Search

Your search keyword '"Hilker, Rüdiger"' showing total 199 results
Start Over Author "Hilker, Rüdiger"
199 results on '"Hilker, Rüdiger"'

28. Manual MRI morphometry in Parkinsonian syndromes

Author

Möller, Leona, Kassubek, Jan, Möller, Franz, Schnitzler, Alfons, Oertel, Wolfgang H, Knake, Susanne, Huppertz, Hans-Jürgen, Höglinger, Günter U, Südmeyer, Martin, Hilker, Rüdiger, Hattingen, Elke, Egger, Karl, Amtage, Florian, Pinkhardt, Elmar H, Respondek, Gesine, and Stamelou, Maria

Subjects
Adult, Aged, 80 and over, Male, Reproducibility of Results, Middle Aged, diagnostic imaging [Multiple System Atrophy], diagnostic imaging [Parkinsonian Disorders], Magnetic Resonance Imaging, physiopathology [Multiple System Atrophy], ROC Curve, Case-Control Studies, physiopathology [Parkinsonian Disorders], diagnostic imaging [Parkinson Disease], Humans, Female, ddc:610, diagnostic imaging [Supranuclear Palsy, Progressive], diagnostic imaging [Brain], Aged
Abstract

Manual MRI morphometry in Parkinsonian syndromes.

Published
2017

29. Apolipoprotein E ε4 does not affect cognitive performance in patients with Parkinson's disease

Author

Mengel, David, Dams, Judith, Ziemek, Jannis, Becker, Julian, Balzer-Geldsetzer, Monika, Hilker, Rüdiger, Baudrexel, Simon, Kalbe, Elke, Schmidt, Nele, Witt, Karsten, Liepelt-Scarfone, Inga, Gräber, Susanne, Petrelli, Annette, Neuser, Petra, Schulte, Claudia, Linse, Katharina, Storch, Alexander, Wittchen, Hans-Ulrich, Riedel, Oliver, Mollenhauer, Brit, Ebentheuer, Jens, Trenkwalder, Claudia, Klockgether, Thomas, Spottke, Annika, Wüllner, Ullrich, Schulz, Jörg B., Reetz, Kathrin, Heber, Ines Ann, Ramirez, Alfredo, and Dodel, Richard

Published
2016
Full Text
View/download PDF

30. Longitudinal changes of cortical microstructure in Parkinson's disease assessed with T1 relaxometry

Author

Nürnberger, Lucas, Gracien, René-Maxime, Hok, Pavel, Hof, Stephanie-Michelle, Rüb, Udo, Steinmetz, Helmuth, Hilker, Rüdiger, Klein, Johannes Christian, Deichmann, Ralf, Baudrexel, Simon, Nürnberger, Lucas, Gracien, René-Maxime, Hok, Pavel, Hof, Stephanie-Michelle, Rüb, Udo, Steinmetz, Helmuth, Hilker, Rüdiger, Klein, Johannes Christian, Deichmann, Ralf, and Baudrexel, Simon

Abstract

Background: Histological evidence suggests that pathology in Parkinson's disease (PD) goes beyond nigrostriatal degeneration and also affects the cerebral cortex. Quantitative MRI (qMRI) techniques allow the assessment of changes in brain tissue composition. However, the development and pattern of disease-related cortical changes have not yet been demonstrated in PD with qMRI methods. The aim of this study was to investigate longitudinal cortical microstructural changes in PD with quantitative T1 relaxometry. Methods: 13 patients with mild to moderate PD and 20 matched healthy subjects underwent high resolution T1 mapping at two time points with an interval of 6.4 years (healthy subjects: 6.5 years). Data from two healthy subjects had to be excluded due to MRI artifacts. Surface-based analysis of cortical T1 values was performed with the FreeSurfer toolbox. Results: In PD patients, a widespread decrease of cortical T1 was detected during follow-up which affected large parts of the temporo-parietal and occipital cortices and also frontal areas. In contrast, age-related T1 decrease in the healthy control group was much less pronounced and only found in lateral frontal, parietal and temporal areas. Average cortical T1 values did not differ between the groups at baseline (p = 0.17), but were reduced in patients at follow-up (p = 0.0004). Annualized relative changes of cortical T1 were higher in patients vs. healthy subjects (patients: − 0.72 ± 0.64%/year; healthy subjects: − 0.17 ± 0.41%/year, p = 0.007). Conclusions: In patients with PD, the development of widespread changes in cortical microstructure was observed as reflected by a reduction of cortical T1. The pattern of T1 decrease in PD patients exceeded the normal T1 decrease as found in physiological aging and showed considerable overlap with the pattern of cortical thinning demonstrated in previous PD studies. Therefore, cortical T1 might be a promising additional imaging marker for future longitudinal PD studies

Published
2017

31. Differentiation of neurodegenerative parkinsonian syndromes by volumetric magnetic resonance imaging analysis and support vector machine classification

Author

Huppertz, Hans-Jürgen, Möller, Leona, Pinkhardt, Elmar H, Oertel, Wolfgang H, Knake, Susanne, Kassubek, Jan, Höglinger, Günter U, Südmeyer, Martin, Hilker, Rüdiger, Hattingen, Elke, Egger, Karl, Amtage, Florian, Respondek, Gesine, Stamelou, Maria, and Schnitzler, Alfons

