Search

Your search keyword '"Giese, Armin"' showing total 768 results
Start Over Author "Giese, Armin"
768 results on '"Giese, Armin"'

1. Risk willingness in multiple system atrophy and Parkinson’s disease understanding patient preferences

Author

Bernhardt, Alexander Maximilian, Oeller, Marc, Friedrich, Isabel, Kocakavuk, Emre, Nachman, Eliana, Peikert, Kevin, Roderigo, Malte, Rossmann, Andreas, Schröter, Tabea, Wilhelm, Lea Olivia, Prell, Tino, van Riesen, Christoph, Nieweler, Johanna, Katzdobler, Sabrina, Weiler, Markus, Jacobi, Heike, Warnecke, Tobias, Claus, Inga, Palleis, Carla, Breimann, Stephan, Falkenburger, Björn, Brandt, Moritz, Hermann, Andreas, Rumpf, Jost-Julian, Claßen, Joseph, Höglinger, Günter, Gandor, Florin, Levin, Johannes, Giese, Armin, Janzen, Annette, and Oertel, Wolfgang Hermann

Published
2024
Full Text
View/download PDF

2. Tau deposition patterns are associated with functional connectivity in primary tauopathies

Author

Franzmeier, Nicolai, Brendel, Matthias, Beyer, Leonie, Slemann, Luna, Kovacs, Gabor G, Arzberger, Thomas, Kurz, Carolin, Respondek, Gesine, Lukic, Milica J, Biel, Davina, Rubinski, Anna, Frontzkowski, Lukas, Hummel, Selina, Müller, Andre, Finze, Anika, Palleis, Carla, Joseph, Emanuel, Weidinger, Endy, Katzdobler, Sabrina, Song, Mengmeng, Biechele, Gloria, Kern, Maike, Scheifele, Maximilian, Rauchmann, Boris-Stephan, Perneczky, Robert, Rullman, Michael, Patt, Marianne, Schildan, Andreas, Barthel, Henryk, Sabri, Osama, Rumpf, Jost J, Schroeter, Matthias L, Classen, Joseph, Villemagne, Victor, Seibyl, John, Stephens, Andrew W, Lee, Edward B, Coughlin, David G, Giese, Armin, Grossman, Murray, McMillan, Corey T, Gelpi, Ellen, Molina-Porcel, Laura, Compta, Yaroslau, van Swieten, John C, Laat, Laura Donker, Troakes, Claire, Al-Sarraj, Safa, Robinson, John L, Xie, Sharon X, Irwin, David J, Roeber, Sigrun, Herms, Jochen, Simons, Mikael, Bartenstein, Peter, Lee, Virginia M, Trojanowski, John Q, Levin, Johannes, Höglinger, Günter, and Ewers, Michael

Subjects
Biochemistry and Cell Biology, Biological Sciences, Acquired Cognitive Impairment, Rare Diseases, Brain Disorders, Pick's Disease, Alzheimer's Disease, Dementia, Frontotemporal Dementia (FTD), Neurosciences, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Neurodegenerative, Aging, Alzheimer's Disease Related Dementias (ADRD), Biomedical Imaging, Aetiology, 2.1 Biological and endogenous factors, Neurological, Brain, Humans, Magnetic Resonance Imaging, Supranuclear Palsy, Progressive, Tauopathies, tau Proteins
Abstract

Tau pathology is the main driver of neuronal dysfunction in 4-repeat tauopathies, including cortico-basal degeneration and progressive supranuclear palsy. Tau is assumed to spread prion-like across connected neurons, but the mechanisms of tau propagation are largely elusive in 4-repeat tauopathies, characterized not only by neuronal but also by astroglial and oligodendroglial tau accumulation. Here, we assess whether connectivity is associated with 4R-tau deposition patterns by combining resting-state fMRI connectomics with both 2nd generation 18F-PI-2620 tau-PET in 46 patients with clinically diagnosed 4-repeat tauopathies and post-mortem cell-type-specific regional tau assessments from two independent progressive supranuclear palsy patient samples (n = 97 and n = 96). We find that inter-regional connectivity is associated with higher inter-regional correlation of both tau-PET and post-mortem tau levels in 4-repeat tauopathies. In regional cell-type specific post-mortem tau assessments, this association is stronger for neuronal than for astroglial or oligodendroglial tau, suggesting that connectivity is primarily associated with neuronal tau accumulation. Using tau-PET we find further that patient-level tau patterns are associated with the connectivity of subcortical tau epicenters. Together, the current study provides combined in vivo tau-PET and histopathological evidence that brain connectivity is associated with tau deposition patterns in 4-repeat tauopathies.

