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2. Structural parameters are superior to eigenvector centrality in detecting progressive supranuclear palsy with machine learning & multimodal MRI

Author

Danek, Adrian, Diehl-Schmid, Janine, Jahn, Holger, Kassubek, Jan, Kornhuber, Johannes, Landwehrmeyer, Bernhard, Lauer, Martin, Prudlo, Johannes, Schneider, Anja, Ludolph, Albert C., Fliesbach, Klaus, Anderl-Straub, Sarah, Brüggen, Katharina, Fischer, Marie, Förstl, Hans, Hammer, Anke, Homola, György, Just, Walter, Levin, Johannes, Marroquin, Nicolai, Marschhauser, Anke, Pino, Danielé, Nagl, Magdalena, Oberstein, Timo, Hüper, Lea, Polyakova, Maryna, Pellkofer, Hannah, Richter-Schmidinger, Tanja, Rossmeier, Carola, Kulko, Marianna, Semler, Elisa, Spottke, Annika, Steinacker, Petra, Thöne-Otto, Angelika, Uttner, Ingo, Zech, Heike, Albrecht, Franziska, Mueller, Karsten, Ballarini, Tommaso, Fassbender, Klaus, Wiltfang, Jens, Otto, Markus, Jech, Robert, and Schroeter, Mattias L.

Published
2024
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5. Author Correction: Integrative genetic analysis illuminates ALS heritability and identifies risk genes

Author

Megat, Salim, Mora, Natalia, Sanogo, Jason, Roman, Olga, Catanese, Alberto, Alami, Najwa Ouali, Freischmidt, Axel, Mingaj, Xhuljana, De Calbiac, Hortense, Muratet, François, Dirrig-Grosch, Sylvie, Dieterle, Stéphane, Van Bakel, Nick, Müller, Kathrin, Sieverding, Kirsten, Weishaupt, Jochen, Andersen, Peter Munch, Weber, Markus, Neuwirth, Christoph, Margelisch, Markus, Sommacal, Andreas, Van Eijk, Kristel R., Veldink, Jan H., Lautrette, Géraldine, Couratier, Philippe, Camuzat, Agnès, Le Ber, Isabelle, Grassano, Maurizio, Chio, Adriano, Boeckers, Tobias, Ludolph, Albert C., Roselli, Francesco, Yilmazer-Hanke, Deniz, Millecamps, Stéphanie, Kabashi, Edor, Storkebaum, Erik, Sellier, Chantal, and Dupuis, Luc

Published
2023
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6. Cystatin C based estimation of chronic kidney disease and amyotrophic lateral sclerosis in the ALS registry Swabia: associated risk and prognostic value

Author

Nagel, Gabriele, Kurz, Deborah, Peter, Raphael S., Rosenbohm, Angela, Koenig, Wolfgang, Dupuis, Luc, Bäzner, Hansjörg, Börtlein, Axel, Dempewolf, Silke, Schabet, Martin, Hecht, Martin, Kohler, Andreas, Opherk, Christian, Naegele, Andrea, Sommer, Norbert, Lindner, Alfred, Tumani, Hayrettin, Ludolph, Albert C., and Rothenbacher, Dietrich

Published
2023
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12. Integrative genetic analysis illuminates ALS heritability and identifies risk genes

Author

Megat, Salim, Mora, Natalia, Sanogo, Jason, Roman, Olga, Catanese, Alberto, Alami, Najwa Ouali, Freischmidt, Axel, Mingaj, Xhuljana, De Calbiac, Hortense, Muratet, François, Dirrig-Grosch, Sylvie, Dieterle, Stéphane, Van Bakel, Nick, Müller, Kathrin, Sieverding, Kirsten, Weishaupt, Jochen, Andersen, Peter Munch, Weber, Markus, Neuwirth, Christoph, Margelisch, Markus, Sommacal, Andreas, Van Eijk, Kristel R., Veldink, Jan H., Lautrette, Géraldine, Couratier, Philippe, Camuzat, Agnès, Le Ber, Isabelle, Grassano, Maurizio, Chio, Adriano, Boeckers, Tobias, Ludolph, Albert C., Roselli, Francesco, Yilmazer-Hanke, Deniz, Millecamps, Stéphanie, Kabashi, Edor, Storkebaum, Erik, Sellier, Chantal, and Dupuis, Luc

Published
2023
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13. Tau-targeting antisense oligonucleotide MAPTRx in mild Alzheimer’s disease: a phase 1b, randomized, placebo-controlled trial

Author

Mummery, Catherine J., Börjesson-Hanson, Anne, Blackburn, Daniel J., Vijverberg, Everard G. B., De Deyn, Peter Paul, Ducharme, Simon, Jonsson, Michael, Schneider, Anja, Rinne, Juha O., Ludolph, Albert C., Bodenschatz, Ralf, Kordasiewicz, Holly, Swayze, Eric E., Fitzsimmons, Bethany, Mignon, Laurence, Moore, Katrina M., Yun, Chris, Baumann, Tiffany, Li, Dan, Norris, Daniel A., Crean, Rebecca, Graham, Danielle L., Huang, Ellen, Ratti, Elena, Bennett, C. Frank, Junge, Candice, and Lane, Roger M.

Published
2023
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14. Long-term efficacy and safety of nusinersen in adults with 5q spinal muscular atrophy: a prospective European multinational observational study

Author

Günther, René, Wurster, Claudia Diana, Brakemeier, Svenja, Osmanovic, Alma, Schreiber-Katz, Olivia, Petri, Susanne, Uzelac, Zeljko, Hiebeler, Miriam, Thiele, Simone, Walter, Maggie C., Weiler, Markus, Kessler, Tobias, Freigang, Maren, Lapp, Hanna Sophie, Cordts, Isabell, Lingor, Paul, Deschauer, Marcus, Hahn, Andreas, Martakis, Kyriakos, Steinbach, Robert, Ilse, Benjamin, Rödiger, Annekathrin, Bellut, Julia, Nentwich, Julia, Zeller, Daniel, Muhandes, Mohamad Tareq, Baum, Tobias, Christoph Koch, Jan, Schrank, Bertold, Fischer, Sophie, Hermann, Andreas, Kamm, Christoph, Naegel, Steffen, Mensch, Alexander, Weber, Markus, Neuwirth, Christoph, Lehmann, Helmar C., Wunderlich, Gilbert, Stadler, Christian, Tomforde, Maike, George, Annette, Groß, Martin, Pechmann, Astrid, Kirschner, Janbernd, Türk, Matthias, Schimmel, Mareike, Bernert, Günther, Martin, Pascal, Rauscher, Christian, Meyer zu Hörste, Gerd, Baum, Petra, Löscher, Wolfgang, Flotats-Bastardas, Marina, Köhler, Cornelia, Probst-Schendzielorz, Kristina, Goldbach, Susanne, Schara-Schmidt, Ulrike, Müller-Felber, Wolfgang, Lochmüller, Hanns, von Velsen, Otgonzul, Kleinschnitz, Christoph, Ludolph, Albert C., and Hagenacker, Tim

