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11 results on '"Rohan, Zdenek"'

1. Deleterious ABCA7 mutations and transcript rescue mechanisms in early onset Alzheimer’s disease

Author

De Roeck, Arne, Van den Bossche, Tobi, van der Zee, Julie, Verheijen, Jan, De Coster, Wouter, Van Dongen, Jasper, Dillen, Lubina, Baradaran-Heravi, Yalda, Heeman, Bavo, Sanchez-Valle, Raquel, Lladó, Albert, Nacmias, Benedetta, Sorbi, Sandro, Gelpi, Ellen, Grau-Rivera, Oriol, Gómez-Tortosa, Estrella, Pastor, Pau, Ortega-Cubero, Sara, Pastor, Maria A., Graff, Caroline, Thonberg, Håkan, Benussi, Luisa, Ghidoni, Roberta, Binetti, Giuliano, de Mendonça, Alexandre, Martins, Madalena, Borroni, Barbara, Padovani, Alessandro, Almeida, Maria Rosário, Santana, Isabel, Diehl-Schmid, Janine, Alexopoulos, Panagiotis, Clarimon, Jordi, Lleó, Alberto, Fortea, Juan, Tsolaki, Magda, Koutroumani, Maria, Matěj, Radoslav, Rohan, Zdenek, De Deyn, Peter, Engelborghs, Sebastiaan, Cras, Patrick, Van Broeckhoven, Christine, Sleegers, Kristel, Bessi, Valentina, Bagnoli, Silvia, do Couto, Frederico Simões, Verdelho, Ana, Fratiglioni, Laura, Padovani, Alessandro, Rohan, Zdenek, Razquin, Cristina, Lorenzo, Elena, Iglesias, Elena, Seijo-Martínez, Manuel, Rene, Ramon, Gascon, Jordi, Campdelacreu, Jaume, Blesa, Rafael, and On behalf of the European Early-Onset Dementia (EU EOD) consortium

Published
2017
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3. CSF biomarker variability in the Alzheimer's Association quality control program

Author

Rojo, Aladro José A., Albert, Marilyn, Alcolea, Daniel, Andreasson, Ulf, Antonell, Anna, Arai, Hiroyuki, Archetti, Silvana, Arkblad, Eva, Baldeiras, Inês, Bartos, Ales, Batish, Dev, Bedel, Aurélie, Bentue-Ferrer, Daniele, Berisha, Flora, Bernardini, Sergio, Blankenstein, Marinus, Blennow, Kaj, Bousiges, Olivier, Camuso, Michael C., Carrillo, Maria, Casoli, Tiziana, Cavallaro, Sebastiano, Chalbot, Sonia, Collins, Steven, Cruz e Silva, Odete, Cutler, Neal, Cuvelier, Isabelle, Delaroche, Odile, Dufour-Rainfray, Diane, Dyer, Roy, Engelborghs, Sebastiaan, Fagan, Anne M., Fogli, Anne, Forlenza, Orestes V., Fox, Nick, Frisoni, Giovanni, Galimberti, Daniela, Galloni, Elisabetta, Gritti, Silvana, Gylys, Karen H., Hampel, Harald, Haustein, Sabine, Heath, Theresa, Heegaard, Niels H.H., Heneka, Michael T., Herukka, Sanna-Kaisa, Holtzman, David, Hsiung, Ging-Yuek Robin, Humpel, Christian, Hyman, Bradley, Iwatsubo, Takeshi, Iqbal, Khalid, Jardel, Claude, Jucker, Mathias, Kapaki, Elisabeth, Käser, Stephan A., Kidd, Daniel, Klivenyi, Peter, Kuwano, Ryozo, Lachno, D. Richard, Lamari, Foudil, Laplanche, Jean-Louis, Laser, Jordan, Lehmann, Sylvian, Lewczuk, Piotr, Li, Qiao-Xin, Lleó, Alberto, Maetzler, Walter, Malaplate-Armand, Catherine, Martin, Ralph, Martone, Robert L., Masters, Colin, Mattsson, Niklas, Mercken, Marc, Molinuevo, José Luis, Montine, Tom, Nowatzke, William, Otto, Markus, Parchi, Piero, Parent, Xavier, Parnetti, Lucilla, Persson, Staffan, Petersen, Ronald, Poesen, Koen, Quadrio, Isabelle, Quillard, Muriel, Regeniter, Axel, Rello, Vara Luis, Rissman, Robert, Rohan, Zdenek, Rosenmann, Hanna, Sancesario, Giuseppe, Schröder, Johannes, Shaw, Leslie M., Sisowath, Christin, Skinningsrud, Anders, Soares, Holly, Soininen, Hilkka, Søndersø, Knudsen Cindy, Spreer, Annette, Suardi, Silvia, Teunissen, Charlotte, Trojanowski, John Q., Umek, Robert, Van Broeck, Bianca, Vandenberghe, Rik, Vanderstichele, Hugo, Vandijck, Manu, Vecsei, Laszlo, Verbeek, Marcel, Vostiar, Igor, Windisch, Manfred, Zetterberg, Henrik, Carrillo, Maria C., Robin Hsiung, Ging-Yuek, Molinuevo, José L., Teunissen, Charlotte E., and Verbeek, Marcel M.