Published
2022

3. Distribution patterns of tau pathology in progressive supranuclear palsy

Author

Kovacs, Gabor G, Lukic, Milica Jecmenica, Irwin, David J, Arzberger, Thomas, Respondek, Gesine, Lee, Edward B, Coughlin, David, Giese, Armin, Grossman, Murray, Kurz, Carolin, McMillan, Corey T, Gelpi, Ellen, Compta, Yaroslau, van Swieten, John C, Laat, Laura Donker, Troakes, Claire, Al-Sarraj, Safa, Robinson, John L, Roeber, Sigrun, Xie, Sharon X, Lee, Virginia M-Y, Trojanowski, John Q, and Höglinger, Günter U

Subjects
Biomedical and Clinical Sciences, Neurosciences, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Rare Diseases, Acquired Cognitive Impairment, Aging, Alzheimer's Disease, Frontotemporal Dementia (FTD), Dementia, Neurodegenerative, Brain Disorders, Underpinning research, 1.1 Normal biological development and functioning, Neurological, Aged, Brain, Cohort Studies, Female, Humans, Male, Middle Aged, Supranuclear Palsy, Progressive, tau Proteins, Coiled body, Neurofibrillary tangle, Progressive supranuclear palsy, Propagation, Richardson syndrome, Sequential involvement, Stage, Tau, Tauopathy, Tufted astrocyte, Clinical Sciences, Neurology & Neurosurgery
Abstract

Progressive supranuclear palsy (PSP) is a 4R-tauopathy predominated by subcortical pathology in neurons, astrocytes, and oligodendroglia associated with various clinical phenotypes. In the present international study, we addressed the question of whether or not sequential distribution patterns can be recognized for PSP pathology. We evaluated heat maps and distribution patterns of neuronal, astroglial, and oligodendroglial tau pathologies and their combinations in different clinical subtypes of PSP in postmortem brains. We used conditional probability and logistic regression to model the sequential distribution of tau pathologies across different brain regions. Tau pathology uniformly predominates in the neurons of the pallido-nigro-luysian axis in different clinical subtypes. However, clinical subtypes are distinguished not only by total tau load but rather cell-type (neuronal versus glial) specific vulnerability patterns of brain regions suggesting distinct dynamics or circuit-specific segregation of propagation of tau pathologies. For Richardson syndrome (n = 81) we recognize six sequential steps of involvement of brain regions by the combination of cellular tau pathologies. This is translated to six stages for the practical neuropathological diagnosis by the evaluation of the subthalamic nucleus, globus pallidus, striatum, cerebellum with dentate nucleus, and frontal and occipital cortices. This system can be applied to further clinical subtypes by emphasizing whether they show caudal (cerebellum/dentate nucleus) or rostral (cortical) predominant, or both types of pattern. Defining cell-specific stages of tau pathology helps to identify preclinical or early-stage cases for the better understanding of early pathogenic events, has implications for understanding the clinical subtype-specific dynamics of disease-propagation, and informs tau-neuroimaging on distribution patterns.

Published
2020

4. Validation of the movement disorder society criteria for the diagnosis of 4-repeat tauopathies.

Author

Respondek, Gesine, Grimm, Max-Joseph, Piot, Ines, Arzberger, Thomas, Compta, Yaroslau, Englund, Elisabet, Ferguson, Leslie, Gelpi, Ellen, Roeber, Sigrun, Giese, Armin, Grossman, Murray, Irwin, David, Meissner, Wassilios, Nilsson, Christer, Pantelyat, Alexander, Rajput, Alex, van Swieten, John, Troakes, Claire, and Höglinger, Günter

Subjects
Four-repeat tauopathies, corticobasal degeneration, diagnostic criteria, progressive supranuclear palsy, Aged, Brain, Female, Humans, Male, Middle Aged, Multiple System Atrophy, Parkinson Disease, Parkinsonian Disorders, Supranuclear Palsy, Progressive, Tauopathies
Abstract