Published
2024
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15. Common and rare variant association analyses in amyotrophic lateral sclerosis identify 15 risk loci with distinct genetic architectures and neuron-specific biology

Author

van Rheenen, Wouter, van der Spek, Rick AA, Bakker, Mark K, van Vugt, Joke JFA, Hop, Paul J, Zwamborn, Ramona AJ, de Klein, Niek, Westra, Harm-Jan, Bakker, Olivier B, Deelen, Patrick, Shireby, Gemma, Hannon, Eilis, Moisse, Matthieu, Baird, Denis, Restuadi, Restuadi, Dolzhenko, Egor, Dekker, Annelot M, Gawor, Klara, Westeneng, Henk-Jan, Tazelaar, Gijs HP, van Eijk, Kristel R, Kooyman, Maarten, Byrne, Ross P, Doherty, Mark, Heverin, Mark, Al Khleifat, Ahmad, Iacoangeli, Alfredo, Shatunov, Aleksey, Ticozzi, Nicola, Cooper-Knock, Johnathan, Smith, Bradley N, Gromicho, Marta, Chandran, Siddharthan, Pal, Suvankar, Morrison, Karen E, Shaw, Pamela J, Hardy, John, Orrell, Richard W, Sendtner, Michael, Meyer, Thomas, Başak, Nazli, van der Kooi, Anneke J, Ratti, Antonia, Fogh, Isabella, Gellera, Cinzia, Lauria, Giuseppe, Corti, Stefania, Cereda, Cristina, Sproviero, Daisy, D’Alfonso, Sandra, Sorarù, Gianni, Siciliano, Gabriele, Filosto, Massimiliano, Padovani, Alessandro, Chiò, Adriano, Calvo, Andrea, Moglia, Cristina, Brunetti, Maura, Canosa, Antonio, Grassano, Maurizio, Beghi, Ettore, Pupillo, Elisabetta, Logroscino, Giancarlo, Nefussy, Beatrice, Osmanovic, Alma, Nordin, Angelica, Lerner, Yossef, Zabari, Michal, Gotkine, Marc, Baloh, Robert H, Bell, Shaughn, Vourc’h, Patrick, Corcia, Philippe, Couratier, Philippe, Millecamps, Stéphanie, Meininger, Vincent, Salachas, François, Mora Pardina, Jesus S, Assialioui, Abdelilah, Rojas-García, Ricardo, Dion, Patrick A, Ross, Jay P, Ludolph, Albert C, Weishaupt, Jochen H, Brenner, David, Freischmidt, Axel, Bensimon, Gilbert, Brice, Alexis, Durr, Alexandra, Payan, Christine AM, Saker-Delye, Safa, Wood, Nicholas W, Topp, Simon, Rademakers, Rosa, Tittmann, Lukas, Lieb, Wolfgang, Franke, Andre, Ripke, Stephan, Braun, Alice, and Kraft, Julia

Subjects
Human Genome, Neurodegenerative, Clinical Research, Rare Diseases, Prevention, ALS, Neurosciences, Genetics, Brain Disorders, Aetiology, 2.1 Biological and endogenous factors, Neurological, Amyotrophic Lateral Sclerosis, Brain, Cholesterol, Disease Progression, Female, Genome-Wide Association Study, Glutamine, Humans, Male, Mendelian Randomization Analysis, Microsatellite Repeats, Mutation, Neurodegenerative Diseases, Neurons, Quantitative Trait Loci, RNA-Seq, Risk Factors, SLALOM Consortium, PARALS Consortium, SLAGEN Consortium, SLAP Consortium, Biological Sciences, Medical and Health Sciences, Developmental Biology
Abstract

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease with a lifetime risk of one in 350 people and an unmet need for disease-modifying therapies. We conducted a cross-ancestry genome-wide association study (GWAS) including 29,612 patients with ALS and 122,656 controls, which identified 15 risk loci. When combined with 8,953 individuals with whole-genome sequencing (6,538 patients, 2,415 controls) and a large cortex-derived expression quantitative trait locus (eQTL) dataset (MetaBrain), analyses revealed locus-specific genetic architectures in which we prioritized genes either through rare variants, short tandem repeats or regulatory effects. ALS-associated risk loci were shared with multiple traits within the neurodegenerative spectrum but with distinct enrichment patterns across brain regions and cell types. Of the environmental and lifestyle risk factors obtained from the literature, Mendelian randomization analyses indicated a causal role for high cholesterol levels. The combination of all ALS-associated signals reveals a role for perturbations in vesicle-mediated transport and autophagy and provides evidence for cell-autonomous disease initiation in glutamatergic neurons.

Published
2021

16. Effect of the addition of a mental health specialist for evaluation of undiagnosed patients in centres for rare diseases (ZSE-DUO): a prospective, controlled trial with a two-phase cohort design

