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001-es BibID:	BIBFORM082378
035-os BibID:	(cikkazonosító)5 (WoS)000455320300001 (Scopus)85059798236
Első szerző:	Ashton, Nicholas J.
Cím:	Increased plasma neurofilament light chain concentration correlates with severity of post-mortem neurofibrillary tangle pathology and neurodegeneration / Nicholas J. Ashton, Antoine Leuzy, Yau Mun Lim, Claire Troakes, Tibor Hortobágyi, Kina Höglund, Dag Aarsland, Simon Lovestone, Michael Schöll, Kaj Blennow, Henrik Zetterberg, Abdul Hye
Dátum:	2019
ISSN:	2051-5960
Megjegyzések:	Alzheimer's disease (AD) is pathologically characterized by the accumulation of amyloid- (A) plaques, neurofibrillary tangles and widespread neuronal loss in the brain. In recent years, blood biomarkers have emerged as a realistic prospect to highlight accumulating pathology for secondary prevention trials. Neurofilament light chain (NfL), a marker of axonal degeneration, is robustly elevated in the blood of many neurological and neurodegenerative conditions, including AD. A strong relationship with cerebrospinal fluid (CSF) NfL suggests that these biomarker modalities reflect the same pathological process. Yet, the connection between blood NfL and brain tissue pathology has not been directly compared. In this study, longitudinal plasma NfL from cognitively healthy controls (n=12) and AD participants (n=57) were quantified by the Simoa platform. On reaching post-mortem, neuropathological assessment was performed on all participants, with additional frozen and paraffin-embedded tissue acquired from 26 participants for further biochemical (A(1-42), A(1-40), tau) and histological (NfL) evaluation. Plasma NfL concentrations were significantly increased in AD and correlated with cognitive decline, independent of age. Retrospective stratification based on Braak staging revealed that baseline plasma NfL concentrations were associated with higher neurofibrillary tangle pathology at post-mortem. Longitudinal increases in plasma NfL were observed in all Braak groupings; a significant negative association, however, was found between plasma NfL at time point 1 and both its rate of change and annual percentage increase. Immunohistochemical evaluation of NfL in the medial temporal gyrus (MTG) demonstrated an inverse relationship between Braak stages and NfL staining. Importantly, a significant negative correlation was found between the plasma NfL measurement closest to death and the level of NfL staining in the MTG at post-mortem. For the first time, we demonstrate that plasma NfL associates with the severity of neurofibrillary tangle pathology and neurodegeneration in the post-mortem brain.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk
Megjelenés:	Acta Neuropathologica Communications. - 7 : 1 (2019), p. 1-11. -
További szerzők:	Leuzy, Antoine Lim, Yau Mun Troakes, Claire Hortobágyi Tibor (1965-) (patológus) Höglund, Kina Aarsland, Dag Lovestone, Simon Schöll, Michael Blennow, Kaj Zetterberg, Henrik Hye, Abdul
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM090909
035-os BibID:	(WOS)000605104600001 (Scopus)85098720952
Első szerző:	Attems, Johannes
Cím:	Neuropathological consensus criteria for the evaluation of Lewy pathology in post-mortem brains : a multi-centre study / Attems Johannes, Toledo Jon B., Walker Lauren, Gelpi Ellen, Gentleman Steve, Halliday Glenda, Hortobagyi Tibor, Jellinger Kurt, Kovacs Gabor G., Lee Edward B., Love Seth, McAleese Kirsty E., Nelson Peter T., Neumann Manuela, Parkkinen Laura, Polvikoski Tuomo, Sikorska Beata, Smith Colin, Grinberg Lea Tenenholz, Thal Dietmar R., Trojanowski John Q., McKeith Ian G.
Dátum:	2021
ISSN:	0001-6322
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk
Megjelenés:	Acta Neuropathologica. - 141 (2021), p. 159-172. -
További szerzők:	Toledo, Jon B. Walker, Lauren Gelpi, Ellen Gentleman, Steve Halliday, Glenda Hortobágyi Tibor (1965-) (patológus) Jellinger, Kurt Kovács Gábor Géza (1969-) (neurológus) Lee, Edward B. Love, Seth McAleese, Kirsty E. Nelson, Peter T. Neumann, Manuela Parkkinen, Laura Polvikoski, Tuomo Sikorska, Beata Smith, Colin Grinberg, Lea T. Thal, Dietmar R. Trojanowski, John Q. McKeith, Ian G.
Pályázati támogatás:	2017-1.2.1-NKP-2017-00002 Egyéb Egyéb OTKA
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001-es BibID:	BIBFORM075028
035-os BibID:	(WoS)000441903500008 (Scopus)85050314318
Első szerző:	Fekete Rebeka
Cím:	Microglia control the spread of neurotropic virus infection via P2Y12 signalling and recruit monocytes through P2Y12-independent mechanisms / Rebeka Fekete, Csaba Cserép, Nikolett Lénárt, Krisztina Tóth, Barbara Orsolits, Bernadett Martinecz, Előd Méhes, Bálint Szabó, Valéria Németh, Balázs Gönci, Beáta Sperlágh, Zsolt Boldogkői, Ágnes Kittel, Mária Baranyi, Szilamér Ferenczi, Krisztina Kovács, Gergely Szalay, Balázs Rózsa, Connor Webb, Gabor G. Kovacs, Tibor Hortobágyi, Brian L. West, Zsuzsanna Környei, Ádám Dénes
Dátum:	2018
ISSN:	0001-6322
Megjegyzések:	Neurotropic herpesviruses can establish lifelong infection in humans and contribute to severe diseases including encephalitis and neurodegeneration. However, the mechanisms through which the brain's immune system recognizes and controls viral infections propagating across synaptically linked neuronal circuits have remained unclear. Using a well-established model of alphaherpesvirus infection that reaches the brain exclusively via retrograde transsynaptic spread from the periphery, and in vivo two-photon imaging combined with high resolution microscopy, we show that microglia are recruited to and isolate infected neurons within hours. Selective elimination of microglia results in a marked increase in the spread of infection and egress of viral particles into the brain parenchyma, which are associated with diverse neurological symptoms. Microglia recruitment and clearance of infected cells require cell-autonomous P2Y12 signalling in microglia, triggered by nucleotides released from affected neurons. In turn, we identify microglia as key contributors to monocyte recruitment into the inflamed brain, which process is largely independent of P2Y12. P2Y12-positive microglia are also recruited to infected neurons in the human brain during viral encephalitis and both microglial responses and leukocyte numbers correlate with the severity of infection. Thus, our data identify a key role for microglial P2Y12 in defence against neurotropic viruses, whilst P2Y12-independent actions of microglia may contribute to neuroinflammation by facilitating monocyte recruitment to the sites of infection.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk Microglia P2Y12 Neurotropic virus Transsynaptic spread Neuroinflammation
Megjelenés:	Acta Neuropathologica. - 136 : 3 (2018), p. 461-482. -
További szerzők:	Cserép Csaba Lénárt Nikolett Tóth Krisztina Orsolits Barbara Martinecz Bernadett Méhes Előd Szabó Bálint Németh Valéria Gönci Balázs Sperlágh Beáta Boldogkői Zsolt Kittel Ágnes Baranyi Mária Ferenczi Szilamér (1977-) (biológus) Kovács Krisztina Szalay Gergely Rózsa Balázs Webb, Connor Kovács Gábor Géza (1969-) (neurológus) Hortobágyi Tibor (1965-) (patológus) West, Brian L. Környei Zsuzsanna Dénes Ádám
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