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1.

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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2.

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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3.

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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4.

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
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5.

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
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6.

001-es BibID:BIBFORM076126
035-os BibID:(WoS)000446548400016 (Scopus)85054395402
Első szerző:Solomon, Daniel A.
Cím:A feedback loop between dipeptide-repeat protein, TDP-43 and karyopherin-[alfa] mediates C9orf72-related neurodegeneration / Solomon Daniel A., Stepto Alan., Au Wing Hei, Adachi Yoshitsugu, Diaper Danielle C., Hall Rachel, Rekhi Anjeet, Boudi Adel, Tziortzouda Paraskevi, Lee Youn-Bok, Smith Bradley, Bridi Jessika C., Spinelli Greta, Dearlove Jonah, Humphrey Dickon M., Gallo Jean-Marc, Troakes Claire, Fanto Manolis, Soller Matthias, Rogelj Boris, Parsons Richard B., Shaw Christopher E., Hortobágyi Tibor, Hirth Frank
Dátum:2018
ISSN:0006-8950
Megjegyzések:Accumulation and aggregation of TDP-43 is a major pathological hallmark of amyotrophic lateral sclerosis and frontotemporal dementia. TDP-43 inclusions also characterize patients with GGGGCC (G4C2) hexanucleotide repeat expansion in C9orf72 that causes the most common genetic form of amyotrophic lateral sclerosis and frontotemporal dementia (C9ALS/FTD). Functional studies in cell and animal models have identified pathogenic mechanisms including repeat-induced RNA toxicity and accumulation of G4C2-derived dipeptide-repeat proteins. The role of TDP-43 dysfunction in C9ALS/FTD, however, remains elusive. We found G4C2-derived dipeptide-repeat protein but not G4C2-RNA accumulation caused TDP-43 proteinopathy that triggered onset and progression of disease in Drosophila models of C9ALS/FTD. Timing and extent of TDP-43 dysfunction was dependent on levels and identity of dipeptide-repeat proteins produced, with poly-GR causing early and poly-GA/poly-GP causing late onset of disease. Accumulating cytosolic, but not insoluble aggregated TDP-43 caused karyopherin-?2/4 (KPNA2/4) pathology, increased levels of dipeptide-repeat proteins and enhanced G4C2-related toxicity. Comparable KPNA4 pathology was observed in both sporadic frontotemporal dementia and C9ALS/FTD patient brains characterized by its nuclear depletion and cytosolic accumulation, irrespective of TDP-43 or dipeptide-repeat protein aggregates. These findings identify a vicious feedback cycle for dipeptide-repeat protein-mediated TDP-43 and subsequent KPNA pathology, which becomes self-sufficient of the initiating trigger and causes C9-related neurodegeneration.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Brain. - 141 : 10 (2018), p. 2908-2924. -
További szerzők:Stepto, Alan Au, Wing Hei Adachi, Yoshitsugu Diaper, Danielle C. Hall, Rachel Rekhi, Anjeet Boudi, Adel Tziortzouda, Paraskevi Lee, Younbok Smith, Bradley Bridi, Jessika C. Spinelli, Greta Dearlove, Jonah Humphrey, Dickon M. Gallo, Jean-Marc Troakes, Claire Fanto, Manolis Soller, Matthias Rogelj, Boris Parsons, Richard B. Shaw, Christopher E. Hortobágyi Tibor (1965-) (patológus) Hirth, Frank
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7.

001-es BibID:BIBFORM065658
Első szerző:Tiwari, Sachin Suresh
Cím:Alzheimer-related decrease in CYFIP2 links amyloid production to tau hyperphosphorylation and memory loss / Sachin Suresh Tiwari, Keiko Mizuno, Anshua Ghosh, Wajeeha Aziz, Claire Troakes, Jason Daoud, Vidushi Golash, Wendy Noble, Tibor Hortobágyi, Karl Peter Giese
Dátum:2016
ISSN:0006-8950
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Brain 139 : Pt10 (2016), p. 2751-2765. -
További szerzők:Mizuno, Keiko Ghosh, Anshua Aziz, Wajeeha Troakes, Claire Daoud, Jason Golash, Vidushi Noble, Wendy Hortobágyi Tibor (1965-) (patológus) Giese, Karl Peter
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8.

001-es BibID:BIBFORM063338
Első szerző:Tiwari, Sachin Suresh
Cím:Evidence that the presynaptic vesicle protein CSPalpha is a key player in synaptic degeneration and protection in Alzheimer's disease / Sachin S. Tiwari, Marie d'Orange, Claire Troakes, Badrun N. Shurovi, Olivia Engmann, Wendy Noble, Tibor Hortobágyi, Karl P. Giese
Dátum:2015
ISSN:1756-6606
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Molecular Brain. - 8 : 1 (2015), p. 1-12. -
További szerzők:d'Orange, Marie Troakes, Claire Shurovi, Badrun N. Engmann, Olivia Noble, Wendy Hortobágyi Tibor (1965-) (patológus) Giese, Karl Peter
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