Author

Akkaya, Federica, Babka, Christine, Bannert, Lisa, Bärsch-Michelmann, Anja, Böhm, Leonie, Brinkmann, Folke, Bullinger, Monika, Cario, Holger, de Greck, Moritz, Debatin, Klaus-Michael, Dillmann-Jehn, Katrin, Eymann, Jutta, Frisch, Julia, Glode, Anja, Gödecke, Vega, Grasemann, Corinna, Grauer, Eva, Haas, Astrid, Haisch, Lea, Isabell, Heinrich, Held, Melissa, Hennermann, Julia, Herpertz, Stephan, Herrmann-Werner, Anne, Hett, Julian, Heuschmann, Peter, Hilbig, Bettina, Holthöfer, Laura, Imhof, Christiane, Junne, Florian, Kassubek, Jan, Koschitzki, Kevin-Thomas, Krassort, Heike, Kropff, Birgit, Kuhn, Julia, Latzko, Philipp, Loew, Thomas, Ludolph, Albert C., Meyer, Torsten, Meyer dos Santos, Isabell, Mohnike, Klaus, Monninger, Martina, Mücke, Martin, Müller, Susanne, Musacchio, Thomas, Nießen, Margret, Nöhre, Mariel, Ott, Stephan, Petermann-Meyer, Andrea, Pfeifer-Duck, Christina, Piduhn, Lea-Sophie, Rampp, Carina, Rieß, Olaf, Schaubert, Kristina, Schmidt, Annika, Schneider, Simone, Schoels, Ludger, Schwalba, Martina, Selig, Udo, Sroka, Alexandra, Steinbüchel, Toni, Stösser, Sebastian, Suchant, Steffi, Ungethüm, Kathrin, Vogel, Matthias, Volk, Daniela, Vollmuth, Christoph, Volnov, Solange, Wagner, Thomas O.F., Walter, Sabrina, Warrings, Bodo, Zajt, Kamil, Zenker, Karola, Zhang, David, Zipfel, Stephan, Hebestreit, Helge, Lapstich, Anne-Marie, Brandstetter, Lilly, Krauth, Christian, Deckert, Jürgen, Haas, Kirsten, Pfister, Lisa, Witt, Stefanie, Schippers, Christopher, Dieris-Hirche, Jan, Maisch, Tim, Tüscher, Oliver, Bârlescu, Lavinia Aurelia, Berger, Alexandra, Berneburg, Mark, Britz, Vanessa, Deibele, Anna, Graeßner, Holm, Gündel, Harald, Heuft, Gereon, Lücke, Thomas, Mundlos, Christine, Quitmann, Julia Hannah, Rutsch, Frank, Schubert, Katharina, Schulz, Jörg B., Schweiger, Susann, Zeidler, Cornelia, Zeltner, Lena Margarete, de Zwaan, Martina, Bârlescu, Lavinia, Quitmann, Julia, Schulz, Jörg Bernhard, and Zeltner, Lena

Published
2023
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17. Author Correction: Tau-targeting antisense oligonucleotide MAPTRx in mild Alzheimer’s disease: a phase 1b, randomized, placebo-controlled trial

Author

Mummery, Catherine J., Börjesson-Hanson, Anne, Blackburn, Daniel J., Vijverberg, Everard G. B., De Deyn, Peter Paul, Ducharme, Simon, Jonsson, Michael, Schneider, Anja, Rinne, Juha O., Ludolph, Albert C., Bodenschatz, Ralf, Kordasiewicz, Holly, Swayze, Eric E., Fitzsimmons, Bethany, Mignon, Laurence, Moore, Katrina M., Yun, Chris, Baumann, Tiffany, Li, Dan, Norris, Daniel A., Crean, Rebecca, Graham, Danielle L., Huang, Ellen, Ratti, Elena, Bennett, C. Frank, Junge, Candice, and Lane, Roger M.

Published
2024
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21. Use and subjective experience of the impact of motor-assisted movement exercisers in people with amyotrophic lateral sclerosis: a multicenter observational study

Author

Maier, André, Gaudlitz, Marcel, Grehl, Torsten, Weyen, Ute, Steinbach, Robert, Grosskreutz, Julian, Rödiger, Annekathrin, Koch, Jan Christoph, Lengenfeld, Teresa, Weydt, Patrick, Günther, René, Wolf, Joachim, Baum, Petra, Metelmann, Moritz, Dorst, Johannes, Ludolph, Albert C., Kettemann, Dagmar, Norden, Jenny, Koc, Ruhan Yasemin, Walter, Bertram, Hildebrandt, Barbara, Münch, Christoph, Meyer, Thomas, and Spittel, Susanne

Published
2022
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25. Pattern of pareses in 5q-spinal muscular atrophy.

Author

Uzelac, Zeljko, Schwäble, Beate, Dorst, Johannes, Rosenbohm, Angela, Wollinsky, Kurt, Wurster, Claudia D., Steinbreier, Janna S., and Ludolph, Albert C.

Subjects
MUSCULAR atrophy, SPINAL muscular atrophy, AMYOTROPHIC lateral sclerosis, PARALYSIS, MUSCLE weakness
Abstract

Background: This prospective study investigates the pattern of pareses in 5q-associated spinal muscular atrophy (SMA) to identify disease-specific characteristics and potential differences from amyotrophic lateral sclerosis (ALS) and spinobulbar muscular atrophy (SBMA). Detailed knowledge about pareses patterns in SMA facilitates differential diagnosis and supports therapeutic monitoring. Methods: Between January 2021, and June 2021, 66 SMA patients (59.1% male, aged 33.6 ± 15.2 years) were included in the study. Most patients had SMA type II (n = 28) or SMA type III (n = 28), seven patients had SMA type I, and three patients had SMA type IV. We analyzed the pattern of pareses using the UK Medical Research Council (MRC) scoring system. Results: In both, upper and lower limbs muscle weakness was less pronounced in distal (upper limbs: MRC median 3.0 (interquartile range 1.5–3.5); lower limbs: 1.5 (0.5–3.0)) compared to proximal muscle groups (upper limbs: 2.0 (1.5–2.6); p < 0.001; lower limbs: 0.5 (0.5–1.5); p < 0.001). Thenar muscles were stronger than other small hand muscles (3.0 (2.0–3.5) vs 3.0 (1.5–3.5); p = 0.004). Muscles had more strength in upper (2.3 (1.5–3.1)) compared to lower limbs (1.1 (0.5–2.3); p < 0.001) and in flexors compared to extensors. Conclusion: We identified a specific pattern of muscle paresis in SMA which is different from the pattern of paresis in ALS and SBMA. As a rule of thumb, the pattern of pareses is similar, but not identical to ALS in distal, but different in proximal muscle groups. [ABSTRACT FROM AUTHOR]

Published
2024
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30. Screening instruments of cognition: The relation of the mini-mental state examination to the Edinburgh cognitive and behavioural ALS screen in amyotrophic lateral sclerosis.