BACKGROUND: The Movement Disorder Society criteria for progressive supranuclear palsy introduced the category probable 4-repeat (4R)-tauopathy for joint clinical diagnosis of progressive supranuclear palsy and corticobasal degeneration. OBJECTIVES: To validate the accuracy of these clinical criteria for probable 4R-tauopathy to predict underlying 4R-tauopathy pathology. METHODS: Diagnostic accuracy for 4R-tauopathies according to the established criteria was estimated retrospectively in autopsy-confirmed patients with progressive supranuclear palsy and corticobasal degeneration (grouped as 4R-tauopathies), and Parkinsons disease, multiple system atrophy, and frontotemporal lobar degeneration (grouped as non-4R-tauopathies). RESULTS: We identified 250 cases with progressive supranuclear palsy (N = 195) and corticobasal degeneration (N = 55) and with and non-4R-tauopathies (N = 161). Sensitivity and specificity of probable 4R-tauopathy was 10% and 99% in the first year and 59% and 88% at final record. CONCLUSIONS: The new diagnostic category probable 4R-tauopathy showed high specificity and may be suitable for the recruitment of patients with progressive supranuclear palsy and corticobasal degeneration into therapeutic trials targeting 4R-tauopathy. The low sensitivity underpins the need for diagnostic biomarkers. © 2019 International Parkinson and Movement Disorder Society.

Published
2020

5. How to apply the movement disorder society criteria for diagnosis of progressive supranuclear palsy.

Author

Grimm, Max-Joseph, Respondek, Gesine, Stamelou, Maria, Arzberger, Thomas, Ferguson, Leslie, Gelpi, Ellen, Giese, Armin, Grossman, Murray, Irwin, David J, Pantelyat, Alexander, Rajput, Alex, Roeber, Sigrun, van Swieten, John C, Troakes, Claire, Antonini, Angelo, Bhatia, Kailash P, Colosimo, Carlo, van Eimeren, Thilo, Kassubek, Jan, Levin, Johannes, Meissner, Wassilios G, Nilsson, Christer, Oertel, Wolfgang H, Piot, Ines, Poewe, Werner, Wenning, Gregor K, Boxer, Adam, Golbe, Lawrence I, Josephs, Keith A, Litvan, Irene, Morris, Huw R, Whitwell, Jennifer L, Compta, Yaroslau, Corvol, Jean-Christophe, Lang, Anthony E, Rowe, James B, Höglinger, Günter U, and Movement Disorder Society-endorsed PSP Study Group

Subjects
Movement Disorder Society-endorsed PSP Study Group, Brain, Humans, Parkinsonian Disorders, Supranuclear Palsy, Progressive, Ocular Motility Disorders, Sensation Disorders, Autopsy, Retrospective Studies, Cohort Studies, Adult, Aged, Aged, 80 and over, Middle Aged, Societies, Medical, Female, Male, Postural Balance, Cognitive Dysfunction, autopsy, diversity, phenotype, progressive supranuclear palsy, Brain Disorders, Pediatric, Neurosciences, Rare Diseases, Clinical Research, Perinatal Period - Conditions Originating in Perinatal Period, 4.2 Evaluation of markers and technologies, Neurology & Neurosurgery, Clinical Sciences, Human Movement and Sports Sciences
Abstract

BackgroundThe Movement Disorder Society criteria for progressive supranuclear palsy define diagnostic allocations, stratified by certainty levels and clinical predominance types. We aimed to study the frequency of ambiguous multiple allocations and to develop rules to eliminate them.MethodsWe retrospectively collected standardized clinical data by chart review in a multicenter cohort of autopsy-confirmed patients with progressive supranuclear palsy, to classify them by diagnostic certainty level and predominance type and to identify multiple allocations.ResultsComprehensive data were available from 195 patients. More than one diagnostic allocation occurred in 157 patients (80.5%). On average, 5.4 allocations were possible per patient. We developed four rules for Multiple Allocations eXtinction (MAX). They reduced the number of patients with multiple allocations to 22 (11.3%), and the allocations per patient to 1.1.ConclusionsThe proposed MAX rules help to standardize the application of the Movement Disorder Society criteria for progressive supranuclear palsy. © 2019 International Parkinson and Movement Disorder Society.