Published
2013
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4. Common and rare TBK1 variants in early-onset Alzheimer disease in a European cohort

Author

Goeman, Johan, Nuytten, Dirk, Vandenbulcke, Mathieu, Santens, Patrick, De Bleecker, Jan, Sieben, Anne, Dermaut, Bart, Versijpt, Jan, Michotte, Alex, Deryck, Olivier, Bergmans, Bruno, Willems, Christiana, Ivanoiu, Adrian, Salmon, Eric, Alexopoulos, Panagiotis, Sorbi, Sandro, Bessi, Valentina, Bagnoli, Silvia, Santana, Isabel, Simões do Couto, Frederico, Martins, Madalena, Thonberg, Håkan, Fratiglioni, Laura, Padovani, Alessandro, Rohan, Zdenek, Razquin, Cristina, Lorenzo, Elena, Iglesias, Elena, Seijo-Martínez, Manuel, Rene, Ramon, Gascon, Jordi, Campdelacreu, Jaume, Koutroumani, Maria, Lleó, Alberto, Fortea, Juan, Blesa, Rafael, Verheijen, Jan, van der Zee, Julie, Gijselinck, Ilse, Van den Bossche, Tobi, Dillen, Lubina, Heeman, Bavo, Gómez-Tortosa, Estrella, Lladó, Albert, Sanchez-Valle, Raquel, Graff, Caroline, Pastor, Pau, Pastor, Maria A., Benussi, Luisa, Ghidoni, Roberta, Binetti, Giuliano, Clarimon, Jordi, de Mendonça, Alexandre, Gelpi, Ellen, Tsolaki, Magda, Diehl-Schmid, Janine, Nacmias, Benedetta, Almeida, Maria Rosário, Borroni, Barbara, Matej, Radoslav, Ruiz, Agustín, Engelborghs, Sebastiaan, Vandenberghe, Rik, De Deyn, Peter P., Cruts, Marc, Van Broeckhoven, Christine, and Sleegers, Kristel

Published
2018
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5. Rare Variants in PLD3 Do Not Affect Risk for Early-Onset Alzheimer Disease in a European Consortium Cohort