Author

Serian, Angela, Finsel, Julia, Ludolph, Albert C., Uttner, Ingo, and Lulé, Dorothée

Subjects
MINI-Mental State Examination, MEDICAL screening, AMYOTROPHIC lateral sclerosis, NEUROPSYCHOLOGICAL tests, NONLINEAR regression, COGNITION, COGNITION disorders
Abstract

Objective: The Edinburgh Cognitive and Behavioural ALS Screen (ECAS) is an established cognitive screening instrument for patients with amyotrophic lateral sclerosis (ALS). Different from tools like the Mini-Mental State Examination (MMSE), it is adjusted for motor impairment, yet, the latter remains one of the most widely used screening instruments, also in ALS studies. Thus, it is of utmost importance to relate outcome scores of both instruments to allow for comparison in ALS patients. This study reports on the performance of ALS patients in both tests with regard to incidence and degree of cognitive impairment, and the correspondence of both, ECAS and MMSE scores. Methods: We examined N = 84 ALS patients with the German versions of the ECAS and the MMSE. Performance in both tests regarding incidence and degree of cognitive impairment, and correspondence of frequency of cognitive impairment according to both tests was examined. The relationship between ECAS and MMSE scores was modelled with a non-linear regression model. Results: All ALS patients were able to complete the ECAS, 89.3% (N = 75) were capable to complete the MMSE. Prevalence of cognitive impairment was in both tests 22.7%, however agreement was only 52.9%. Despite, regression analyses yielded a strong positive relationship (adjusted R2 =.68) between the ECAS total score and the MMSE total score. Both tests were able to identify all patients with dementia. Conclusion: These results suggest that the MMSE is not ideal for cognitive screening in early-stage ALS patients. However, a rough translation of MMSE scores in ECAS scores is possible to estimate the cognitive performance level of patients, with the ECAS being more discriminative in the lower range of cognitive dysfunction (ECAS score: 80–136), for which the MMSE does not define cognitive impairment (corresponding MMSE score: 27–30). [ABSTRACT FROM AUTHOR]

Published
2024
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31. Explorative study of emerging blood biomarkers in progressive multiple sclerosis (EmBioProMS): Design of a prospective observational multicentre pilot study

Author

Abdelhak, Ahmed, Huss, Andre, Stahmann, Alexander, Senel, Makbule, Krumbholz, Markus, Kowarik, Markus C., Havla, Joachim, Kümpfel, Tania, Kleiter, Ingo, Wüstinger, Isabella, Zettl, Uwe K., Schwartz, Margit, Roesler, Romy, Friede, Tim, Ludolph, Albert C., Ziemann, Ulf, and Tumani, Hayrettin

Published
2020
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33. Toxic gain of function from mutant FUS protein is crucial to trigger cell autonomous motor neuron loss

Author

Scekic-Zahirovic, Jelena, Sendscheid, Oliver, El Oussini, Hajer, Jambeau, Mélanie, Sun, Ying, Mersmann, Sina, Wagner, Marina, Dieterlé, Stéphane, Sinniger, Jérome, Dirrig-Grosch, Sylvie, Drenner, Kevin, Birling, Marie-Christine, Qiu, Jinsong, Zhou, Yu, Li, Hairi, Fu, Xiang-Dong, Rouaux, Caroline, Shelkovnikova, Tatyana, Witting, Anke, Ludolph, Albert C, Kiefer, Friedemann, Storkebaum, Erik, Lagier-Tourenne, Clotilde, and Dupuis, Luc

Subjects
Neurosciences, Brain Disorders, Genetics, Dementia, Neurodegenerative, Rare Diseases, Acquired Cognitive Impairment, ALS, 2.1 Biological and endogenous factors, Aetiology, Neurological, Animals, Brain, Cytoplasm, Mice, Inbred C57BL, Mice, Transgenic, Motor Neurons, Mutation, RNA-Binding Protein FUS, Spinal Cord, amyotrophic lateral sclerosis, frontotemporal dementia, FUS, motor neuron degeneration, PY-NLS, PY‐NLS, Biological Sciences, Information and Computing Sciences, Medical and Health Sciences, Developmental Biology
Abstract

FUS is an RNA-binding protein involved in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). Cytoplasmic FUS-containing aggregates are often associated with concomitant loss of nuclear FUS Whether loss of nuclear FUS function, gain of a cytoplasmic function, or a combination of both lead to neurodegeneration remains elusive. To address this question, we generated knockin mice expressing mislocalized cytoplasmic FUS and complete FUS knockout mice. Both mouse models display similar perinatal lethality with respiratory insufficiency, reduced body weight and length, and largely similar alterations in gene expression and mRNA splicing patterns, indicating that mislocalized FUS results in loss of its normal function. However, FUS knockin mice, but not FUS knockout mice, display reduced motor neuron numbers at birth, associated with enhanced motor neuron apoptosis, which can be rescued by cell-specific CRE-mediated expression of wild-type FUS within motor neurons. Together, our findings indicate that cytoplasmic FUS mislocalization not only leads to nuclear loss of function, but also triggers motor neuron death through a toxic gain of function within motor neurons.

Published
2016

34. Serum glial fibrillary acidic protein and disability progression in progressive multiple sclerosis

Author

Abdelhak, Ahmed, primary, Antweiler, Kai, additional, Kowarik, Markus C., additional, Senel, Makbule, additional, Havla, Joachim, additional, Zettl, Uwe K., additional, Kleiter, Ingo, additional, Skripuletz, Thomas, additional, Haarmann, Axel, additional, Stahmann, Alexander, additional, Huss, Andre, additional, Gingele, Stefan, additional, Krumbholz, Markus, additional, Benkert, Pascal, additional, Kuhle, Jens, additional, Friede, Tim, additional, Ludolph, Albert C., additional, Ziemann, Ulf, additional, Kümpfel, Tania, additional, and Tumani, Hayrettin, additional

Published
2023
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42. Coping as a resource to allow for psychosocial adjustment in fatal disease: results from patients with amyotrophic lateral sclerosis.

Author

Finsel, Julia, Rosenbohm, Angela, Peter, Raphael S., Bäzner, Hansjörg, Börtlein, Axel, Dempewolf, Silke, Schabet, Martin, Hecht, Martin, Kohler, Andreas, Opherk, Christian, Nägele, Andrea, Sommer, Norbert, Lindner, Alfred, Rothenbacher, Dietrich, Ludolph, Albert C., Nagel, Gabriele, and Lulé, Dorothée E.

