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1.

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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2.

001-es BibID:BIBFORM019984
Első szerző:Halleskog, Carina
Cím:WNT signaling in activated microglia is proinflammatory / Carina Halleskog, Jan Mulder, Jenny Dahlström, Ken Mackie, Tibor Hortobágyi, Heikki Tanila, Lakshman Kumar Puli, Katrin Färber, Tibor Harkany, Gunnar Schulte
Dátum:2011
ISSN:0894-1491
Megjegyzések:Microglia activation is central to the neuroinflammation associated with neurological and neurodegenerative diseases, particularly because activated microglia are often a source of proinflammatory cytokines. Despite decade-long research, the molecular cascade of proinflammatory transformation of microglia in vivo remains largely elusive. Here, we report increased β-catenin expression, a central intracellular component of WNT signaling, in microglia undergoing a proinflammatory morphogenic transformation under pathogenic conditions associated with neuroinflammation such as Alzheimer's disease. We substantiate disease-associated β-catenin signaling in microglia in vivo by showing age-dependent β-catenin accumulation in mice with Alzheimer's-like pathology (APdE9). In cultured mouse microglia expressing the WNT receptors Frizzled FZD(4,5,7,8) and LDL receptor-related protein 5/6 (LRP5/6), we find that WNT-3A can stabilize β-catenin. WNT-3A dose dependently induces LRP6 phosphorylation with downstream activation of disheveled, β-catenin stabilization, and nuclear import. Gene-expression profiling reveals that WNT-3A stimulation specifically increases the expression of proinflammatory immune response genes in microglia and exacerbates the release of de novo IL-6, IL-12, and tumor necrosis factor α. In summary, our data suggest that the WNT family of lipoglycoproteins can instruct proinflammatory microglia transformation and emphasize the pathogenic significance of β-catenin-signaling networks in this cell type.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Glia. - 59 : 1 (2011), p. 119-131. -
További szerzők:Mulder, Jan Dahlström, Jenny Mackie, Ken Hortobágyi Tibor (1965-) (patológus) Tanila, Heikki Kumar Puli, Lakshman Färber, Katrin Harkány Tibor Schulte, Gunnar
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3.

001-es BibID:BIBFORM020087
Első szerző:Harkány Tibor
Cím:Short-term consequences of N-methyl-D-aspartate excitotoxicity in rat magnocellular nucleus basalis : effects on in vivo labelling of cholinergic neurons / T. Harkany, J. Grosche, J. Mulder, K. M. Horvath, J. Keijser, T. Hortobágyi, P. G. M. Luiten, W. Härtig
Dátum:2001
ISSN:0306-4522
Megjegyzések:Cholinergic neurons of the basal forebrain form one of the neuron populations that are susceptible to excitotoxic injury. Whereas neuropharmacological studies have aimed at rescuing cholinergic neurons from acute excitotoxic attacks, the short-term temporal profile of excitotoxic damage to cholinergic nerve cells remains largely elusive. The effects of N-methyl-D-aspartate (NMDA) infusion on cytochemical markers of cholinergic neurons in rat magnocellular nucleus basalis were therefore determined 4, 24 and 48 h post-lesion. Additionally, the influence of excitotoxic damage on the efficacy of in vivo labelling of cholinergic neurons with carbocyanine 3-192IgG was investigated. Carbocyanine 3-192IgG was unilaterally injected in the lateral ventricle. Twenty-four hours later, NMDA (60 nM/microl) was infused in the right magnocellular nucleus basalis, while control lesions were performed contralaterally. Triple immunofluorescence labelling for carbocyanine 3-192IgG, NMDA receptor 2A and B subunits and choline-acetyltransferase (ChAT) was employed to determine temporal changes in NMDA receptor immunoreactivity on cholinergic neurons. The extent of neuronal degeneration was studied by staining with Fluoro-Jade. Moreover, changes in the numbers of ChAT or p75 low-affinity neurotrophin receptor immunoreactive neurons, and the degree of their co-labelling with carbocyanine 3-192IgG were determined in basal forebrain nuclei. The effects of NMDA-induced lesions on cortical projections of cholinergic nucleus basalis neurons were studied by acetylcholinesterase (AChE) histochemistry. Characteristic signs of cellular damage, as indicated by decreased immunoreactivity for NMDA receptors, ChAT and p75 low-affinity neurotrophin receptors, were already detected at the shortest post-lesion interval investigated. Fluoro-Jade at 4 h post-lesion only labelled the core of the excitotoxic lesion. Longer survival led to enhanced Fluoro-Jade staining, and to the decline of ChAT immunoreactivity reaching a maximum 24 h post-surgery. Significant loss of p75 low-affinity neurotrophin receptor immunoreactivity and of cortical AChE-positive projections only became apparent 48 h post-lesion. Carbocyanine 3-192IgG labelling in the ipsilateral basal forebrain exceeded that of the contralateral hemisphere at all time points investigated and progressively declined in the damaged magnocellular nucleus basalis up to 48 h after NMDA infusion. The present study indicates that excitotoxic lesion-induced alteration of cholinergic neuronal markers is a rapid and gradual process reaching its maximum 24 h post-surgery. Furthermore, in vivo labelling of cholinergic neurons may be applied to indicate neuronal survival under pathological conditions, and enable to follow their degeneration process under a variety of experimental conditions.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Neuroscience. - 108 : 4 (2001), p. 611-627. -
További szerzők:Grosche, Jens Mulder, Jan Horváth Katalin M. Keijser, J. Hortobágyi Tibor (1965-) (patológus) Luiten, Paul G. M. Härtig, Wolfgang
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Intézményi repozitóriumban (DEA) tárolt változat
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4.