Subjects
Support Vector Machine, Brain, Multiple System Atrophy, diagnostic imaging [Multiple System Atrophy], diagnostic imaging [Parkinsonian Disorders], Magnetic Resonance Imaging, methods [Magnetic Resonance Imaging], Parkinsonian Disorders, Cerebellar Diseases, Humans, ddc:610, diagnostic imaging [Supranuclear Palsy, Progressive], Supranuclear Palsy, Progressive, diagnostic imaging [Cerebellar Diseases], classification [Parkinsonian Disorders], diagnostic imaging [Brain]
Abstract

Clinical differentiation of parkinsonian syndromes is still challenging.A fully automated method for quantitative MRI analysis using atlas-based volumetry combined with support vector machine classification was evaluated for differentiation of parkinsonian syndromes in a multicenter study.Atlas-based volumetry was performed on MRI data of healthy controls (n = 73) and patients with PD (204), PSP with Richardson's syndrome phenotype (106), MSA of the cerebellar type (21), and MSA of the Parkinsonian type (60), acquired on different scanners. Volumetric results were used as input for support vector machine classification of single subjects with leave-one-out cross-validation.The largest atrophy compared to controls was found for PSP with Richardson's syndrome phenotype patients in midbrain (-15%), midsagittal midbrain tegmentum plane (-20%), and superior cerebellar peduncles (-13%), for MSA of the cerebellar type in pons (-33%), cerebellum (-23%), and middle cerebellar peduncles (-36%), and for MSA of the parkinsonian type in the putamen (-23%). The majority of binary support vector machine classifications between the groups resulted in balanced accuracies of >80%. With MSA of the cerebellar and parkinsonian type combined in one group, support vector machine classification of PD, PSP and MSA achieved sensitivities of 79% to 87% and specificities of 87% to 96%. Extraction of weighting factors confirmed that midbrain, basal ganglia, and cerebellar peduncles had the largest relevance for classification.Brain volumetry combined with support vector machine classification allowed for reliable automated differentiation of parkinsonian syndromes on single-patient level even for MRI acquired on different scanners. © 2016 International Parkinson and Movement Disorder Society.

Published
2016

32. Naturally occurring Autoantibodies against tau protein are reduced in Parkinson's disease dementia

Author

Kronimus, Yannick, Albus, Alexandra, Balzer-Geldsetzer, Monika, Straub, Sarah, Semler, Elisa, Otto, Markus, Klotsche, Jens, Dodel, Richard, Mengel, David, Hilker, Rüdiger, Baudrexel, Simon, Kalbe, Elke, Schmidt, Nele, Witt, Karsten, Liepelt-Scarfone, Inga, Gräber, Susanne, Schulte, Claudia, Wittchen, Hans-Ulrich, Riedel, Oliver, Mollenhauer, Brit, Trenkwalder, Claudia, Klockgether, Thomas, Spottke, Annika, Wüllner, Ullrich, Schulz, Jörg B., Reetz, Kathrin, and Heber, Ines Ann

Subjects
mental disorders, Medizin
Abstract

Background and Objective: Altered levels of naturally occurring autoantibodies (nAbs) against disease-associated neuronal proteins have been reported for neurodegenerative diseases, such as Alzheimer's (AD) and Parkinson's disease (PD). Recent histopathologic studies suggest a contribution of both Lewy body- and AD-related pathology to Parkinson's disease dementia (PDD). Therefore, we explored nAbs against alpha-synuclein (αS), tau and β-amyloid (Aβ) in PDD compared to cognitively normal PD patients. Materials and Methods: We established three different ELISAs to quantify the nAbs-tau, nAbs-αS, and nAbs-Aβ levels and avidity towards their specific antigen in serum samples of 18 non-demented (PDND) and 18 demented PD patients (PDD), which were taken from an ongoing multi-center cohort study (DEMPARK/LANDSCAPE). Results: PDD patients had significantly decreased nAbs-tau serum levels compared to PDND patients (p = 0.007), whereas the serum titers of nAbs-αS and nAbs-Aβ were unchanged. For all three nAbs, no significant differences in avidity were found between PDD and PDND cohorts. However, within both patient groups, nAbs-tau showed lowest avidity to their antigen, followed by nAbs-αS, and nAbs-Aβ. Though, due to a high interassay coefficient of variability and the exclusion of many samples below the limit of detection, conclusions for nAbs-Aβ are only conditionally possible. Conclusion: We detected a significantly decreased nAbs-tau serum level in PDD patients, indicating a potential linkage between nAbs-tau serum titer and cognitive deficits in PD. Thus, further investigation in larger samples is justified to confirm our findings. OA gold

Published
2016

33. Manual MRI morphometry in Parkinsonian syndromes

Author

Möller, Leona, primary, Kassubek, Jan, additional, Südmeyer, Martin, additional, Hilker, Rüdiger, additional, Hattingen, Elke, additional, Egger, Karl, additional, Amtage, Florian, additional, Pinkhardt, Elmar H., additional, Respondek, Gesine, additional, Stamelou, Maria, additional, Möller, Franz, additional, Schnitzler, Alfons, additional, Oertel, Wolfgang H., additional, Knake, Susanne, additional, Huppertz, Hans-Jürgen, additional, and Höglinger, Günter U., additional