Subjects
AMYOTROPHIC lateral sclerosis, PSYCHOLOGICAL adaptation, FAILURE (Psychology), FEAR of failure, PATIENTS' attitudes
Abstract

Background: Amyotrophic lateral sclerosis (ALS) is a fatal disorder, which imposes a severe emotional burden on patients. Appropriate copingmechanisms may alleviate this burden and facilitate wellbeing, with social support known to be a successful coping strategy. This observational study aimed to determine the interplay of general coping traits of hope for success and fear of failure, coping behavior of social activity, and patients' wellbeing. Methods: In this cross-sectional study, patients with ALS from a clinical-epidemiological registry in Southwestern Germany were interviewed regarding coping traits (achievement-motivated behavior: hope for success and fear of failure), coping behavior of social activity, and psychosocial adjustment, determined using measures of depressiveness, anxiety [both measured by Hospital Anxiety and Depression Scale (HADS)], and quality of life [Anamnestic Comparative Self-Assessment (ACSA)]. Demographics, clinical [ALS Functional Rating Scale revised version (ALSFRS-R)], and survival data were recorded. Results: A total of 868 patients [60.70% male patients, mean age: 64.70 (±10.83) years, mean ALSFRS-R: 37.36 ± 7.07] were interviewed. Anxiety in patients was found to be associated with a high fear of failure. In contrast, a generally positive attitude in patients exemplified in high hopes for success was associated with better wellbeing. Finally, coping behavior of social activity explained up to 65% of the variance of depressiveness among the patients with ALS. Conclusion: In this study, we present evidence that the wellbeing of patients with ALS is not an immediate fatalistic consequence of physical degradation but rather determined by coping traits and behavior, which may be trained to substantially increase the wellbeing of patients with ALS. [ABSTRACT FROM AUTHOR]

Published
2024
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43. Development of an algorithm for identifying paraneoplastic ischemic stroke in association with lung, pancreatic, and colorectal cancer.

Author

Kassubek, Rebecca, Winter, Marc-Andre G. R., Dreyhaupt, Jens, Laible, Mona, Kassubek, Jan, Ludolph, Albert C., and Lewerenz, Jan

Subjects
STROKE prognosis, PANCREATIC cancer, COLORECTAL cancer, LUNG cancer, C-reactive protein, LACTATE dehydrogenase
Abstract

Background: Paraneoplastic ischemic stroke has a poor prognosis. We have recently reported an algorithm based on the number of ischemic territories, C-reactive protein (CRP), lactate dehydrogenase (LDH), and granulocytosis to predict the underlying active cancer in a case-control setting. However, co-occurrence of cancer and stroke might also be merely incidental. Objective: To detect cancer-associated ischemic stroke in a large, unselected cohort of consecutive stroke patients by detailed analysis of ischemic stroke associated with specific cancer subtypes and comparison to patients with bacterial endocarditis. Methods: Retrospective single-center cohort study of consecutive 1612 ischemic strokes with magnetic resonance imaging, CRP, LDH, and relative granulocytosis data was performed, including identification of active cancers, history of now inactive cancers, and the diagnosis of endocarditis. The previously developed algorithm to detect paraneoplastic cancer was applied. Tumor types associated with paraneoplastic stroke were used to optimize the diagnostic algorithm. Results: Ischemic strokes associated with active cancer, but also endocarditis, were associated with more ischemic territories as well as higher CRP and LDH levels. Our previous algorithm identified active cancer-associated strokes with a specificity of 83% and sensitivity of 52%. Ischemic strokes associated with lung, pancreatic, and colorectal (LPC) cancers but not with breast and prostate cancers showed more frequent and prominent characteristics of paraneoplastic stroke. A multiple logistic regression model optimized to identify LPC cancers detected active cancer with a sensitivity of 77.8% and specificity of 81.4%. The positive predictive value (PPV) for all active cancers was 13.1%. Conclusion: Standard clinical examinations can be employed to identify suspect paraneoplastic stroke with an adequate sensitivity, specificity, and PPV when it is considered that the association of ischemic stroke with breast and prostate cancers in the stroke-prone elderly population might be largely incidental. [ABSTRACT FROM AUTHOR]

Published
2024
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44. Longitudinal course of neurofilament light chain levels in amyotrophic lateral sclerosis—insights from a completed randomized controlled trial with rasagiline.

Author

Witzel, Simon, Statland, Jeffrey M., Steinacker, Petra, Otto, Markus, Dorst, Johannes, Schuster, Joachim, Barohn, Richard J., and Ludolph, Albert C.

Subjects
AMYOTROPHIC lateral sclerosis, RANDOMIZED controlled trials, CYTOPLASMIC filaments, CLUSTER randomized controlled trials, DISEASE progression, DISEASE duration
Abstract

Background and purpose: Rasagiline might be disease modifying in patients with amyotrophic lateral sclerosis (ALS). The aim was to evaluate the effect of rasagiline 2 mg/day on neurofilament light chain (NfL), a prognostic biomarker in ALS. Methods: In 65 patients with ALS randomized in a 3:1 ratio to rasagiline 2 mg/day (n = 48) or placebo (n = 17) in a completed randomized controlled multicentre trial, NfL levels in plasma were measured at baseline, month 6 and month 12. Longitudinal changes in NfL levels were evaluated regarding treatment and clinical parameters. Results: Baseline NfL levels did not differ between the study arms and correlated with disease progression rates both pre‐baseline (r = 0.64, p < 0.001) and during the study (r = 0.61, p < 0.001). NfL measured at months 6 and 12 did not change significantly from baseline in both arms, with a median individual NfL change of +1.4 pg/mL (interquartile range [IQR] −5.6, 14.2) across all follow‐up time points. However, a significant difference in NfL change at month 12 was observed between patients with high and low NfL baseline levels treated with rasagiline (high [n = 13], −6.9 pg/mL, IQR −20.4, 6.0; low [n = 18], +5.9 pg/mL, IQR −1.4, 19.7; p = 0.025). Additionally, generally higher longitudinal NfL variability was observed in patients with high baseline levels, whereas disease progression rates and disease duration at baseline had no impact on the longitudinal NfL course. Conclusion: Post hoc NfL measurements in completed clinical trials are helpful in interpreting NfL data from ongoing and future interventional trials and could provide hypothesis‐generating complementary insights. Further studies are warranted to ultimately differentiate NfL response to treatment from other factors. [ABSTRACT FROM AUTHOR]

Published
2024
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45. Serum glial fibrillary acidic protein and disability progression in progressive multiple sclerosis.