Published
2019

10. The diphenylpyrazole compound anle138b blocks Aβ channels and rescues disease phenotypes in a mouse model for amyloid pathology

Author

Martinez Hernandez, Ana, Urbanke, Hendrik, Gillman, Alan L, Lee, Joon, Ryazanov, Sergey, Agbemenyah, Hope Y, Benito, Eva, Jain, Gaurav, Kaurani, Lalit, Grigorian, Gayane, Leonov, Andrei, Rezaei‐Ghaleh, Nasrollah, Wilken, Petra, Arce, Fernando Teran, Wagner, Jens, Fuhrmann, Martin, Caruana, Mario, Camilleri, Angelique, Vassallo, Neville, Zweckstetter, Markus, Benz, Roland, Giese, Armin, Schneider, Anja, Korte, Martin, Lal, Ratnesh, Griesinger, Christian, Eichele, Gregor, and Fischer, Andre

Subjects
Biochemistry and Cell Biology, Biological Sciences, Neurodegenerative, Dementia, Alzheimer's Disease, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Aging, Acquired Cognitive Impairment, Genetics, Brain Disorders, Neurosciences, 2.1 Biological and endogenous factors, 5.1 Pharmaceuticals, Neurological, Alzheimer Disease, Amyloid beta-Peptides, Animals, Benzodioxoles, Disease Models, Animal, Hippocampus, Male, Mice, Mice, Inbred C57BL, Neuronal Plasticity, Phenotype, Pyrazoles, Spatial Memory, Transcriptome, Alzheimer's disease, amyloid pathology, A beta channels, gene expression, membrane pores, Aβ channels, Medical and Health Sciences, Biochemistry and cell biology
Abstract

Alzheimer's disease is a devastating neurodegenerative disease eventually leading to dementia. An effective treatment does not yet exist. Here we show that oral application of the compound anle138b restores hippocampal synaptic and transcriptional plasticity as well as spatial memory in a mouse model for Alzheimer's disease, when given orally before or after the onset of pathology. At the mechanistic level, we provide evidence that anle138b blocks the activity of conducting Aβ pores without changing the membrane embedded Aβ-oligomer structure. In conclusion, our data suggest that anle138b is a novel and promising compound to treat AD-related pathology that should be investigated further.

Published
2018

12. Which ante mortem clinical features predict progressive supranuclear palsy pathology?

Author

Respondek, Gesine, Kurz, Carolin, Arzberger, Thomas, Compta, Yaroslau, Englund, Elisabet, Ferguson, Leslie W, Gelpi, Ellen, Giese, Armin, Irwin, David J, Meissner, Wassilios G, Nilsson, Christer, Pantelyat, Alexander, Rajput, Alex, van Swieten, John C, Troakes, Claire, Josephs, Keith A, Lang, Anthony E, Mollenhauer, Brit, Müller, Ulrich, Whitwell, Jennifer L, Antonini, Angelo, Bhatia, Kailash P, Bordelon, Yvette, Corvol, Jean‐Christophe, Colosimo, Carlo, Dodel, Richard, Grossman, Murray, Kassubek, Jan, Krismer, Florian, Levin, Johannes, Lorenzl, Stefan, Morris, Huw, Nestor, Peter, Oertel, Wolfgang H, Rabinovici, Gil D, Rowe, James B, van Eimeren, Thilo, Wenning, Gregor K, Boxer, Adam, Golbe, Lawrence I, Litvan, Irene, Stamelou, Maria, Höglinger, Günter U, and Group, for the Movement Disorder Society‐Endorsed PSP Study

Subjects
Biomedical and Clinical Sciences, Ophthalmology and Optometry, Brain Disorders, Dementia, Alzheimer's Disease Related Dementias (ADRD), Pick's Disease, Rare Diseases, Acquired Cognitive Impairment, Neurodegenerative, Neurosciences, Aging, Parkinson's Disease, Frontotemporal Dementia (FTD), Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Aetiology, 2.1 Biological and endogenous factors, Detection, screening and diagnosis, 4.2 Evaluation of markers and technologies, Neurological, Humans, Supranuclear Palsy, Progressive, Progressive supranuclear palsy, clinical features, diagnosis, clinico-pathological series, systematic review, Movement Disorder Society-Endorsed PSP Study Group, Clinical Sciences, Human Movement and Sports Sciences, Neurology & Neurosurgery, Clinical sciences
Abstract

