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Danielle Seilhean
Researcher at University of Paris
Publications - 174
Citations - 11034
Danielle Seilhean is an academic researcher from University of Paris. The author has contributed to research in topics: Amyotrophic lateral sclerosis & Frontotemporal lobar degeneration. The author has an hindex of 54, co-authored 158 publications receiving 9153 citations. Previous affiliations of Danielle Seilhean include French Institute of Health and Medical Research & Pasteur Institute.
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Journal ArticleDOI
Neuroinvasion of SARS-CoV-2 in human and mouse brain.
Eric Song,Ce Zhang,Benjamin Israelow,Alice Lu-Culligan,Alba Vieites Prado,Sophie Skriabine,Peiwen Lu,Orr-El Weizman,Feimei Liu,Yile Dai,Klara Szigeti-Buck,Yuki Yasumoto,Guilin Wang,Christopher Castaldi,Jaime Heltke,Evelyn Ng,John Wheeler,Mia Madel Alfajaro,Etienne Levavasseur,Benjamin Fontes,Neal G. Ravindra,David van Dijk,Shrikant Mane,Murat Gunel,Aaron M. Ring,Syed A. Jaffar Kazmi,Kai Zhang,Craig B. Wilen,Tamas L. Horvath,Isabelle Plu,Stéphane Haïk,Jean-Leon Thomas,Jean-Leon Thomas,Angeliki Louvi,Shelli F. Farhadian,Anita Huttner,Danielle Seilhean,Nicolas Renier,Kaya Bilguvar,Akiko Iwasaki,Akiko Iwasaki +40 more
Abstract: Although COVID-19 is considered to be primarily a respiratory disease, SARS-CoV-2 affects multiple organ systems including the central nervous system (CNS). Yet, there is no consensus on the consequences of CNS infections. Here, we used three independent approaches to probe the capacity of SARS-CoV-2 to infect the brain. First, using human brain organoids, we observed clear evidence of infection with accompanying metabolic changes in infected and neighboring neurons. However, no evidence for type I interferon responses was detected. We demonstrate that neuronal infection can be prevented by blocking ACE2 with antibodies or by administering cerebrospinal fluid from a COVID-19 patient. Second, using mice overexpressing human ACE2, we demonstrate SARS-CoV-2 neuroinvasion in vivo. Finally, in autopsies from patients who died of COVID-19, we detect SARS-CoV-2 in cortical neurons and note pathological features associated with infection with minimal immune cell infiltrates. These results provide evidence for the neuroinvasive capacity of SARS-CoV-2 and an unexpected consequence of direct infection of neurons by SARS-CoV-2.
Journal ArticleDOI
Common variants at 7p21 are associated with frontotemporal lobar degeneration with TDP-43 inclusions
Vivianna M. Van Deerlin,Patrick M. A. Sleiman,Maria Martinez-Lage,Maria Martinez-Lage,Alice Chen-Plotkin,Li-San Wang,Neill R. Graff-Radford,Dennis W. Dickson,Rosa Rademakers,Bradley F. Boeve,Murray Grossman,Steven E. Arnold,David M. A. Mann,Stuart Pickering-Brown,Harro Seelaar,Peter Heutink,John C. van Swieten,Jill R. Murrell,Bernardino Ghetti,Salvatore Spina,Salvatore Spina,Jordan Grafman,John R. Hodges,Maria Grazia Spillantini,Sid Gilman,Andrew P. Lieberman,Jeffrey Kaye,Randall L. Woltjer,Eileen H. Bigio,M.-Marsel Mesulam,Safa Al-Sarraj,Claire Troakes,Roger N. Rosenberg,Charles L. White,Isidro Ferrer,Albert Lladó,Manuela Neumann,Hans A. Kretzschmar,Christine M. Hulette,Kathleen A. Welsh-Bohmer,Bruce L. Miller,Ainhoa Alzualde,Adolfo López de Munain,Ann C. McKee,Ann C. McKee,Marla Gearing,Allan I. Levey,James J. Lah,John Hardy,Jonathan D. Rohrer,Tammaryn Lashley,Ian R. A. Mackenzie,Howard Feldman,Ronald L. Hamilton,Steven T. DeKosky,Julie van der Zee,Julie van der Zee,Samir Kumar-Singh,Samir Kumar-Singh,Christine Van Broeckhoven,Christine Van Broeckhoven,Richard Mayeux,Jean Paul G. Vonsattel,Juan C. Troncoso,Jillian J. Kril,John B.J. Kwok,Glenda M. Halliday,Thomas D. Bird,Paul G. Ince,Pamela J. Shaw,Nigel J. Cairns,John C. Morris,Catriona McLean,Charles DeCarli,William G. Ellis,Stefanie H. Freeman,Matthew P. Frosch,John H. Growdon,Daniel P. Perl,Mary Sano,Mary Sano,David A. Bennett,Julie A. Schneider,Thomas G. Beach,Eric M. Reiman,Bryan K. Woodruff,Jeffrey L. Cummings,Harry V. Vinters,Carol A. Miller,Helena C. Chui,Irina Alafuzoff,Irina Alafuzoff,Päivi Hartikainen,Danielle Seilhean,Douglas Galasko,Eliezer Masliah,Carl W. Cotman,M. Teresa Tũón,M. Cristina Caballero Martínez,David G. Munoz,Steven L. Carroll,Daniel C. Marson,Peter Riederer,Nenad Bogdanovic,Gerard D. Schellenberg,Hakon Hakonarson,John Q. Trojanowski,Virginia M.-Y. Lee +107 more
TL;DR: It is found that FTLD-TDP associates with multiple SNPs mapping to a single linkage disequilibrium block on 7p21 that contains TMEM 106B, which implicate variants in TMEM106B as a strong risk factor for FTLD, suggesting an underlying pathogenic mechanism.
