Kermer, Pawel

[["dc.bibliographiccitation.firstpage","551"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of Alzheimer's Disease"],["dc.bibliographiccitation.lastpage","565"],["dc.bibliographiccitation.volume","38"],["dc.contributor.author","Schmitz, M."],["dc.contributor.author","Wulf, K."],["dc.contributor.author","Signore, S. C."],["dc.contributor.author","Schulz-Schaeffer, W. J."],["dc.contributor.author","Kermer, P."],["dc.contributor.author","Baehr, M."],["dc.contributor.author","Wouters, F. S."],["dc.contributor.author","Zafar, S."],["dc.contributor.author","Zerr, I."],["dc.date.accessioned","2017-09-07T11:46:57Z"],["dc.date.available","2017-09-07T11:46:57Z"],["dc.date.issued","2014"],["dc.description.abstract","Previous studies indicate an important role for the cellular prion protein (PrPC) in the development of Alzheimer's disease (AD) pathology. In the present study, we analyzed the involvement of PrPC in different pathological mechanisms underlying AD: the processing of the amyloid-beta protein precursor (A beta PP) and its interaction with A beta PP, tau, and different phosphorylated forms of the tau protein (p-tau). The effect of PrPC on tau expression was investigated in various cellular compartments using a HEK293 cell model expressing a tau mutant (3PO-tau) or wild type (WT)-tau. We could show that PrPC reduces A beta PP cleavage, leading to decreased levels of A beta(40) and sA beta PP without changing the protein expression of A beta PP, beta-secretase, or gamma-secretase. Tau and its phosphorylated forms were identified as interactions partners for PrPC, raising the question as to whether PrPC might also be involved in tau pathology. Overexpression of PrPC in PRNP and 3PO-tau transfected cells resulted in a reduction of 3PO-tau and p-tau as well as a decrease of 3PO-tau-related toxicity. In addition, we used the transgenic PrPC knockout (Prnp0/0) mouse line to study the dynamics of tau phosphorylation, an important pathological hallmark in the pathogenesis of AD in vivo. There, an effect of PrPC on tau expression could be observed under oxidative stress conditions but not during aging. In summary, we provide further evidence for interactions of PrPC with proteins that are known to be the key players in AD pathogenesis. We identified tau and its phosphorylated forms as potential PrP-interactors and report a novel protective function of PrPC in AD-like tau pathology."],["dc.identifier.doi","10.3233/JAD-130566"],["dc.identifier.gro","3142228"],["dc.identifier.isi","000327598500009"],["dc.identifier.pmid","24028865"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10657"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/5954"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.eissn","1875-8908"],["dc.relation.issn","1387-2877"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.title","Impact of the Cellular Prion Protein on Amyloid-beta and 3PO-Tau Processing"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","190"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Medical Case Reports"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Liman, Jan"],["dc.contributor.author","von Gottberg, Philipp"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Kermer, Pawel"],["dc.date.accessioned","2018-03-08T09:21:27Z"],["dc.date.available","2018-03-08T09:21:27Z"],["dc.date.issued","2011"],["dc.description.abstract","Introduction Infectious ileopectineal bursitis is a rare complication after total hip replacement and is associated mainly with rheumatoid arthritis. The main complications are local swelling and pain, but communication of the inflamed bursa with the joint can occur, leading to subsequent cartilage damage and bone destruction. Case presentation We report a case of a 47-year-old Caucasian woman without rheumatoid arthritis who reported pain and palsy in her left leg almost one year after total hip replacement. She was diagnosed with an ileopectineal bursitis after total hip replacement, leading to femoral nerve palsy. The diagnosis was obtained by thorough clinical examination, the results of focused computed tomography and magnetic resonance imaging. Conclusion To the best of our knowledge, this is the first report of non-infectious ileopectineal bursitis in a patient without rheumatoid arthritis as a complication of total hip replacement. This rare case underlines the importance of proper neurologic examination of persistent conditions after orthopedic intervention in otherwise healthy individuals. We believe this case should be useful for a broad spectrum of medical specialties, including orthopedics, neurology, radiology, and general practice."],["dc.identifier.doi","10.1186/1752-1947-5-190"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6375"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/12889"],["dc.language.iso","en"],["dc.notes.intern","GRO-Li-Import"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation.doi","10.1186/1752-1947-5-190"],["dc.relation.issn","1752-1947"],["dc.relation.issn","1752-1947"],["dc.rights","CC BY 2.