Author

Abdelhak, Ahmed, Antweiler, Kai, Kowarik, Markus C., Senel, Makbule, Havla, Joachim, Zettl, Uwe K., Kleiter, Ingo, Skripuletz, Thomas, Haarmann, Axel, Stahmann, Alexander, Huss, Andre, Gingele, Stefan, Krumbholz, Markus, Benkert, Pascal, Kuhle, Jens, Friede, Tim, Ludolph, Albert C., Ziemann, Ulf, Kümpfel, Tania, and Tumani, Hayrettin

Abstract

Objective: Progression prediction is a significant unmet need in people with progressive multiple sclerosis (pwPMS). Studies on glial fibrillary acidic protein (GFAP) have either been limited to single center with relapsing MS or were based solely on Expanded Disability Status Scale (EDSS), which limits its generalizability to state‐of‐the‐art clinical settings and trials applying combined outcome parameters. Methods: Serum GFAP and NfL (neurofilament light chain) were investigated in EmBioProMS participants with primary (PP) or secondary progressive MS. Six months confirmed disability progression (CDP) was defined using combined outcome parameters (EDSS, timed‐25‐foot walk test (T25FW), and nine‐hole‐peg‐test (9HPT)). Results: 243 subjects (135 PPMS, 108 SPMS, age 55.5, IQR [49.7–61.2], 135 female, median follow‐up: 29.3 months [17.9–40.9]) were included. NfL (age‐) and GFAP (age‐ and sex‐) adjusted Z scores were higher in pwPMS compared to HC (p < 0.001 for both). 111 (32.8%) CDP events were diagnosed in participants with ≥3 visits (n = 169). GFAP Z score >3 was associated with higher risk for CDP in participants with low NfL Z score (i.e., ≤1.0) (HR: 2.38 [1.12–5.08], p = 0.025). In PPMS, GFAP Z score >3 was associated with higher risk for CDP (HR: 2.88 [1.21–6.84], p = 0.016). Risk was further increased in PPMS subjects with high GFAP when NfL is low (HR: 4.31 [1.53–12.13], p = 0.006). Interpretation: Blood GFAP may help identify pwPPMS at risk of progression. Combination of high GFAP and low NfL levels could distinguish non‐active pwPMS with particularly high progression risk. [ABSTRACT FROM AUTHOR]

Published
2024
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46. Author Correction: Tau-targeting antisense oligonucleotide MAPTRx in mild Alzheimer’s disease: a phase 1b, randomized, placebo-controlled trial

Author

Mummery, Catherine J., primary, Börjesson-Hanson, Anne, additional, Blackburn, Daniel J., additional, Vijverberg, Everard G. B., additional, De Deyn, Peter Paul, additional, Ducharme, Simon, additional, Jonsson, Michael, additional, Schneider, Anja, additional, Rinne, Juha O., additional, Ludolph, Albert C., additional, Bodenschatz, Ralf, additional, Kordasiewicz, Holly, additional, Swayze, Eric E., additional, Fitzsimmons, Bethany, additional, Mignon, Laurence, additional, Moore, Katrina M., additional, Yun, Chris, additional, Baumann, Tiffany, additional, Li, Dan, additional, Norris, Daniel A., additional, Crean, Rebecca, additional, Graham, Danielle L., additional, Huang, Ellen, additional, Ratti, Elena, additional, Bennett, C. Frank, additional, Junge, Candice, additional, and Lane, Roger M., additional

Published
2023
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47. Incidence of Syndromes Associated With Frontotemporal Lobar Degeneration in 9 European Countries

Author

the FRONTIERS group, Logroscino, Giancarlo, Piccininni, Marco, Graff, Caroline, Hardiman, Orla, Ludolph, Albert C., Moreno, Fermin, Otto, Markus, Remes, Anne M., Rowe, James B., Seelaar, Harro, Solje, Eino, Stefanova, Elka, Traykov, Latchezar, Jelic, Vesna, Rydell, Melissa Taheri, Pender, Niall, Anderl-Straub, Sarah, Barandiaran, Myriam, Gabilondo, Alazne, Kruger, Johanna, Murley, Alexander G., Rittman, Timothy, van der Ende, Emma L., van Swieten, John C., Hartikainen, Paeivi, Stojmenovic, Gorana Mandic, Mehrabian, Shima, Benussi, Luisa, Alberici, Antonella, Dell'Abate, Maria Teresa, Zecca, Chiara, Borroni, Barbara, Neurology, Department of Neurosciences, Faculty of Medicine, Clinicum, HUS Neurocenter, Belezhanska, Diyana, Bianchetti, Angelo, Binetti, Giuliano, Cotelli, Maria, Cotelli, Maria Sofia, Dreharova, Irena, Filardi, Marco, Fostinelli, Silvia, Ghidoni, Roberta, Gnoni, Valentina, Nacheva, Genoveva, Novaković, Ivana, Padovani, Alessandro, Popivanov, Ivo, Raycheva, Margarita, Stockton, Katherine, Stoyanova, Katya, Suhonen, Noora-Maria, Tainta, Mikel, Toncheva, Draga, Urso, Daniele, Zlatareva, Dora, and Zulaica, Miren

Subjects
Subtypes, Amyotrophic-lateral-sclerosis, Diagnosis, Prevalence, Pathology, Dementia, ddc:610, Neurology (clinical), Criteria, 3124 Neurology and psychiatry
Abstract

ImportanceDiagnostic incidence data for syndromes associated with frontotemporal lobar degeneration (FTLD) in multinational studies are urgent in light of upcoming therapeutic approaches.ObjectiveTo assess the incidence of FTLD across Europe.Design, Setting, and ParticipantsThe Frontotemporal Dementia Incidence European Research Study (FRONTIERS) was a retrospective cohort study conducted from June 1, 2018, to May 31, 2019, using a population-based registry from 13 tertiary FTLD research clinics from the UK, the Netherlands, Finland, Sweden, Spain, Bulgaria, Serbia, Germany, and Italy and including all new FTLD-associated cases during the study period, with a combined catchment population of 11 023 643 person-years. Included patients fulfilled criteria for the behavioral variant of frontotemporal dementia (BVFTD), the nonfluent variant or semantic variant of primary progressive aphasia (PPA), unspecified PPA, progressive supranuclear palsy, corticobasal syndrome, or frontotemporal dementia with amyotrophic lateral sclerosis (FTD-ALS). Data were analyzed from July 19 to December 7, 2021.Main Outcomes and MeasuresRandom-intercept Poisson models were used to obtain estimates of the European FTLD incidence rate accounting for geographic heterogeneity.ResultsBased on 267 identified cases (mean [SD] patient age, 66.70 [9.02] years; 156 males [58.43%]), the estimated annual incidence rate for FTLD in Europe was 2.36 cases per 100 000 person-years (95% CI, 1.59-3.51 cases per 100 000 person-years). There was a progressive increase in FTLD incidence across age, reaching its peak at the age of 71 years, with 13.09 cases per 100 000 person-years (95% CI, 8.46-18.93 cases per 100 000 person-years) among men and 7.88 cases per 100 000 person-years (95% CI, 5.39-11.60 cases per 100 000 person-years) among women. Overall, the incidence was higher among men (2.84 cases per 100 000 person-years; 95% CI, 1.88-4.27 cases per 100 000 person-years) than among women (1.91 cases per 100 000 person-years; 95% CI, 1.26-2.91 cases per 100 000 person-years). BVFTD was the most common phenotype (107 cases [40.07%]), followed by PPA (76 [28.46%]) and extrapyramidal phenotypes (69 [25.84%]). FTD-ALS was the rarest phenotype (15 cases [5.62%]). A total of 95 patients with FTLD (35.58%) had a family history of dementia. The estimated number of new FTLD cases per year in Europe was 12 057.Conclusions and RelevanceThe findings suggest that FTLD-associated syndromes are more common than previously recognized, and diagnosis should be considered at any age. Improved knowledge of FTLD incidence may contribute to appropriate health and social care planning and in the design of future clinical trials.