Published
2017
Full Text
View/download PDF

35. Subtypes of mild cognitive impairment in patients with Parkinson's disease: evidence from the LANDSCAPE study

Author

Kalbe, Elke, primary, Rehberg, Sarah Petra, additional, Heber, Ines, additional, Kronenbuerger, Martin, additional, Schulz, Jörg B, additional, Storch, Alexander, additional, Linse, Katharina, additional, Schneider, Christine, additional, Gräber, Susanne, additional, Liepelt-Scarfone, Inga, additional, Berg, Daniela, additional, Dams, Judith, additional, Balzer-Geldsetzer, Monika, additional, Hilker, Rüdiger, additional, Oberschmidt, Carola, additional, Witt, Karsten, additional, Schmidt, Nele, additional, Mollenhauer, Brit, additional, Trenkwalder, Claudia, additional, Spottke, Annika, additional, Roeske, Sandra, additional, Wittchen, Hans-Ulrich, additional, Riedel, Oliver, additional, and Dodel, Richard, additional

Published
2016
Full Text
View/download PDF

36. Association of LRRK2 exonic variants with susceptibility to Parkinson's disease: a case-control study

Author

Ross, Owen A, Soto-Ortolaza, Alexandra I, Brighina, Laura, Riess, Olaf, Klein, Christine, Djarmati, Ana, Hagenah, Johann, Lohmann, Katja, van de Loo, Simone, Abahuni, Nadine, Gispert-Sánchez, Suzana, Hilker, Rüdiger, Auburger, Georg, Van Broeckhoven, Christine, Xiromerisiou, Georgia, Tsimourtou, Vaia, Ralli, Styliani, Kountra, Persa, Markou, Katerina, Patramani, Gianna, Vogiatzi, Christina, Lynch, Tim, Gibson, J Mark, Craig, Dr David, Carr, Jonathan, Valente, Enza Maria, Ferraris, Alessandro, Bentivoglio, Anna Rita, Ialongo, Tamara, Guidubaldi, Arianna, Piano, Carla, Ferrarese, Carlo, Tarantino, Patrizia, Annesi, Ferdinanda, Chartier-Harlin, Marie-Christine, Annesi, Grazia, Quattrone, Aldo, Hattori, Nobutaka, Tomiyama, Hiroyuki, Funayama, Manabu, Yoshino, Hiroyo, Li, Yuanzhe, Imamichi, Yoko, Toda, Tatsushi, Satake, Wataru, Dardiotis, Efthimios, Aasly, J., Opala, Grzegorz, Jasinska-Myga, Barbara, Boczarska-Jedynak, Magdalena, Tan, Eng King, Bardien, Soraya, Jeon, Beom Seok, Park, Sung Sup, Kim, Yun Joong, Dickson, Dennis W, Sohn, Young Ho, Belin, Andrea Carmine, Olson, Lars, Galter, Dagmar, Westerlund, Marie, Sydow, Olof, Pedersen, Nancy L, Wirdefeldt, Karin, Nilsson, Christer, Puschmann, Andreas, Diehl, Nancy N, Wu, Ruey-Meei, Maraganore, Demetrius M, Ahlskog, Eric, de Andrade, Mariza, Lesnick, Timothy G, Rocca, Walter A, Checkoway, Harvey, Farrer, M., Elbaz, Alexis, Heckman, Michael G, Fiske, Brian, Gibson, Rachel, Hadjigeorgiou, Georgios M, Ioannidis, John P A, Jeon, Beom S, Aasly, Jan O, Kruger, Rejko, Kyratzi, Elli, Lesage, Suzanne, Lin, Chin-Hsien, Lynch, Timothy, Mellick, George D, Mutez, Eugénie, Sharma, Manu, Silburn, Peter A, Stefanis, Leonidas, Tadic, Vera, Theuns, Jessie, Uitti, Ryan J, Vassilatis, Demetrios K, Vilariño-Güell, Carles, White, Linda R, Wszolek, Zbigniew K, Farrer, Matthew J, Bacon, Justin A, Disease, Genetic Epidemiology Of Parkinson's, Sutherland, G. T., Siebert, G. A., Nuytemans, Karen, Meeus, Bram, Crosiers, David, Pickut, Barbara, Engelborghs, Sebastiaan, De Deyn, Peter P, Cras, Patrick, Rogaeve, Ekaterina, Destée, A., Agid, Y., Anheim, M., Bonnet, A-M, Borg, M., Bozi, Maria, Brice, A., Broussolle, E., Corvol, J. C., Damier, P., Dürr, A., Durif, F., Lesage, S., Lohmann, E., Pollak, P., Brice, Alexis, Rascol, O., Tison, F., Tranchant, C., Viallet, F., Vidailhet, M., Gasser, Thomas, Krüger, Rejko, Berg, Daniela, Schulte, Claudia, Ross, O, Soto Ortolaza, A, Heckman, M, Aasly, J, Abahuni, N, Annesi, G, Bacon, J, Bardien, S, Bozi, M, Brice, A, Brighina, L, Van Broeckhoven, C, Carr, J, Chartier Harlin, M, Dardiotis, E, Dickson, D, Diehl, N, Elbaz, A, Ferrarese, C, Ferraris, A, Fiske, B, Gibson, J, Gibson, R, Hadjigeorgiou, G, Hattori, N, Ioannidis, J, Jasinska Myga, B, Jeon, B, Kim, Y, Klein, C, Kruger, R, Kyratzi, E, Lesage, S, Lin, C, Lynch, T, Maraganore, D, Mellick, G, Mutez, E, Nilsson, C, Opala, G, Park, S, Puschmann, A, Quattrone, A, Sharma, M, Silburn, P, Sohn, Y, Stefanis, L, Tadic, V, Theuns, J, Tomiyama, H, Uitti, R, Valente, E, van de Loo, S, Vassilatis, D, Vilariño Güell, C, White, L, Wirdefeldt, K, Wszolek, Z, Wu, R, Farrer, M, Engelborghs, Sebastiaan, De Deyn, Peter Paul, Cras, Patrick, Genetic Epidemiology Of Parkinson's Disease (GEO-PD) Consortium, Pathologic Biochemistry and Physiology, and Pollak, Pierre