BackgroundProgressive supranuclear palsy (PSP) is a neuropathologically defined disease presenting with a broad spectrum of clinical phenotypes.ObjectiveTo identify clinical features and investigations that predict or exclude PSP pathology during life, aiming at an optimization of the clinical diagnostic criteria for PSP.MethodsWe performed a systematic review of the literature published since 1996 to identify clinical features and investigations that may predict or exclude PSP pathology. We then extracted standardized data from clinical charts of patients with pathologically diagnosed PSP and relevant disease controls and calculated the sensitivity, specificity, and positive predictive value of key clinical features for PSP in this cohort.ResultsOf 4166 articles identified by the database inquiry, 269 met predefined standards. The literature review identified clinical features predictive of PSP, including features of the following 4 functional domains: ocular motor dysfunction, postural instability, akinesia, and cognitive dysfunction. No biomarker or genetic feature was found reliably validated to predict definite PSP. High-quality original natural history data were available from 206 patients with pathologically diagnosed PSP and from 231 pathologically diagnosed disease controls (54 corticobasal degeneration, 51 multiple system atrophy with predominant parkinsonism, 53 Parkinson's disease, 73 behavioral variant frontotemporal dementia). We identified clinical features that predicted PSP pathology, including phenotypes other than Richardson's syndrome, with varying sensitivity and specificity.ConclusionsOur results highlight the clinical variability of PSP and the high prevalence of phenotypes other than Richardson's syndrome. The features of variant phenotypes with high specificity and sensitivity should serve to optimize clinical diagnosis of PSP. © 2017 International Parkinson and Movement Disorder Society.

Published
2017

13. Clinical diagnosis of progressive supranuclear palsy: The movement disorder society criteria.

Author

Höglinger, Günter U, Respondek, Gesine, Stamelou, Maria, Kurz, Carolin, Josephs, Keith A, Lang, Anthony E, Mollenhauer, Brit, Müller, Ulrich, Nilsson, Christer, Whitwell, Jennifer L, Arzberger, Thomas, Englund, Elisabet, Gelpi, Ellen, Giese, Armin, Irwin, David J, Meissner, Wassilios G, Pantelyat, Alexander, Rajput, Alex, van Swieten, John C, Troakes, Claire, Antonini, Angelo, Bhatia, Kailash P, Bordelon, Yvette, Compta, Yaroslau, Corvol, Jean-Christophe, Colosimo, Carlo, Dickson, Dennis W, Dodel, Richard, Ferguson, Leslie, Grossman, Murray, Kassubek, Jan, Krismer, Florian, Levin, Johannes, Lorenzl, Stefan, Morris, Huw R, Nestor, Peter, Oertel, Wolfgang H, Poewe, Werner, Rabinovici, Gil, Rowe, James B, Schellenberg, Gerard D, Seppi, Klaus, van Eimeren, Thilo, Wenning, Gregor K, Boxer, Adam L, Golbe, Lawrence I, Litvan, Irene, and Movement Disorder Society-endorsed PSP Study Group

Subjects
Movement Disorder Society-endorsed PSP Study Group, Humans, Supranuclear Palsy, Progressive, Societies, Medical, Practice Guidelines as Topic, clinical diagnostic criteria, consensus-based, evidence-based, progressive supranuclear palsy, Brain Disorders, Neurosciences, Neurological, Clinical Sciences, Human Movement and Sports Sciences, Neurology & Neurosurgery
Abstract