Author

Cacace, Rita, Van den Bossche, Tobi, Engelborghs, Sebastiaan, Geerts, Nathalie, Laureys, Annelies, Dillen, Lubina, Graff, Caroline, Thonberg, Håkan, Chiang, Huei-Hsin, Pastor, Pau, Ortega-Cubero, Sara, Pastor, Maria A., Diehl-Schmid, Janine, Alexopoulos, Panagiotis, Benussi, Luisa, Ghidoni, Roberta, Binetti, Giuliano, Nacmias, Benedetta, Sorbi, Sandro, Sanchez-Valle, Raquel, Lladó, Albert, Gelpi, Ellen, Almeida, Maria Rosário, Santana, Isabel, Tsolaki, Magda, Koutroumani, Maria, Clarimon, Jordi, Lleó, Alberto, Fortea, Juan, de Mendonça, Alexandre, Martins, Madalena, Borroni, Barbara, Padovani, Alessandro, Matej, Radoslav, Rohan, Zdenek, Vandenbulcke, Mathieu, Vandenberghe, Rik, De Deyn, Peter P., Cras, Patrick, van der Zee, Julie, Sleegers, Kristel, and Van Broeckhoven, Christine

Published
2015
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7. Genetic variability in SQSTM1 and risk of early-onset Alzheimer dementia: a European early-onset dementia consortium study

Author

Cuyvers, Elise, van der Zee, Julie, Bettens, Karolien, Engelborghs, Sebastiaan, Vandenbulcke, Mathieu, Robberecht, Caroline, Dillen, Lubina, Merlin, Céline, Geerts, Nathalie, Graff, Caroline, Thonberg, Håkan, Chiang, Huei-Hsin, Pastor, Pau, Ortega-Cubero, Sara, Pastor, Maria A., Diehl-Schmid, Janine, Alexopoulos, Panagiotis, Benussi, Luisa, Ghidoni, Roberta, Binetti, Giuliano, Nacmias, Benedetta, Sorbi, Sandro, Sanchez-Valle, Raquel, Lladó, Albert, Gelpi, Ellen, Almeida, Maria Rosário, Santana, Isabel, Clarimon, Jordi, Lleó, Alberto, Fortea, Juan, de Mendonça, Alexandre, Martins, Madalena, Borroni, Barbara, Padovani, Alessandro, Matěj, Radoslav, Rohan, Zdenek, Ruiz, Agustín, Frisoni, Giovanni B., Fabrizi, Gian Maria, Vandenberghe, Rik, De Deyn, Peter P., Van Broeckhoven, Christine, and Sleegers, Kristel

Published
2015
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8. Current Concepts in the Classification and Diagnosis of Frontotemporal Lobar Degenerations: A Practical Approach

Author

Rohan, Zdenek and Matej, Radoslav

Subjects
Protein binding, Movement disorders -- Diagnosis, Dementia -- Diagnosis, Sarcoma -- Diagnosis, Aphasia -- Diagnosis, Proteins, Neurons, Health
Abstract

Frontotemporal lobar degenerations are clinically, genetically, and molecularly heterogeneous diseases characterized by mainly frontal and temporal atrophy and affecting behavioral, language, cognitive, and motor functions. The term frontotemporal dementia incorporates 3 distinct clinical syndromes seen in frontotemporal degenerations: behavioral variant of frontotemporal dementia, progressive nonfluent aphasia, and semantic dementia. Progressive supranuclear palsy syndrome, corticobasal syndrome, and motor neuron disease syndrome are also associated with frontotemporal lobar degenerations. The neuropathologic hallmark of frontotemporal lobar degenerations is accumulation of abnormal proteins in the cytoplasm and nuclei of neurons and glial cells. Proteins involved in pathologic processes that represent the basis for frontotemporal lobar degeneration classification are tau protein, transactive response DNA-binding protein of 43 kDa, and 'fused in sarcoma' protein. The aim of this review is to provide a summary of practical approaches for neuropathologic diagnostics of the rapidly evolving classifications of frontotemporal lobar degenerations. (Arch Pathol Lab Med. 2014; 138:132-138; doi: 10.5858/arpa.2012-0510-RS), CLINICAL FEATURES Frontotemporal lobar degeneration (FTLD) is a rather rare cause of dementia; however, it is a common cause of dementia in individuals younger than 65 years, second only to [...]