Subjects
Male, Polymorphism, Single Nucleotide/*genetics, International Cooperation, Ethnic Groups/genetics, Ethnic Group, Genome-wide association study, Protein-Serine-Threonine Kinase, methods [Genome-Wide Association Study], genetics [Ethnic Groups], 0302 clinical medicine, Gene Frequency, genetics [Parkinson Disease], Risk Factors, Exons/genetics, Ethnicity, Parkinson Disease/genetics, Medicine(all), Genetics, Aged, 80 and over, 0303 health sciences, Parkinson Disease, Exons, genetics [Exons], Middle Aged, Polymorphism, Single Nucleotide/genetics, Protein-Serine-Threonine Kinases, LRRK2, 3. Good health, genetics [Polymorphism, Single Nucleotide], Genome-Wide Association Study/methods, Female, Case-Control Studie, Human, Adult, Parkinson Disease/*genetics, Genotype, Adolescent, Protein-Serine-Threonine Kinases/*genetics, Protein-Serine-Threonine Kinases/genetics, Exon, Protein Serine-Threonine Kinases, Biology, Leucine-Rich Repeat Serine-Threonine Protein Kinase-2, genetics [Protein-Serine-Threonine Kinases], Polymorphism, Single Nucleotide, 03 medical and health sciences, Young Adult, Humans, Genetic Predisposition to Disease, ddc:610, LRRK2 protein, human, Risk factor, Allele frequency, 030304 developmental biology, Aged, Risk Factor, Case-control study, Exons/*genetics, Odds ratio, nervous system diseases, ddc:616.8, Minor allele frequency, Genetic epidemiology, Case-Control Studies, Neurology (clinical), Human medicine, 030217 neurology & neurosurgery, Genome-Wide Association Study
Abstract

BACKGROUND: Background The leucine-rich repeat kinase 2 gene (LRRK2) harbours highly penetrant mutations that are linked to familial parkinsonism. However, the extent of its polymorphic variability in relation to risk of Parkinson's disease (PD) has not been assessed systematically. We therefore assessed the frequency of LRRK2 exonic variants in individuals with and without PD, to investigate the role of the variants in PD susceptibility. METHODS: LRRK2 was genotyped in patients with PD and controls from three series (white, Asian, and Arab-Berber) from sites participating in the Genetic Epidemiology of Parkinson's Disease Consortium. Genotyping was done for exonic variants of LRRK2 that were identified through searches of literature and the personal communications of consortium members. Associations with PD were assessed by use of logistic regression models. For variants that had a minor allele frequency of 0.5% or greater, single variant associations were assessed, whereas for rarer variants information was collapsed across variants. FINDINGS: 121 exonic LRRK2 variants were assessed in 15 540 individuals: 6995 white patients with PD and 5595 controls, 1376 Asian patients and 962 controls, and 240 Arab-Berber patients and 372 controls. After exclusion of carriers of known pathogenic mutations, new independent risk associations were identified for polymorphic variants in white individuals (M1646T, odds ratio 1.43, 95% CI 1.15-1.78; p=0.0012) and Asian individuals (A419V, 2.27, 1.35-3.83; p=0.0011). A protective haplotype (N551K-R1398H-K1423K) was noted at a frequency greater than 5% in the white and Asian series, with a similar finding in the Arab-Berber series (combined odds ratio 0.82, 0.72-0.94; p=0.0043). Of the two previously reported Asian risk variants, G2385R was associated with disease (1.73, 1.20-2.49; p=0.0026), but no association was noted for R1628P (0.62, 0.36-1.07; p=0.087). In the Arab-Berber series, Y2189C showed potential evidence of risk association with PD (4.48, 1.33-15.09; p=0.012). INTERPRETATION: The results for LRRK2 show that several rare and common genetic variants in the same gene can have independent effects on disease risk. LRRK2, and the pathway in which it functions, is important in the cause and pathogenesis of PD in a greater proportion of patients with this disease than previously believed. These results will help discriminate those patients who will benefit most from therapies targeted at LRRK2 pathogenic activity. FUNDING: Michael J Fox Foundation and National Institutes of Health. Lancet Neurol