001-es BibID:BIBFORM020073
Első szerző:Harkány Tibor
Cím:Distinct subsets of nucleus basalis neurons exhibit similar sensitivity to excitotoxicity / Tibor Harkany, Csaba Varga, Jens Grosche, Jan Mulder, Paul G. M. Luiten, Tibor Hortobágyi, Botond Penke, Wolfgang Härtig
Dátum:2002
ISSN:0959-4965
Megjegyzések:Excitotoxic lesions in the magnocellular nucleus basalis (MBN) lead to a significant damage of cholinergic neurons concomitant with increased amyloid precursor protein (APP) expression in the cerebral cortex. However, the sensitivity of non-cholinergic neurons to excitotoxicity, and changes of APP expression in the damaged MBN are still elusive. Hence, we performed multiple-labeling immunocytochemistry for choline-acetyltransferase (ChAT), neuron-specific nuclear protein (NeuN) and APP 4, 24, and 48 h after NMDA infusion in the MBN. Whereas all cholinergic neurons were immunoreactive for NeuN, this neuronal marker also labeled a population of ChAT-immunonegative non-cholinergic neurons. Both neuron populations exhibited a similar degree of sensitivity to NMDA excitotoxicity that became evident as early as 4 h post-lesion. Cholinergic MBN neurons showed abundant APP immunoreactivity (approximately 90%), while only a fraction (approximately 20-30%) of non-cholinergic neurons expressed the protein. Remarkably, cholinergic but not non-cholinergic neurons retained their APP immunoreactivity after NMDA infusion. In conclusion, cholinergic MBN neurons are not preferentially sensitive to short-term excitotoxicity, but are one of the major sources of APP in the basal forebrain.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Neuroreport. - 13 : 6 (2002), p. 767-772. -
További szerzők:Varga Csaba (orvos) Grosche, Jens Mulder, Jan Luiten, Paul G. M. Hortobágyi Tibor (1965-) (patológus) Penke Botond Härtig, Wolfgang
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5.