Journal ArticleDOI
Hallucinations, REM sleep, and Parkinson's disease: a medical hypothesis.
Isabelle Arnulf,Anne-Marie Bonnet,P. Damier,B. P. Bejjani,Danielle Seilhean,J.-P. Derenne,Yves Agid +6 more
TL;DR: The visual hallucinations that coincide with daytime episodes of REM sleep in patients who also experience post-REM delusions at night may be dream imagery and Psychosis in patients with PD may reflect a narcolepsy-like REM sleep disorder.
Journal ArticleDOI
Staging of Neurofibrillary Pathology in Alzheimer's Disease: A Study of the BrainNet Europe Consortium
Irina Alafuzoff,Thomas Arzberger,Safa Al-Sarraj,Istvan Bodi,Nenad Bogdanovic,Heiko Braak,Orso Bugiani,Kelly Del-Tredici,Isidro Ferrer,Ellen Gelpi,Giorgio Giaccone,Manuel B. Graeber,Paul G. Ince,Wouter Kamphorst,Andrew T. King,Penelope Korkolopoulou,Gabor G. Kovacs,Sergey Larionov,David Meyronet,Camelia M. Monoranu,Piero Parchi,Efstratios Patsouris,Wolfgang Roggendorf,Danielle Seilhean,Fabrizio Tagliavini,Christine Stadelmann,Nathalie Streichenberger,Dietmar Rudolf Thal,Dietmar Rudolf Thal,Stephen B. Wharton,Hans A. Kretzschmar +30 more
TL;DR: The results indicate that good agreement can be reached when the lesions are substantial, i.e., the lesions have reached isocortical structures, whereas when only mild subtle lesions were present the agreement was poorer, and it is strongly recommended that the assessment of lesions should be carried out by at least two independent observers.
Journal ArticleDOI
Aging-related tau astrogliopathy (ARTAG): harmonized evaluation strategy
Gabor G. Kovacs,Isidro Ferrer,Lea T. Grinberg,Lea T. Grinberg,Irina Alafuzoff,Johannes Attems,Herbert Budka,Nigel J. Cairns,John F. Crary,Charles Duyckaerts,Bernardino Ghetti,Glenda M. Halliday,James W. Ironside,Seth Love,Ian R. A. Mackenzie,David G. Munoz,Melissa E. Murray,Peter T. Nelson,Hitoshi Takahashi,John Q. Trojanowski,Olaf Ansorge,Thomas Arzberger,Atik Baborie,Thomas G. Beach,Kevin F. Bieniek,Eileen H. Bigio,Istvan Bodi,Brittany N. Dugger,Mel B. Feany,Ellen Gelpi,Stephen M. Gentleman,Giorgio Giaccone,Kimmo J. Hatanpaa,Richard Heale,Patrick R. Hof,Monika Hofer,Tibor Hortobágyi,Kurt A. Jellinger,Gregory A. Jicha,Paul G. Ince,Julia Kofler,Eniko Veronika Kovari,Jillian J. Kril,David M. A. Mann,Radoslav Matej,Ann C. McKee,Catriona McLean,Ivan Milenkovic,Thomas J. Montine,Shigeo Murayama,Edward B. Lee,Jasmin Rahimi,Roberta Diehl Rodriguez,Annemieke J.M. Rozemuller,Julie A. Schneider,Christian Schultz,William W. Seeley,Danielle Seilhean,Colin Smith,Fabrizio Tagliavini,Masaki Takao,Dietmar Rudolf Thal,Dietmar Rudolf Thal,Jon B. Toledo,Markus Tolnay,Juan C. Troncoso,Harry V. Vinters,Serge Weis,Stephen B. Wharton,Charles L. White,Thomas Wisniewski,John Woulfe,Masahito Yamada,Dennis W. Dickson +73 more
Abstract: Pathological accumulation of abnormally phosphorylated tau protein in astrocytes is a frequent, but poorly characterized feature of the aging brain. Its etiology is uncertain, but its presence is sufficiently ubiquitous to merit further characterization and classification, which may stimulate clinicopathological studies and research into its pathobiology. This paper aims to harmonize evaluation and nomenclature of aging-related tau astrogliopathy (ARTAG), a term that refers to a morphological spectrum of astroglial pathology detected by tau immunohistochemistry, especially with phosphorylation-dependent and 4R isoform-specific antibodies. ARTAG occurs mainly, but not exclusively, in individuals over 60 years of age. Tau-immunoreactive astrocytes in ARTAG include thorn-shaped astrocytes at the glia limitans and in white matter, as well as solitary or clustered astrocytes with perinuclear cytoplasmic tau immunoreactivity that extends into the astroglial processes as fine fibrillar or granular immunopositivity, typically in gray matter. Various forms of ARTAG may coexist in the same brain and might reflect different pathogenic processes. Based on morphology and anatomical distribution, ARTAG can be distinguished from primary tauopathies, but may be concurrent with primary tauopathies or other disorders. We recommend four steps for evaluation of ARTAG: (1) identification of five types based on the location of either morphologies of tau astrogliopathy: subpial, subependymal, perivascular, white matter, gray matter; (2) documentation of the regional involvement: medial temporal lobe, lobar (frontal, parietal, occipital, lateral temporal), subcortical, brainstem; (3) documentation of the severity of tau astrogliopathy; and (4) description of subregional involvement. Some types of ARTAG may underlie neurological symptoms; however, the clinical significance of ARTAG is currently uncertain and awaits further studies. The goal of this proposal is to raise awareness of astroglial tau pathology in the aged brain, facilitating communication among neuropathologists and researchers, and informing interpretation of clinical biomarkers and imaging studies that focus on tau-related indicators.