Published
2011

37. Independent and joint effects of the MAPT and SNCA genes in Parkinson disease

Author

Elbaz, Alexis, Ross, Owen A, Destée, Alain, Ferrarese, Carlo, Ferraris, Alessandro, Gibson, J Mark, Gispert, Suzana, Hadjigeorgiou, Georgios M, Jasinska-Myga, Barbara, Klein, Christine, Krüger, Rejko, Lambert, Jean-Charles, Ioannidis, John P A, Lohmann, Katja, van de Loo, Simone, Loriot, Marie-Anne, Lynch, Timothy, Mellick, George D, Mutez, Eugénie, Nilsson, Christer, Opala, Grzegorz, Puschmann, Andreas, Quattrone, Aldo, Soto-Ortolaza, Alexandra I, Sharma, Manu, Silburn, Peter A, Stefanis, Leonidas, Uitti, Ryan J, Valente, Enza Maria, Vilariño-Güell, Carles, Wirdefeldt, Karin, Wszolek, Zbigniew K, Xiromerisiou, Georgia, Maraganore, Demetrius M, Moisan, Frédéric, Farrer, Matthew J, Disease, Genetic Epidemiology of Parkinson's, Amouyel, Philippe, Tzourio, Christophe, Mulot, Claire, Bacon, Justin A, Cobb, Stephanie A, Sutherland, Greg T, Siebert, Gerhard A, Dissanayaka, Nadeeka, Aasly, Jan, O'Sullivan, John D, Boyle, Richard S, Pasquier, Florence, Bordet, Régis, Legendre, Jean-Philippe, Auburger, Georg, Hilker, Rüdiger, Abahuni, Nadine, Geisen, Christof, Winkler, Susen, Annesi, Grazia, Gasser, Thomas, Riess, Olaf, Berg, Daniela, Schulte, Claudia, Vassilatis, Demitris, Stamboulis, Eleftherios, Dardiotis, Efthimios, Patramani, Ioanna, Kountra, Persa-Maria, Vogiatzi, Christina, Bozi, Maria, Markou, Katerina, Tarantino, Patrizia, Annesi, Ferdinanda, Bentivoglio, Anna Rita, Guidubaldi, Arianna, Caccialupi, Matilde, De Nigris, Francesca, Riva, Chiara, Pedersen, Nancy L, Nilsson, Karin, Brighina, Laura, Reimer, Jan, Van Gerpen, Jay, Lash, Jennifer, Searcy, Jill, Strongosky, Audrey, Chartier-Harlin, Marie-Christine, Elbaz, A, Ross, O, Ioannidis, J, Soto Ortolaza, A, Moisan, F, Aasly, J, Annesi, G, Bozi, M, Brighina, L, Chartier Harlin, M, Destée, A, Ferrarese, C, Ferraris, A, Gibson, J, Gispert, S, Hadjigeorgiou, G, Jasinska Myga, B, Klein, C, Krüger, R, Lambert, J, Lohmann, K, van de Loo, S, Loriot, M, Lynch, T, Mellick, G, Mutez, E, Nilsson, C, Opala, G, Puschmann, A, Quattrone, A, Sharma, M, Silburn, P, Stefanis, L, Uitti, R, Valente, E, Vilariño Güell, C, Wirdefeldt, K, Wszolek, Z, Xiromerisiou, G, Maraganore, D, and Farrer, M

Subjects
Adult, Male, Parkinson Disease/*genetics, Logistic Model, Polymorphism, Single Nucleotide/*genetics, Single-nucleotide polymorphism, Genome-wide association study, MAPT protein, human, tau Proteins, Biology, alpha-Synuclein/*genetics, Polymorphism, Single Nucleotide, Article, Gene interaction, genetics [Parkinson Disease], Retrospective Studie, Genotype, Odds Ratio, SNP, Humans, genetics, Genetic Predisposition to Disease, ddc:610, SNCA protein, human, Age of Onset, Retrospective Studies, Aged, Genetics, Aged, 80 and over, Haplotype, tau Protein, Parkinson Disease, Middle Aged, genetics [tau Proteins], Settore MED/26 - NEUROLOGIA, Logistic Models, Neurology, Genetic epidemiology, Case-Control Studies, Multiple comparisons problem, genetics [Polymorphism, Single Nucleotide], genetics [alpha-Synuclein], alpha-Synuclein, Female, Neurology (clinical), tau Proteins/*genetics, Case-Control Studie, Human
Abstract