BackgroundPSP is a neuropathologically defined disease entity. Clinical diagnostic criteria, published in 1996 by the National Institute of Neurological Disorders and Stroke/Society for PSP, have excellent specificity, but their sensitivity is limited for variant PSP syndromes with presentations other than Richardson's syndrome.ObjectiveWe aimed to provide an evidence- and consensus-based revision of the clinical diagnostic criteria for PSP.MethodsWe searched the PubMed, Cochrane, Medline, and PSYCInfo databases for articles published in English since 1996, using postmortem diagnosis or highly specific clinical criteria as the diagnostic standard. Second, we generated retrospective standardized clinical data from patients with autopsy-confirmed PSP and control diseases. On this basis, diagnostic criteria were drafted, optimized in two modified Delphi evaluations, submitted to structured discussions with consensus procedures during a 2-day meeting, and refined in three further Delphi rounds.ResultsDefined clinical, imaging, laboratory, and genetic findings serve as mandatory basic features, mandatory exclusion criteria, or context-dependent exclusion criteria. We identified four functional domains (ocular motor dysfunction, postural instability, akinesia, and cognitive dysfunction) as clinical predictors of PSP. Within each of these domains, we propose three clinical features that contribute different levels of diagnostic certainty. Specific combinations of these features define the diagnostic criteria, stratified by three degrees of diagnostic certainty (probable PSP, possible PSP, and suggestive of PSP). Clinical clues and imaging findings represent supportive features.ConclusionsHere, we present new criteria aimed to optimize early, sensitive, and specific clinical diagnosis of PSP on the basis of currently available evidence. © 2017 International Parkinson and Movement Disorder Society.

Published
2017

15. Genetic determinants of survival in progressive supranuclear palsy: a genome-wide association study

Author

Mok, Kin Y., Murphy, David P., Al-Sarraj, Safa, Troakes, Claire, Gentleman, Steve M., Allinson, Kieren S.J., Jaunmuktane, Zane, Holton, Janice L., Lees, Andrew J., Morris, Christopher M., Compta, Yaroslau, Gelpi, Ellen, van Swieten, John C., Rajput, Alex, Ferguson, Leslie, Cookson, Mark R., Gibbs, J. Raphael, Blauwendraat, Cornelis, Ding, Jinhui, Chia, Ruth, Traynor, Bryan J., Pantelyat, Alexander, Viollet, Coralie, Pletnikova, Olga, Troncoso, Juan C., Rosenthal, Liana S., Boxer, Adam L., Respondek, Gesine, Arzberger, Thomas, Roeber, Sigrun, Giese, Armin, Burn, David J., Pavese, Nicola, Gerhard, Alexander, Kobylecki, Christopher, Leigh, P. Nigel, Church, Alistair, T.M. Hu, Michele, Jabbari, Edwin, Koga, Shunsuke, Valentino, Rebecca R, Reynolds, Regina H, Ferrari, Raffaele, Tan, Manuela M X, Rowe, James B, Dalgard, Clifton L, Scholz, Sonja W, Dickson, Dennis W, Warner, Thomas T, Revesz, Tamas, Höglinger, Günter U, Ross, Owen A, Ryten, Mina, Hardy, John, Shoai, Maryam, and Morris, Huw R

Published
2021
Full Text
View/download PDF

18. A meta-analysis of epigenome-wide association studies in Alzheimer’s disease highlights novel differentially methylated loci across cortex

Author

Smith, Rebecca G., Pishva, Ehsan, Shireby, Gemma, Smith, Adam R., Roubroeks, Janou A. Y., Hannon, Eilis, Wheildon, Gregory, Mastroeni, Diego, Gasparoni, Gilles, Riemenschneider, Matthias, Giese, Armin, Sharp, Andrew J., Schalkwyk, Leonard, Haroutunian, Vahram, Viechtbauer, Wolfgang, van den Hove, Daniel L. A., Weedon, Michael, Brokaw, Danielle, Francis, Paul T., Thomas, Alan J., Love, Seth, Morgan, Kevin, Walter, Jörn, Coleman, Paul D., Bennett, David A., De Jager, Philip L., Mill, Jonathan, and Lunnon, Katie

Published
2021
Full Text
View/download PDF

20. Safety and efficacy of epigallocatechin gallate in multiple system atrophy (PROMESA): a randomised, double-blind, placebo-controlled trial