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.0"],["dc.title","Femoral nerve palsy caused by ileopectineal bursitis after total hip replacement: a case report"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e0216530"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","PLoS One"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Wasser, Katrin"],["dc.contributor.author","Weber-Krüger, Mark"],["dc.contributor.author","Jürries, Falko"],["dc.contributor.author","Liman, Jan"],["dc.contributor.author","Hamann, Gerhard F."],["dc.contributor.author","Kermer, Pawel"],["dc.contributor.author","Uphaus, Timo"],["dc.contributor.author","Protsenko, Evgeny"],["dc.contributor.author","Seegers, Joachim"],["dc.contributor.author","Mende, Meinhard"],["dc.contributor.author","Gröschel, Klaus"],["dc.contributor.author","Wachter, Rolf"],["dc.date.accessioned","2019-07-09T11:51:30Z"],["dc.date.available","2019-07-09T11:51:30Z"],["dc.date.issued","2019"],["dc.description.abstract","BACKGROUND: The cardiac diagnostic workup of stroke patients, especially the value of echocardiography and enhanced and prolonged Holter-ECG monitoring, is still a matter of debate. We aimed to analyse the impact of pathologies detected by echocardiography and ECG monitoring on therapeutic decisions and prognosis. METHODS: Find-AFRANDOMISED was a prospective multicenter study which randomised 398 acute ischemic stroke patients ≥ 60 years to enhanced and prolonged Holter-ECG monitoring or usual stroke unit care. This substudy compared therapeutic consequences of echocardiography and routine Holter-ECG or enhanced and prolonged Holter-ECG monitoring, respectively, and prognosis of patients with or without pathologic findings in echocardiography or Holter-ECG monitoring. RESULTS: 50.3% received enhanced and prolonged Holter-ECG monitoring and 49.7% routine ECG monitoring. 82.9% underwent transthoracic echocardiography (TTE), 38.9% transesophageal echocardiography (TEE) and 25.6% both procedures. 14/89 TEE pathologies and 1/90 TTE pathology led to a change in therapy, resulting in a number needed to change decision (NNCD) of 12 and 330 (p < 0.001), respectively. In comparison, enhanced and prolonged Holter-ECG monitoring found atrial fibrillation (AF) in 27 of 200 patients, and routine ECG monitoring in twelve of 198 patients, leading to therapeutic changes in all patients (NNCD 8 and 17, respectively, p < 0.001). CONCLUSIONS: Most changes in therapeutic decisions were triggered by enhanced and prolonged Holter-ECG monitoring, which should therefore play a more prominent role in future guidelines. Echocardiography identifies a patient group at high cardiovascular risk, but rarely result in therapeutic changes. Whether this patient group requires further cardiovascular workup remains unknown. This should be further investigated by interdisciplinary neurocardiologic teams and in appropriate future trials."],["dc.identifier.doi","10.1371/journal.pone.0216530"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16141"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59961"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","The cardiac diagnostic work-up in stroke patients—A subanalysis of the Find-AFRANDOMISED trial"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","269"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Medical Case Reports"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Gawehn, Annemarie"],["dc.contributor.author","Ayari, Yassine"],["dc.contributor.author","Heuschkel, Christian"],["dc.contributor.author","Kaste, Matthias"],["dc.contributor.author","Kermer, Pawel"],["dc.date.accessioned","2019-07-09T11:42:51Z"],["dc.date.available","2019-07-09T11:42:51Z"],["dc.date.issued","2016"],["dc.description.abstract","Abstract Background Effective anticoagulation