Objective: We studied the independent and joint effects of the genes encoding alpha-synuclein (SNCA) and microtubule-associated protein tau (MAPT) in Parkinson disease (PD) as part of a large meta-analysis of individual data from case-control studies participating in the Genetic Epidemiology of Parkinson's Disease (GEO-PD) consortium. Methods: Participants of Caucasian ancestry were genotyped for a total of 4 SNCA (rs2583988, rs181489, rs356219, rs11931074) and 2 MAPT (rs1052553, rs242557) single nucleotide polymorphism (SNPs). Individual and joint effects of SNCA and MAPT SNPs were investigated using fixed- and random-effects logistic regression models. Interactions were studied on both a multiplicative and an additive scale, and using a case-control and case-only approach. Results: Fifteen GEO-PD sites contributed a total of 5,302 cases and 4,161 controls. All 4 SNCA SNPs and the MAPT H1-haplotype-defining SNP (rs1052553) displayed a highly significant marginal association with PD at the significance level adjusted for multiple comparisons. For SNCA, the strongest associations were observed for SNPs located at the 30 end of the gene. There was no evidence of statistical interaction between any of the 4 SNCA SNPs and rs1052553 or rs242557, neither on the multiplicative nor on the additive scale. Interpretation: This study confirms the association between PD and both SNCA SNPs and the H1 MAPT haplotype. It shows, based on a variety of approaches, that the joint action of variants in these 2 loci is consistent with independent effects of the genes without additional interacting effects. ANN NEUROL 2011; 69: 778-792

Published
2011

39. Does Navigated Transcranial Stimulation Increase the Accuracy of Tractography? A Prospective Clinical Trial Based on Intraoperative Motor Evoked Potential Monitoring During Deep Brain Stimulation

Author

Forster, Marie-Therese, primary, Hoecker, Alexander Claudius, additional, Kang, Jun-Suk, additional, Quick, Johanna, additional, Seifert, Volker, additional, Hattingen, Elke, additional, Hilker, Rüdiger, additional, and Weise, Lutz Martin, additional

Published
2015
Full Text
View/download PDF

41. Screening for cognitive deficits in Parkinson's disease with the Parkinson neuropsychometric dementia assessment (PANDA) instrument

Author

Kalbe, Elke, Calabrese, Pasquale, Kohn, Nils, Hilker, Rüdiger, Riedel, Oliver, Wittchen, Hans-Ulrich, Dodel, Richard, Otto, Jörg, Ebersbach, Georg, Kessler, Josef, Kalbe, Elke, Calabrese, Pasquale, Kohn, Nils, Hilker, Rüdiger, Riedel, Oliver, Wittchen, Hans-Ulrich, Dodel, Richard, Otto, Jörg, Ebersbach, Georg, and Kessler, Josef

Abstract

Cognitive and affective dysfunctions are frequent but often neglected symptoms in Parkinson’s disease (PD). We developed the screening tool Parkinson neuropsychometric dementia assessment (PANDA) with five cognitive tasks and a short depression questionnaire. Healthy subjects and patients without cognitive impairment (PD), mild cognitive disorder (PD-MCD), or dementia (PDD) were examined. The cognition part had a specificity of 91% and a sensitivity of 90% for PDD and 77% for PDD plus PD-MCD patients. The mood questionnaire also had high sensitivity and specificity. We conclude that the PANDA is an economical, easy-to-use and sensitive tool to detect neuropsychological dysfunctions in PD patients in clinical practice.

Published
2013

42. Parkinson’s Disease and Dementia: A Longitudinal Study (DEMPARK)

Author

Balzer-Geldsetzer, Monika, Costa, Ana Sofia Ferreira Braga da, Kronenbürger, Martin, Schulz, Jörg B., Röske, Sandra, Spottke, Annika, Wüllner, Ullrich, Klockgether, Thomas, Storch, Alexander, Schneider, Christine, Riedel, Oliver, Wittchen, Hans-Ulrich, Seifried, Carola, Hilker, Rüdiger, Schmidt, Nele, Witt, Karsten, Deuschl, Günther, Mollenhauer, Brit, Trenkwalder, Claudia, Liepelt-Scarfone, Inga, Gräber-Sultan, Susanne, Berg, Daniela, Gasser, Thomas, Kalbe, Elke, Bodden, Maren, Oertel, Wolfgang H., Dodel, Richard, Balzer-Geldsetzer, Monika, Costa, Ana Sofia Ferreira Braga da, Kronenbürger, Martin, Schulz, Jörg B., Röske, Sandra, Spottke, Annika, Wüllner, Ullrich, Klockgether, Thomas, Storch, Alexander, Schneider, Christine, Riedel, Oliver, Wittchen, Hans-Ulrich, Seifried, Carola, Hilker, Rüdiger, Schmidt, Nele, Witt, Karsten, Deuschl, Günther, Mollenhauer, Brit, Trenkwalder, Claudia, Liepelt-Scarfone, Inga, Gräber-Sultan, Susanne, Berg, Daniela, Gasser, Thomas, Kalbe, Elke, Bodden, Maren, Oertel, Wolfgang H., and Dodel, Richard

