly in areas of the cortex associatedwith higher cognitive functions. This study investigates the contribution of theindividual and combined pathologies in determining the rate of cognitive decline. Cortical?-synuclein, phosphorylated tau (phosphotau) and A? plaque pathology in 34 PDD and 55DLB patients was assessed semi-quantitatively in four regions of the neocortex. The declinein cognition, assessed by Mini Mental State Examination, correlated positively with thecortical ?-synuclein load. Patients also had varying degrees of senile A? plaque andphosphotau pathology. Regression analyses pointed to a combined pathology (A? plaqueplus phosphotau plus ?-synuclein-positive features), particularly in the prefrontal cortex(BA9) and temporal lobe neocortex with the superior and middle temporal gyrus (BA21,22), being a major determining factor in the development of dementia. Thus, cognitivedecline in Lewy body dementias is not a consequence of ?-synuclein-induced neurodegenerationalone but senile plaque and phosphorylated tau pathology also contribute tothe overall deficits.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Brain Pathology. - 25 : 4 (2015), p. 401-408. -
További szerzők:Whitfield, David Johnson, Mary Attems, Johannes O'Brien, John Aarsland, Dag Lai, Mitchell K.P. Lee, Jasinda H. Chen, Christopher Ballard, Clive G. Hortobágyi Tibor (1965-) (patológus) Francis, Paul T.
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12.

001-es BibID:BIBFORM051598
035-os BibID:PMID:23521156 WOS:000325608000002
Első szerző:Howlett, David R.
Cím:Clusterin associates specifically with Aβ40 in Alzheimer's disease brain tissue / David R. Howlett, Tibor Hortobágyi, Paul T. Francis
Dátum:2013
ISSN:1015-6305
Megjegyzések:Genome-wide association studies have pointed to clusterin (apolipoprotein J) as being linked to the occurrence of Alzheimer's disease (AD); studies have identified the protein as a possible biomarker. The association between clusterin and senile plaques in AD brain is well known, and clusterin levels in AD brain are 40% higher than that in control subjects. The present study investigates, immunohistochemically, the association between clusterin and Aβ peptides in AD and control cortex. A unique and specific association between clusterin and Aβ40 was observed in plaques in the cerebral cortex from AD subjects in that only plaques that contained Aβ40 showed clusterin immunoreactivity, while the many plaques with Aβ42 alone lacked clusterin labeling. Cerebrovascular Aβ in AD brain generally lacked Aβ42 but was positively labeled by both the Aβ40 and the clusterin antibodies. In control subjects, however, Aβ40 was absent from plaques, although very occasional plaques were found to be labeled by both the Aβ42 and the clusterin antibodies. Overall, in AD, but not aged control brain, clusterin was associated specifically with the Aβ40 form of Aβ in the brain. The lack of clusterin in association with Aβ42 may be a significant feature in neuronal loss and neurodegeneration in the disease state.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Alzheimer's disease
amyloid beta-protein
apolipoprotein J
biomarker
clusterin
Megjelenés:Brain Pathology. - 23 : 6 (2013), p. 623-632. -
További szerzők:Hortobágyi Tibor (1965-) (patológus) Francis, Paul T.
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