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1.

001-es BibID:BIBFORM020292
Első szerző:Currais, Antonio
Cím:The neuronal cell cycle as a mechanism of pathogenesis in Alzheimer's disease = Nevronski celični ciklus kot patogenetski dejavnik pri Alzhemerjevi bolezni / Antonio Currais, Bilal Malik, Tibor Hortobágyi, Salvador Soriano
Dátum:2008
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Zdravstveni Vestnik. - 77 : 2 (2008), p. 13-20. -
További szerzők:Malik, Bilal Hortobágyi Tibor (1965-) (patológus) Soriano, Salvador
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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2.

001-es BibID:BIBFORM020096
Első szerző:Currais, Antonio
Cím:The neuronal cell cycle as a mechanism of pathogenesis in Alzheimer's disease / Antonio Currais, Tibor Hortobágyi, Salvador Soriano
Dátum:2009
Megjegyzések:Differentiated neurons display specific biochemical, physiological and morphological properties that apparently prevent them from further cell division. Nevertheless, expression of cell cycle modulators persists after neuronal differentiation and is upregulated under stress conditions, such as trophic factor deprivation, oxidative stress and the presence of DNA damaging agents. This apparent reactivation of the cell cycle has been postulated as a sine qua non for neuronal death in response to those stress conditions, particularly in Alzheimer's disease. However, the physiological and pathogenic implications of a putative neuronal cell cycle are far from clear. Here, we discuss the notion of the neuronal cell cycle as a mediator of cell death, with particular emphasis on Alzheimer's disease.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Aging [electronic resource]. - 1 : 4 (2009), p. 363-371. -
További szerzők:Soriano, Salvador Hortobágyi Tibor (1965-) (patológus)
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3.

001-es BibID:BIBFORM016363
Első szerző:Currais, Antonio
Cím:The neuronal cell cycle as a mechanism of pathogenesis in Alzheimer's disease / Antonio Currais, Tibor Hortobágyi, Salvador Soriano
Dátum:2010
ISBN:978 81 7895 447 9
Tárgyszavak:Orvostudományok Klinikai orvostudományok könyvfejezet
Megjelenés:Cell Cycle Regulators in Alzheimer's Disease / ed. Jaya Padmanabhan. - p. 39-53. -
További szerzők:Hortobágyi Tibor (1965-) (patológus) Soriano, Salvador
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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4.

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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5.

001-es BibID:BIBFORM020049
Első szerző:Malik, Bilal
Cím:Loss of neuronal cell cycle control as a mechanism of neurodegeneration in the presenilin-1 Alzheimer's disease brain / Bilal Malik, Antonio Currais, Ana Andres, Christopher Towlson, Didier Pitsi, Ana Nunes, Michael Niblock, Jonathan Cooper, Tibor Hortobágyi, Salvador Soriano
Dátum:2008
ISSN:1538-4101
Megjegyzések:Presenilin-1 (PS1) is a component of the beta-catenin degradation machinery, and PS1 mutations linked to familial Alzheimer's disease (FAD) represent a loss of this function, leading, in non-neuronal cells, to accumulation of cyclin D1, aberrant cell cycle activation and hyperproliferation. In post-mitotic neurons, cell cycle activation is thought to be abortive and initiate apoptosis, thus contributing to AD pathogenesis. Consequently, we tested here the hypothesis that, in the PS1 FAD brain, cyclin D1 accumulation may occur and lead to neuronal apoptosis secondary to an abortive entry into the cell cycle.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Cell Cycle. - 7 : 5 (2008), p. 637-646. -
További szerzők:Currais, Antonio Andres, Ana Towlson, Christopher Pitsi, Didier Nunes, Ana Niblock, Michael Cooper, Jonathan D. Hortobágyi Tibor (1965-) (patológus) Soriano, Salvador
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