Abstract

Background: Parkinson’s disease (PD) is a progressive neurodegenerative motor disorder. However, non-motor complications frequently alter the course of the disease. A particularly disabling non-motor symptom is dementia. Methods/Design: The study is designed as a multicentre prospective, observational cohort study of about 700 PD patients aged 45–80 years with or without dementia and PD-mild cognitive impairment (MCI). The patients will be recruited in eight specialized movement disorder clinics and will be followed for 36 months. Information about the patients’ functional status will be assessed at baseline and 6-/12- month intervals. In addition, 120 patients with dementia with Lewy bodies (DLB) will be included. Well-established standardized questionnaires/tests will be applied for detailed neuropsychological assessment. In addition, patients will be asked to participate in modules including volumetric MRI, genetic parameters, and neuropsychology to detect risk factors, early diagnostic biomarkers and predictors for dementia in PD. Results: The study included 604 PD patients by March 2011; 56.3% were classified as having PD alone, with 30.6% of patients suffering from PD-MCI and 13.1% from PD with dementia. The mean age of the cohort was 68.6 ± 7.9 years, with a mean disease duration of 6.8 ± 5.4 years. There was a preponderance of patients in the earlier Hoehn and Yahr stages. Conclusion: The main aim of the study is to characterize the natural progression of cognitive impairment in PD and to identify factors which contribute to the evolution and/or progression of the cognitive impairment. To accomplish this aim we established a large cohort of PD patients without cognitive dysfunction, PD patients with MCI, and PD patients with dementia, to characterize these patients in a standardized manner, using imaging (serial structural MRI), genetic and proteomic methods in order to improve our understanding of the course of the PD process and the development of cognitiv

Published
2012

43. Pros and cons of a prion-like pathogenesis in Parkinson's disease

Author

Hilker, Rüdiger, Brotchie, Jonathan M., Chapman, Joab, Hilker, Rüdiger, Brotchie, Jonathan M., and Chapman, Joab

Abstract

Background: Parkinson's disease (PD) is a slowly progressive neurodegenerative disorder which affects widespread areas of the brainstem, basal ganglia and cerebral cortex. A number of proteins are known to accumulate in parkinsonian brains including ubiquitin and alpha-synuclein. Prion diseases are sporadic, genetic or infectious disorders with various clinical and histopathological features caused by prion proteins as infectious proteinaceous particles transmitting a misfolded protein configuration through brain tissue. The most important form is Creutzfeldt-Jakob disease which is associated with a self-propagating pathological precursor form of the prion protein that is physiologically widely distributed in the central nervous system. Discussion: It has recently been found that alpha-synuclein may behave similarly to the prion precursor and propagate between cells. The post-mortem proof of alpha-synuclein containing Lewy bodies in embryonic dopamine cells transplants in PD patient suggests that the misfolded protein might be transmitted from the diseased host to donor neurons reminiscent of prion behavior. The involvement of the basal ganglia and brainstem in the degenerative process are other congruencies between Parkinson's and Creutzfeldt-Jakob disease. However, a number of issues advise caution before categorizing Parkinson's disease as a prion disorder, because clinical appearance, brain imaging, cerebrospinal fluid and neuropathological findings exhibit fundamental differences between both disease entities. Most of all, infectiousness, a crucial hallmark of prion diseases, has never been observed in PD so far. Moreover, the cellular propagation of the prion protein has not been clearly defined and it is, therefore, difficult to assess the molecular similarities between the two disease entities. Summary: At the current state of knowledge, the molecular pathways of transmissible pathogenic proteins are not yet fully understood. Their exact involvement in the p

Published
2011

47. Diurnal Variation of Hypothalamic Function and Chronic Subthalamic Nucleus Stimulation in Parkinson's Disease

Author

Seifried, Carola, primary, Boehncke, Sandra, additional, Heinzmann, Jannika, additional, Baudrexel, Simon, additional, Weise, Lutz, additional, Gasser, Thomas, additional, Eggert, Karla, additional, Fogel, Wolfgang, additional, Baas, Horst, additional, Badenhoop, Klaus, additional, Steinmetz, Helmuth, additional, and Hilker, Rüdiger, additional