routinely precludes patients from receiving intravenous thrombolysis with recombinant tissue plasminogen activator to reverse severe symptoms of ischemic stroke. We report what we believe to be the first case of ischemic stroke successfully treated with recombinant tissue plasminogen activator after antagonizing dabigatran with the monoclonal antibody idarucizumab, recently approved worldwide. Case presentation A 75-year-old Caucasian man presented to our hospital with severe aphasia and mild hemiparesis. After providing written consent, he received two doses of 2.5 g of idarucizumab over 20 minutes followed by standard protocol in-label recombinant tissue plasminogen activator application. All symptoms resolved within 1 h. Conclusions Applying a recombinant tissue plasminogen activator after antagonizing dabigatran with idarucizumab is feasible and easy to manage in an emergency room or stroke unit. Thus, idarucizumab represents a new therapeutic option for patients receiving dabigatran treatment, reestablishing their eligibility for recombinant tissue plasminogen activator thrombolysis."],["dc.identifier.doi","10.1186/s13256-016-1050-0"],["dc.identifier.pmid","27686252"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13890"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58766"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Successful thrombolysis with recombinant tissue plasminogen activator after antagonizing dabigatran by idarucizumab: a case report"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e34351"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Wachter, Rolf"],["dc.contributor.author","Lahno, Rosine"],["dc.contributor.author","Haase, Beatrice"],["dc.contributor.author","Weber-Krueger, Mark"],["dc.contributor.author","Seegers, Joachim"],["dc.contributor.author","Edelmann, Frank"],["dc.contributor.author","Wohlfahrt, Janin"],["dc.contributor.author","Gelbrich, Götz"],["dc.contributor.author","Goerlitz, Anke"],["dc.contributor.author","Kermer, Pawel"],["dc.contributor.author","Vollmann, Dirk"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Groeschel, Klaus"],["dc.contributor.author","Stahrenberg, Raoul"],["dc.date.accessioned","2017-09-07T11:48:54Z"],["dc.date.available","2017-09-07T11:48:54Z"],["dc.date.issued","2012"],["dc.description.abstract","Background and Purpose: Diagnosis of paroxysmal atrial fibrillation (AF) can be challenging, but it is highly relevant in patients presenting with sinus rhythm and acute cerebral ischemia. We aimed to evaluate prospectively whether natriuretic peptide levels and kinetics identify patients with paroxysmal AF. Methods: Patients with acute cerebral ischemia were included into the prospective observational Find-AF study. N-terminal pro brain-type natriuretic peptide (NT-proBNP), brain-type natriuretic peptide (BNP) and N-terminal pro atrial-type natriuretic peptide (NT-proANP) plasma levels were measured on admission, after 6 and 24 hours. Patients free from AF at presentation received 7 day Holter monitoring. We prospectively hypothesized that patients presenting in sinus rhythm with NT-proBNP>median were more likely to have paroxysmal AF than patients with NT-proBNPmedian (239 pg/ml), 17.9% had paroxysmal AF in contrast to 7.4% with NT-proBNP<239 pg/ml (p = 0.025). The ratio of early (0 h) to late (24 h) plasma levels of NT-proBNP showed no difference between both groups. For the detection of paroxysmal atrial fibrillation, BNP, NT-proBNP and NT-proANP at admission had an area under the curve in ROC analysis of 0.747 (0.663-0.831), 0.638 (0.531-0.744) and 0.663 (0.566-0.761), respectively. In multivariate analysis, BNP was the only biomarker to be independently predictive for paroxysmal atrial fibrillation. Conclusions: BNP is independently predictive of paroxysmal AF detected by prolonged ECG monitoring in patients with cerebral ischemia and may be used to effectively select patients for prolonged Holter monitoring."