Published
2023

48. Genome-wide Analyses Identify KIF5A as a Novel ALS Gene

Author

Logullo, Francesco O., Simone, Isabella, Logroscino, Giancarlo, Salvi, Fabrizio, Bartolomei, Ilaria, Borghero, Giuseppe, Murru, Maria Rita, Costantino, Emanuela, Pani, Carla, Puddu, Roberta, Caredda, Carla, Piras, Valeria, Tranquilli, Stefania, Cuccu, Stefania, Corongiu, Daniela, Melis, Maurizio, Milia, Antonio, Marrosu, Francesco, Marrosu, Maria Giovanna, Floris, Gianluca, Cannas, Antonino, Capasso, Margherita, Caponnetto, Claudia, Mancardi, Gianluigi, Origone, Paola, Mandich, Paola, Conforti, Francesca L., Cavallaro, Sebastiano, Mora, Gabriele, Marinou, Kalliopi, Sideri, Riccardo, Penco, Silvana, Mosca, Lorena, Lunetta, Christian, Pinter, Giuseppe Lauria, Corbo, Massimo, Riva, Nilo, Carrera, Paola, Volanti, Paolo, Mandrioli, Jessica, Fini, Nicola, Fasano, Antonio, Tremolizzo, Lucio, Arosio, Alessandro, Ferrarese, Carlo, Trojsi, Francesca, Tedeschi, Gioacchino, Monsurrò, Maria Rosaria, Piccirillo, Giovanni, Femiano, Cinzia, Ticca, Anna, Ortu, Enzo, La Bella, Vincenzo, Spataro, Rossella, Colletti, Tiziana, Sabatelli, Mario, Zollino, Marcella, Conte, Amelia, Luigetti, Marco, Lattante, Serena, Marangi, Giuseppe, Santarelli, Marialuisa, Petrucci, Antonio, Pugliatti, Maura, Pirisi, Angelo, Parish, Leslie D., Occhineri, Patrizia, Giannini, Fabio, Battistini, Stefania, Ricci, Claudia, Benigni, Michele, Cau, Tea B., Loi, Daniela, Calvo, Andrea, Moglia, Cristina, Brunetti, Maura, Barberis, Marco, Restagno, Gabriella, Casale, Federico, Marrali, Giuseppe, Fuda, Giuseppe, Ossola, Irene, Cammarosano, Stefania, Canosa, Antonio, Ilardi, Antonio, Manera, Umberto, Grassano, Maurizio, Tanel, Raffaella, Pisano, Fabrizio, Harms, Matthew B., Goldstein, David B., Shneider, Neil A., Goutman, Stephen, Simmons, Zachary, Miller, Timothy M., Chandran, Siddharthan, Pal, Suvankar, Manousakis, Georgios, Appel, Stanley H., Simpson, Ericka, Wang, Leo, Baloh, Robert H., Gibson, Summer, Bedlack, Richard, Lacomis, David, Sareen, Dhruv, Sherman, Alexander, Bruijn, Lucie, Penny, Michelle, Allen, Andrew S., Appel, Stanley, Bedlack, Richard S., Boone, Braden E., Brown, Robert, Carulli, John P., Chesi, Alessandra, Chung, Wendy K., Cirulli, Elizabeth T., Cooper, Gregory M., Couthouis, Julien, Day-Williams, Aaron G., Dion, Patrick A., Gitler, Aaron D., Glass, Jonathan D., Han, Yujun, Harris, Tim, Hayes, Sebastian D., Jones, Angela L., Keebler, Jonathan, Krueger, Brian J., Lasseigne, Brittany N., Levy, Shawn E., Lu, Yi-Fan, Maniatis, Tom, McKenna-Yasek, Diane, Myers, Richard M., Petrovski, Slavé, Pulst, Stefan M., Raphael, Alya R., Ravits, John M., Ren, Zhong, Rouleau, Guy A., Sapp, Peter C., Sims, Katherine B., Staropoli, John F., Waite, Lindsay L., Wang, Quanli, Wimbish, Jack R., Xin, Winnie W., Phatnani, Hemali, Kwan, Justin, Broach, James R., Arcila-Londono, Ximena, Lee, Edward B., Van Deerlin, Vivianna M., Fraenkel, Ernest, Ostrow, Lyle W., Baas, Frank, Zaitlen, Noah, Berry, James D., Malaspina, Andrea, Fratta, Pietro, Cox, Gregory A., Thompson, Leslie M., Finkbeiner, Steve, Dardiotis, Efthimios, Hornstein, Eran, MacGowan, Daniel J., Heiman-Patterson, Terry, Hammell, Molly G., Patsopoulos, Nikolaos A., Dubnau, Joshua, Nath, Avindra, Kaye, Julia, Finkbeiner, Steven, Wyman, Stacia, LeNail, Alexander, Lima, Leandro, Rothstein, Jeffrey D., Svendsen, Clive N., Van Eyk, Jenny, Maragakis, Nicholas J., Kolb, Stephen J., Cudkowicz, Merit, Baxi, Emily, Benatar, Michael, Taylor, J. Paul, Wu, Gang, Rampersaud, Evadnie, Wuu, Joanne, Rademakers, Rosa, Züchner, Stephan, Schule, Rebecca, McCauley, Jacob, Hussain, Sumaira, Cooley, Anne, Wallace, Marielle, Clayman, Christine, Barohn, Richard, Statland, Jeffrey, Ravits, John, Swenson, Andrea, Jackson, Carlayne, Trivedi, Jaya, Khan, Shaida, Katz, Jonathan, Jenkins, Liberty, Burns, Ted, Gwathmey, Kelly, Caress, James, McMillan, Corey, Elman, Lauren, Pioro, Erik, Heckmann, Jeannine, So, Yuen, Walk, David, Maiser, Samuel, Zhang, Jinghui, Silani, Vincenzo, Ticozzi, Nicola, Gellera, Cinzia, Ratti, Antonia, Taroni, Franco, Lauria, Giuseppe, Verde, Federico, Fogh, Isabella, Tiloca, Cinzia, Comi, Giacomo