Author

André, Elisabeth, Blankenstein, Christiane, Canelo, Monica, Düring, Marco, Ebentheuer, Jens, Fricke, Christopher, Gerbes, Alexander, Groiss, Stefan, Gruber, Doreen, Hartmann, Christian, Kirchner, Thomas, Kroneberg, Daniel, Kunz, Martin, Lorenzl, Stefan, Moldovan, Alexia, Noda, Anna, Pape, Heidi, Respondek, Gesine, Schäffer, Eva, Schneider, Martina, Schnitzler, Alfons, Schulz-Schaeffer, Walter, Schwarz, Johannes, Skowronek, Cornelia, Storch, Alexander, Tadic, Vera, Vadász, Dávid, Zimmermann, Benno, Levin, Johannes, Maaß, Sylvia, Schuberth, Madeleine, Giese, Armin, Oertel, Wolfgang H, Poewe, Werner, Trenkwalder, Claudia, Wenning, Gregor K, Mansmann, Ulrich, Südmeyer, Martin, Eggert, Karla, Mollenhauer, Brit, Lipp, Axel, Löhle, Matthias, Classen, Joseph, Münchau, Alexander, Kassubek, Jan, Gandor, Florin, Berg, Daniela, Egert-Schwender, Silvia, Eberhardt, Cornelia, Paul, Friedemann, Bötzel, Kai, Ertl-Wagner, Birgit, Huppertz, Hans-Jürgen, Ricard, Ingrid, and Höglinger, Günter U

Published
2019
Full Text
View/download PDF

22. Development and Radiosynthesis of [11C]MODAG-005 for in vivo Imaging of alpha-synuclein Pathology

Author

Maurer, Andreas, primary, Bonanno, Federica, additional, Saw, Ran Sing, additional, Buss, Sabrina, additional, Kuebler, Laura, additional, Ryazanov, Sergey, additional, Leonov, Andrei, additional, Bleher, Daniel, additional, Grotegerd, Kathrin, additional, Pethe, Madhushree, additional, Schmidt, Felix, additional, Ruf, Viktoria, additional, Dahl, Bernadette, additional, Kahle, Philipp, additional, Pichler, Bernd, additional, Bowden, Gregory, additional, Griesinger, Christian, additional, Giese, Armin, additional, and Herfert, Kristina, additional

Published
2023
Full Text
View/download PDF

26. Anle138b interaction in α-synuclein aggregates by dynamic nuclear polarization NMR

Author

Dervişoğlu, Rıza, primary, Antonschmidt, Leif, additional, Nimerovsky, Evgeny, additional, Sant, Vrinda, additional, Kim, Myeongkyu, additional, Ryazanov, Sergey, additional, Leonov, Andrei, additional, Fuentes-Monteverde, Juan Carlos, additional, Wegstroth, Melanie, additional, Giller, Karin, additional, Mathies, Guinevere, additional, Giese, Armin, additional, Becker, Stefan, additional, Griesinger, Christian, additional, and Andreas, Loren B., additional

Published
2023
Full Text
View/download PDF

34. Late-stage Anle138b treatment ameliorates tau pathology and metabolic decline in a mouse model of human Alzheimer’s disease tau

Author

Brendel, Matthias, Deussing, Maximilian, Blume, Tanja, Kaiser, Lena, Probst, Federico, Overhoff, Felix, Peters, Finn, von Ungern-Sternberg, Barbara, Ryazanov, Sergey, Leonov, Andrei, Griesinger, Christian, Zwergal, Andreas, Levin, Johannes, Bartenstein, Peter, Yakushev, Igor, Cumming, Paul, Boening, Guido, Ziegler, Sibylle, Herms, Jochen, Giese, Armin, and Rominger, Axel

Published
2019
Full Text
View/download PDF

44. Safety, tolerability and pharmacokinetics of the oligomer modulator anle138b with exposure levels sufficient for therapeutic efficacy in a murine Parkinson model: A randomised, double-blind, placebo-controlled phase 1a trial

Author

Levin, Johannes, primary, Sing, Nand, additional, Melbourne, Sue, additional, Morgan, Amber, additional, Mariner, Carla, additional, Spillantini, Maria Grazia, additional, Wegrzynowicz, Michal, additional, Dalley, Jeffrey W., additional, Langer, Simon, additional, Ryazanov, Sergey, additional, Leonov, Andrei, additional, Griesinger, Christian, additional, Schmidt, Felix, additional, Weckbecker, Daniel, additional, Prager, Kai, additional, Matthias, Torsten, additional, and Giese, Armin, additional