001-es BibID:BIBFORM019971
Első szerző:Mulder, Jan
Cím:Molecular reorganization of endocannabinoid signalling in Alzheimer's disease / Jan Mulder, Misha Zilberter, Susana J. Pasquaré, Alán Alpár, Gunnar Schulte, Samira G. Ferreira, Attila Köfalvi, Ana M. Martín-Moreno, Erik Keimpema, Heikki Tanila, Masahiko Watanabe, Ken Mackie, Tibor Hortobágyi, Maria L. de Ceballos, Tibor Harkany
Dátum:2011
ISSN:0006-8950
Megjegyzések:Retrograde messengers adjust the precise timing of neurotransmitter release from the presynapse, thus modulating synaptic efficacy and neuronal activity. 2-Arachidonoyl glycerol, an endocannabinoid, is one such messenger produced in the postsynapse that inhibits neurotransmitter release upon activating presynaptic CB(1) cannabinoid receptors. Cognitive decline in Alzheimer's disease is due to synaptic failure in hippocampal neuronal networks. We hypothesized that errant retrograde 2-arachidonoyl glycerol signalling impairs synaptic neurotransmission in Alzheimer's disease. Comparative protein profiling and quantitative morphometry showed that overall CB(1) cannabinoid receptor protein levels in the hippocampi of patients with Alzheimer's disease remain unchanged relative to age-matched controls, and CB(1) cannabinoid receptor-positive presynapses engulf amyloid-β-containing senile plaques. Hippocampal protein concentrations for the sn-1-diacylglycerol lipase α and β isoforms, synthesizing 2-arachidonoyl glycerol, significantly increased in definite Alzheimer's (Braak stage VI), with ectopic sn-1-diacylglycerol lipase β expression found in microglia accumulating near senile plaques and apposing CB(1) cannabinoid receptor-positive presynapses. We found that microglia, expressing two 2-arachidonoyl glycerol-degrading enzymes, serine hydrolase α/β-hydrolase domain-containing 6 and monoacylglycerol lipase, begin to surround senile plaques in probable Alzheimer's disease (Braak stage III). However, Alzheimer's pathology differentially impacts serine hydrolase α/β-hydrolase domain-containing 6 and monoacylglycerol lipase in hippocampal neurons: serine hydrolase α/β-hydrolase domain-containing 6 expression ceases in neurofibrillary tangle-bearing pyramidal cells. In contrast, pyramidal cells containing hyperphosphorylated tau retain monoacylglycerol lipase expression, although at levels significantly lower than in neurons lacking neurofibrillary pathology. Here, monoacylglycerol lipase accumulates in CB(1) cannabinoid receptor-positive presynapses. Subcellular fractionation revealed impaired monoacylglycerol lipase recruitment to biological membranes in post-mortem Alzheimer's tissues, suggesting that disease progression slows the termination of 2-arachidonoyl glycerol signalling. We have experimentally confirmed that altered 2-arachidonoyl glycerol signalling could contribute to synapse silencing in Alzheimer's disease by demonstrating significantly prolonged depolarization-induced suppression of inhibition when superfusing mouse hippocampi with amyloid-β. We propose that the temporal dynamics and cellular specificity of molecular rearrangements impairing 2-arachidonoyl glycerol availability and actions may differ from those of anandamide. Thus, enhanced endocannabinoid signalling, particularly around senile plaques, can exacerbate synaptic failure in Alzheimer's disease.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Brain. - 134 : 4 (2011), p. 1041-1060. -
További szerzők:Zilberter, Misha Pasquaré, Susana J. Alpár Alán Schulte, Gunnar Ferreira, Samira G. Köfalvi Attila Martín-Moreno, Ana M. Keimpema, Erik Tanila, Heikki Watanabe, Masahiko Mackie, Ken Hortobágyi Tibor (1965-) (patológus) de Ceballos, Maria L. Harkány Tibor
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6.

001-es BibID:BIBFORM069191
Első szerző:Wilhelmsson, Ulrika
Cím:Injury Leads to the Appearance of Cells with Characteristics of Both Microglia and Astrocytes in Mouse and Human Brain / Ulrika Wilhelmsson, Daniel Andersson, Yolanda de Pablo, Roy Pekny, Anders Ståhlberg, Jan Mulder, Nicholas Mitsios, Tibor Hortobágyi, Milos Pekny, Marcela Pekna
Dátum:2017
ISSN:1047-3211
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Cerebral Cortex. - 27 : 6 (2017), p. 3360-3377. -
További szerzők:Andersson, Daniel de Pablo, Yolanda Pekny, Roy Ståhlberg, Anders Mulder, Jan Mitsios, Nicholas Hortobágyi Tibor (1965-) (patológus) Pekny, Milos Pekna, Marcela
Pályázati támogatás:GINOP-2.3.2-15-2016-00043
GINOP
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Intézményi repozitóriumban (DEA) tárolt változat
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7.

001-es BibID:BIBFORM107284
035-os BibID:(scopus)85135939903 (wos)000891285200003 (cikkazonosító)e2123146119
Első szerző:Zhong, Wen
Cím:The neuropeptide landscape of human prefrontal cortex / Zhong Wen, Barde Swapnali, Mitsios Nicholas, Adori Csaba, Oksvold Per, Feilitzen Kalle von, O'Leary Liam, Csiba László, Hortobágyi Tibor, Szocsics Péter, Mechawar Naguib, Maglóczky Zsófia, Renner Éva, Palkovits Miklós, Uhlén Mathias, Mulder Jan, Hökfelt Tomas
Dátum:2022
ISSN:0027-8424 1091-6490
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Proceedings Of The National Academy Of Sciences Of The United States Of America. - 119 : 33 (2022), p. 1-12. -
További szerzők:Barde, Swapnali Mitsios, Nicholas Adori Csaba Oksvold, Per von Feilitzen, Kalle O'Leary, Liam Csiba László (1952-) (neurológus, pszichiáter) Hortobágyi Tibor (1965-) (patológus) Szocsics Péter Mechawar, Naguib Maglóczky Zsófia Renner Éva Palkovits Miklós Uhlén, Mathias Mulder, Jan Hökfelt, Tomas
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