Published
2014
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10. Proteinase-activated receptor 2 and disease biomarkers in cerebrospinal fluid in cases with autopsy-confirmed prion diseases and other neurodegenerative diseases.

Author

Rohan, Zdenek, Smetakova, Magdalena, Kukal, Jaromir, Rusina, Robert, and Matej, Radoslav

Subjects
*PROTEINASES, *AMYLOID beta-protein, *CREUTZFELDT-Jakob disease, *BIOMARKERS, *CEREBROSPINAL fluid, *PRION diseases, *NEURODEGENERATION
Abstract

Background: Proteinase-activated receptor 2 (PAR-2) has been shown to promote both neurotoxic and neuroprotective effects. Similarly, other routinely used nonspecific markers of neuronal damage can be found in cerebrospinal fluid (CSF) and can be used as biomarkers for different neurodegenerative disorders. Methods: Using enzyme-linked immunosorbent assays and western blotting we assessed PAR-2, total-tau, phospho-tau, beta-amyloid levels, and protein 14-3-3 in the CSF of former patients who had undergone a neuropathological autopsy after death and who had been definitively diagnosed with a prion or other neurodegenerative disease. Results: We did not find any significant correlation between levels of PAR-2 and other biomarkers, nor did we find any differences in PAR-2 levels between prion diseases and other neurodegenerative conditions. However, we confirmed that very high total-tau levels were significantly associated with definitive prion diagnoses and exhibited greater sensitivity and specificity than protein 14-3-3, which is routinely used as a marker. Conclusions: Our study showed that PAR-2, in CSF, was not specifically altered in prion diseases compared to other neurodegenerative conditions. Our results also confirmed that very high total-tau protein CSF levels were significantly associated with a definitive Creutzfeldt-Jakob disease (CJD) diagnosis and should be routinely tested as a diagnostic marker. Observed individual variability in CSF biomarkers provide invaluable feedback from neuropathological examinations even in "clinically certain" cases. [ABSTRACT FROM AUTHOR]

Published
2015
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11. Oligodendroglial Response in the Spinal Cord in TDP-43 Proteinopathy with Motor Neuron Involvement.

Author

Rohan, Zdenek, Matej, Radoslav, Rusina, Robert, and Kovacs, Gabor G.

Subjects
*AMYOTROPHIC lateral sclerosis, *MYELIN basic protein, *OLIGODENDROGLIA, *SPINAL cord, *TDP-43 proteinopathies, *NEURODEGENERATION
Abstract

Background: TDP-43 proteinopathies represent a spectrum of neurodegenerative disorders. Variable clinical presentations including frontotemporal dementia, amyotrophic lateral sclerosis (ALS) and mixed forms are associated with the spatial heterogeneity of the TDP-43 pathology. Recent studies have emphasized the role of oligodendrocytes in the pathogenesis of ALS. Objective: To evaluate whether TDP-43 proteinopathies are associated with an oligodendroglial response. Methods: We performed a study on 7 controls and 10 diseased patients with spinal cord involvement. Using the oligodendroglia-specific antibody TPPP/p25, we assessed oligodendrocyte density in the lateral corticospinal tracts (LCSs) along with the presence of perineuronal oligodendrocytes (PNOGs) in the anterior horns. We performed a densitometry of myelin basic protein (MBP) immunoreactivity. The numbers of TDP-43 and p62 immunoreactive inclusions were counted in both the LCSs and the anterior horns. Results: Double immunolabeling confirmed that oligodendrocytes harbor TDP-43 inclusions. In the LCSs, MBP density, but not the number of oligodendrocytes, was decreased in the diseased group. However, oligodendrocyte counts in the LCS correlated positively, and the density of MBP inversely, with the number of neuronal inclusions in the anterior horn, suggestive of a compensatory response of oligodendrocytes. The number of neurons with PNOGs correlated with the amount of inclusions. Conclusion: Our study further emphasizes the importance of oligodendroglia in the pathogenesis of TDP-43 proteinopathies with spinal cord involvement. © 2014 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Published
2014
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