Published
2022
Full Text
View/download PDF

45. Long-Duration Progressive Supranuclear Palsy:Clinical Course and Pathological Underpinnings

Author

Lukic, Milica Jecmenica, Respondek, Gesine, Kurz, Carolin, Compta, Yaroslau, Gelpi, Ellen, Ferguson, Leslie W., Rajput, Alex, Troakes, Claire, van Swieten, John C., Giese, Armin, Roeber, Sigrun, Herms, Jochen, Arzberger, Thomas, Höglinger, Günter, Lukic, Milica Jecmenica, Respondek, Gesine, Kurz, Carolin, Compta, Yaroslau, Gelpi, Ellen, Ferguson, Leslie W., Rajput, Alex, Troakes, Claire, van Swieten, John C., Giese, Armin, Roeber, Sigrun, Herms, Jochen, Arzberger, Thomas, and Höglinger, Günter

Abstract

Objectives: To identify the clinical characteristics of the subgroup of benign progressive supranuclear palsy with particularly long disease duration; to define neuropathological determinants underlying variability in disease duration in progressive supranuclear palsy. Methods: Clinical and pathological features were compared among 186 autopsy-confirmed cases with progressive supranuclear palsy with ≥10 years and shorter survival times. Results: The 45 cases (24.2%) had a disease duration of ≥10 years. The absence of ocular motor abnormalities within the first 3 years from disease onset was the only significant independent clinical predictor of longer survival. Histopathologically, the neurodegeneration parameters in each survival group were paralleled anatomically by the distribution of neuronal cytoplasmic inclusions, whereas the tufted astrocytes displayed anatomically an opposite severity pattern. Most interestingly, we found significantly less coiled bodies in those who survive longer, in contrast to patients with less favorable course. Interpretation: A considerable proportion of patients had a more ”benign” disease course with ≥10 years survival. They had a distinct pattern and evolution of core symptoms compared to patients with short survival. The inverted anatomical patterns of astrocytic tau distribution suggest distinct implications of these cell types in trans-cellular propagation. The tempo of disease progression appeared to be determined mostly by oligodendroglial tau, where the high degree of oligodendroglial tau pathology might affect neuronal integrity and function on top of neuronal tau pathology. The relative contribution of glial tau should be further explored in cellular and animal models. ANN NEUROL 2022;92:637–649.

Published
2022

46. Reducing tau aggregates with anle138b delays disease progression in a mouse model of tauopathies

Author

Wagner, Jens, Krauss, Sybille, Shi, Song, Ryazanov, Sergey, Steffen, Julia, Miklitz, Carolin, Leonov, Andrei, Kleinknecht, Alexander, Göricke, Bettina, Weishaupt, Jochen H., Weckbecker, Daniel, Reiner, Anne M., Zinth, Wolfgang, Levin, Johannes, Ehninger, Dan, Remy, Stefan, Kretzschmar, Hans A., Griesinger, Christian, Giese, Armin, and Fuhrmann, Martin

Published
2015
Full Text
View/download PDF

48. Extracellular vesicle sorting of α-Synuclein is regulated by sumoylation

Author

Kunadt, Marcel, Eckermann, Katrin, Stuendl, Anne, Gong, Jing, Russo, Belisa, Strauss, Katrin, Rai, Surya, Kügler, Sebastian, Falomir Lockhart, Lisandro, Schwalbe, Martin, Krumova, Petranka, Oliveira, Luis M. A., Bähr, Mathias, Möbius, Wiebke, Levin, Johannes, Giese, Armin, Kruse, Niels, Mollenhauer, Brit, Geiss-Friedlander, Ruth, Ludolph, Albert C., Freischmidt, Axel, Feiler, Marisa S., Danzer, Karin M., Zweckstetter, Markus, Jovin, Thomas M., Simons, Mikael, Weishaupt, Jochen H., and Schneider, Anja

Published
2015
Full Text
View/download PDF

50. Toxicity of extracellular alpha-synuclein is independent of intracellular alpha-synuclein

Author

Dening, Yanina, primary, Straßl, Theresa, additional, Ruf, Viktoria, additional, Dirscherl, Petra, additional, Chovsepian, Alexandra, additional, Stievenard, Alicia, additional, Khairnar, Amit, additional, Schmidt, Felix, additional, Giesert, Florian, additional, Herms, Jochen, additional, Levin, Johannes, additional, Dieterich, Marianne, additional, Falkai, Peter, additional, Weisenhorn, Daniela Vogt, additional, Wurst, Wolfgang, additional, Giese, Armin, additional, and Pan-Montojo, Francisco, additional

Published
2022
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results