Published
2012
Full Text
View/download PDF

48. Large-scale replication and heterogeneity in Parkinson disease genetic loci

Author

Sharma, Manu, primary, Ioannidis, John P.A., additional, Aasly, Jan O., additional, Annesi, Grazia, additional, Brice, Alexis, additional, Van Broeckhoven, Christine, additional, Bertram, Lars, additional, Bozi, Maria, additional, Crosiers, David, additional, Clarke, Carl, additional, Facheris, Maurizio, additional, Farrer, Matthew, additional, Garraux, Gaetan, additional, Gispert, Suzana, additional, Auburger, Georg, additional, Vilariño-Güell, Carles, additional, Hadjigeorgiou, Georgios M., additional, Hicks, Andrew A., additional, Hattori, Nobutaka, additional, Jeon, Beom, additional, Lesage, Suzanne, additional, Lill, Christina M., additional, Lin, Juei-Jueng, additional, Lynch, Timothy, additional, Lichtner, Peter, additional, Lang, Anthony E., additional, Mok, Vincent, additional, Jasinska-Myga, Barbara, additional, Mellick, George D., additional, Morrison, Karen E., additional, Opala, Grzegorz, additional, Pramstaller, Peter P., additional, Pichler, Irene, additional, Park, Sung Sup, additional, Quattrone, Aldo, additional, Rogaeva, Ekaterina, additional, Ross, Owen A., additional, Stefanis, Leonidas, additional, Stockton, Joanne D., additional, Satake, Wataru, additional, Silburn, Peter A., additional, Theuns, Jessie, additional, Tan, Eng-King, additional, Toda, Tatsushi, additional, Tomiyama, Hiroyuki, additional, Uitti, Ryan J., additional, Wirdefeldt, Karin, additional, Wszolek, Zbigniew, additional, Xiromerisiou, Georgia, additional, Yueh, Kuo-Chu, additional, Zhao, Yi, additional, Gasser, Thomas, additional, Maraganore, Demetrius, additional, Krüger, Rejko, additional, Boyle, R.S, additional, Sellbach, A, additional, O'Sullivan, J.D., additional, Sutherland, G.T., additional, Siebert, G.A, additional, Dissanayaka, N.N.W, additional, Pickut, Barbara, additional, Engelborghs, Sebastiaan, additional, Meeus, Bram, additional, De Deyn, Peter P., additional, Cras, Patrick, additional, Lang, Anthony E, additional, Agid, Y, additional, Anheim, M, additional, Bonnet, A-M, additional, Borg, M, additional, Brice, A, additional, Broussolle, E, additional, Corvol, JC, additional, Damier, P, additional, Destée, A, additional, Dürr, A, additional, Durif, F, additional, Lesage, S, additional, Lohmann, E, additional, Pollak, P, additional, Rascol, O, additional, Tison, F, additional, Tranchant, C, additional, Viallet, F, additional, Vidailhet, M, additional, Tzourio, Christophe, additional, Amouyel, Philippe, additional, Loriot, Marie-Anne, additional, Mutez, Eugénie, additional, Duflot, Aurélie, additional, Legendre, Jean-Philippe, additional, Waucquier, Nawal, additional, Riess, Olaf, additional, Berg, Daniela, additional, Schulte, Claudia, additional, Klein, Christine, additional, Djarmati, Ana, additional, Hagenah, Johann, additional, Lohmann, Katja, additional, Hilker, Rüdiger, additional, van de Loo, Simone, additional, Dardiotis, Efthimios, additional, Tsimourtou, Vaia, additional, Ralli, Styliani, additional, Kountra, Persa, additional, Patramani, Gianna, additional, Vogiatzi, Cristina, additional, Funayama, Manabu, additional, Yoshino, Hiroyo, additional, Li, Yuanzhe, additional, Imamichi, Yoko, additional, Lynch, Tim, additional, Gibson, J. Mark, additional, Valente, Enza Maria, additional, Ferraris, Alessandro, additional, Dallapiccola, Bruno, additional, Ialongo, Tamara, additional, Brighina, Laura, additional, Corradi, Barbara, additional, Piolti, Roberto, additional, Tarantino, Patrizia, additional, Annesi, Ferdinanda, additional, Jeon, Beom S., additional, Park, Sung-Sup, additional, Aasly, J, additional, Klodowska-Duda, Gabriela, additional, Boczarska-Jedynak, Magdalena, additional, Tan, Eng King, additional, Belin, Andrea Carmine, additional, Olson, Lars, additional, Galter, Dagmar, additional, Westerlund, Marie, additional, Sydow, Olof, additional, Nilsson, Christer, additional, Puschmann, Andreas, additional, Lin, JJ, additional, Maraganore, Demetrius M., additional, Ahlskog, J, Eric, additional, de Andrade, Mariza, additional, Lesnick, Timothy G., additional, Rocca, Walter A., additional, Checkoway, Harvey, additional, Ross, Owen A, additional, and Wszolek, Zbigniew K., additional

Published
2012
Full Text
View/download PDF

49. Glucose metabolism in small subcortical structures in Parkinson’s disease

Author

Borghammer, Per, primary, Hansen, Søren B., additional, Eggers, Carsten, additional, Chakravarty, Mallar, additional, Vang, Kim, additional, Aanerud, Joel, additional, Hilker, Rüdiger, additional, Heiss, Wolf-Dieter, additional, Rodell, Anders, additional, Munk, Ole L., additional, Keator, David, additional, and Gjedde, Albert, additional

Published
2011
Full Text
View/download PDF

50. Parkinson’s Disease and Dementia: A Longitudinal Study (DEMPARK)

Author

Balzer-Geldsetzer, Monika, primary, Braga da Costa, Ana Sofia Ferreira, additional, Kronenbürger, Martin, additional, Schulz, Jörg B., additional, Röske, Sandra, additional, Spottke, Annika, additional, Wüllner, Ullrich, additional, Klockgether, Thomas, additional, Storch, Alexander, additional, Schneider, Christine, additional, Riedel, Oliver, additional, Wittchen, Hans-Ulrich, additional, Seifried, Carola, additional, Hilker, Rüdiger, additional, Schmidt, Nele, additional, Witt, Karsten, additional, Deuschl, Günther, additional, Mollenhauer, Brit, additional, Trenkwalder, Claudia, additional, Liepelt-Scarfone, Inga, additional, Gräber-Sultan, Susanne, additional, Berg, Daniela, additional, Gasser, Thomas, additional, Kalbe, Elke, additional, Bodden, Maren, additional, Oertel, Wolfgang H., additional, and Dodel, Richard, additional

Published
2011
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results