P., Sorarù, Gianni, Cereda, Cristina, D’Alfonso, Sandra, Corrado, Lucia, De Marchi, Fabiola, Corti, Stefania, Ceroni, Mauro, Mazzini, Letizia, Siciliano, Gabriele, Filosto, Massimiliano, Inghilleri, Maurizio, Peverelli, Silvia, Colombrita, Claudia, Poletti, Barbara, Maderna, Luca, Del Bo, Roberto, Gagliardi, Stella, Querin, Giorgia, Bertolin, Cinzia, Pensato, Viviana, Castellotti, Barbara, Camu, William, Mouzat, Kevin, Lumbroso, Serge, Corcia, Philippe, Meininger, Vincent, Besson, Gérard, Lagrange, Emmeline, Clavelou, Pierre, Guy, Nathalie, Couratier, Philippe, Vourch, Patrick, Danel, Véronique, Bernard, Emilien, Lemasson, Gwendal, Al Kheifat, Ahmad, Al-Chalabi, Ammar, Andersen, Peter, Basak, A. Nazli, Blair, Ian P., Chio, Adriano, Cooper-Knock, Jonathan, de Carvalho, Mamede, Dekker, Annelot, Drory, Vivian, Redondo, Alberto Garcia, Gotkine, Marc, Hardiman, Orla, Hide, Winston, Iacoangeli, Alfredo, Glass, Jonathan, Kenna, Kevin, Kiernan, Matthew, Kooyman, Maarten, Landers, John, McLaughlin, Russell, Middelkoop, Bas, Mill, Jonathan, Neto, Miguel Mitne, Moisse, Mattieu, Pardina, Jesus Mora, Morrison, Karen, Newhouse, Stephen, Pinto, Susana, Pulit, Sara, Robberecht, Wim, Shatunov, Aleksey, Shaw, Pamela, Shaw, Chris, Sproviero, William, Tazelaar, Gijs, van Damme, Philip, van den Berg, Leonard, van der Spek, Rick, van Eijk, Kristel, van Es, Michael, van Rheenen, Wouter, van Vugt, Joke, Veldink, Jan, Weber, Markus, Williams, Kelly L., Zatz, Mayana, Bauer, Denis C., Twine, Natalie A., Nicolas, Aude, Kenna, Kevin P., Renton, Alan E., Faghri, Faraz, Chia, Ruth, Dominov, Janice A., Kenna, Brendan J., Nalls, Mike A., Keagle, Pamela, Rivera, Alberto M., Murphy, Natalie A., van Vugt, Joke J.F.A., Geiger, Joshua T., Van der Spek, Rick A., Pliner, Hannah A., Shankaracharya, Smith, Bradley N., Topp, Simon D., Abramzon, Yevgeniya, Gkazi, Athina Soragia, Eicher, John D., Kenna, Aoife, Messina, Sonia, Simone, Isabella L., Ferrucci, Luigi, Moreno, Cristiane de Araujo Martins, Kamalakaran, Sitharthan, Musunuri, Rajeeva Lochan, Evani, Uday Shankar, Abhyankar, Avinash, Zody, Michael C., Wyman, Stacia K., LeNail, Alex, Van Eyk, Jennifer E., Laaksovirta, Hannu, Myllykangas, Liisa, Jansson, Lilja, Valori, Miko, Ealing, John, Hamdalla, Hisham, Rollinson, Sara, Pickering-Brown, Stuart, Orrell, Richard W., Sidle, Katie C., Hardy, John, Singleton, Andrew B., Johnson, Janel O., Arepalli, Sampath, Polak, Meraida, Asress, Seneshaw, Al-Sarraj, Safa, King, Andrew, Troakes, Claire, Vance, Caroline, de Belleroche, Jacqueline, ten Asbroek, Anneloor L.M.A., Muñoz-Blanco, José Luis, Hernandez, Dena G., Ding, Jinhui, Gibbs, J. Raphael, Scholz, Sonja W., Floeter, Mary Kay, Campbell, Roy H., Landi, Francesco, Bowser, Robert, MacGowan, Daniel J.L., Kirby, Janine, Pioro, Erik P., Pamphlett, Roger, Broach, James, Gerhard, Glenn, Dunckley, Travis L., Brady, Christopher B., Kowall, Neil W., Troncoso, Juan C., Le Ber, Isabelle, Heiman-Patterson, Terry D., Kamel, Freya, Van Den Bosch, Ludo, Strom, Tim M., Meitinger, Thomas, Van Eijk, Kristel R., Moisse, Matthieu, McLaughlin, Russell L., Van Es, Michael A., Boylan, Kevin B., Van Blitterswijk, Marka, Morrison, Karen E., Mora, Jesús S., Drory, Vivian E., Shaw, Pamela J., Turner, Martin R., Talbot, Kevin, Fifita, Jennifer A., Nicholson, Garth A., Esteban-Pérez, Jesús, García-Redondo, Alberto, Rogaeva, Ekaterina, Zinman, Lorne, Cooper-Knock, Johnathan, Brice, Alexis, Goutman, Stephen A., Feldman, Eva L., Gibson, Summer B., Van Damme, Philip, Ludolph, Albert C., Andersen, Peter M., Weishaupt, Jochen H., Trojanowski, John Q., Brown, Robert H., Jr., van den Berg, Leonard H., Veldink, Jan H., Stone, David J., Tienari, Pentti, Chiò, Adriano, Shaw, Christopher E., Traynor, Bryan J., and Landers, John E.

Published
2018
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