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2012"],["dc.identifier.doi","10.1371/journal.pone.0034351"],["dc.identifier.gro","3142549"],["dc.identifier.isi","000305336600027"],["dc.identifier.pmid","22509292"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7572"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8912"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.title","Natriuretic Peptides for the Detection of Paroxysmal Atrial Fibrillation in Patients with Cerebral Ischemia - the Find-AF Study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","505"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","The Journal of Cell Biology"],["dc.bibliographiccitation.lastpage","513"],["dc.bibliographiccitation.volume","188"],["dc.contributor.author","Deeg, Sebastian"],["dc.contributor.author","Gralle, Mathias"],["dc.contributor.author","Sroka, Kamila"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Wouters, Fred Silvester"],["dc.contributor.author","Kermer, Pawel"],["dc.date.accessioned","2017-09-07T11:46:08Z"],["dc.date.available","2017-09-07T11:46:08Z"],["dc.date.issued","2010"],["dc.description.abstract","Mutations in the gene coding for DJ-1 protein lead to early-onset recessive forms of Parkinson's disease. It is believed that loss of DJ-1 function is causative for disease, although the function of DJ-1 still remains a matter of controversy. We show that DJ-1 is localized in the cytosol and is associated with membranes and organelles in the form of homodimers. The disease-related mutation L166P shifts its subcellular distribution to the nucleus and decreases its ability to dimerize, impairing cell survival. Using an intracellular foldase biosensor, we found that wild-type DJ-1 possesses chaperone activity, which is abolished by the L166P mutation. We observed that this aberrant phenotype can be reversed by the expression of the cochaperone BAG1 (Bcl-2-associated athanogene 1), restoring DJ-1 subcellular distribution, dimer formation, and chaperone activity and ameliorating cell survival."],["dc.identifier.doi","10.1083/jcb.200904103"],["dc.identifier.gro","3142963"],["dc.identifier.isi","000274723800009"],["dc.identifier.pmid","20156966"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6087"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/425"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: Deutsche Forschungsgemeinschaft (DFG) [EXC171]"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0021-9525"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","BAG1 restores formation of functional DJ-1 L166P dimers and DJ-1 chaperone activity"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","349"],["dc.bibliographiccitation.issue","1-12"],["dc.bibliographiccitation.journal","Perspectives in Medicine"],["dc.bibliographiccitation.lastpage","352"],["dc.bibliographiccitation.volume","1"],["dc.contributor.author","Liman, Jan"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Kermer, Pawel"],["dc.date.accessioned","2019-07-09T11:40:54Z"],["dc.date.available","2019-07-09T11:40:54Z"],["dc.date.issued","2012"],["dc.description.abstract","Since the first discovery, that ultrasound can overcome the skull allowing examination of the intracranial blood-flow as well as the first description of substantia nigra (SN) signal alterations via B-mode sonography, a plethora of applications especially in the field of movement disorders have been fostered. Up to now, however, most studies investigated adult individuals, even though numerous of the diseases studied have their onset already during childhood or adolescence. This overview summarizes recent studies of transcranial B-mode sonography (TCS) within the movement disorder field and outlines potential implications for pediatric applications."],["dc.identifier.doi","10.1016/j.permed.2012.02.003"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11472"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58293"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Transcranial ultrasound in adults and children with movement disorders"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e28855"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Gerhardt, Ellen"],["dc.contributor.author","Graeber, Simone"],["dc.contributor.author","Szego, Eva M."],["dc.contributor.author","Moisoi, Nicoleta"],["dc.contributor.author","Martins, L. Miguel"],["dc.contributor.author","Outeiro, Tiago Fleming"],["dc.contributor.author","Kermer, Pawel"],["dc.date.accessioned","2018-11-07T08:48:56Z"],["dc.date.available","2018-11-07T08:48:56Z"],["dc.date.issued","2011"],["dc.description.abstract","Heterozygous loss-of-function mutation of the human gene for the mitochondrial protease HtrA2 has been associated with increased risk to develop mitochondrial dysfunction, a process known to contribute to neurodegenerative disorders such as Huntington's disease (HD) and Parkinson's disease (PD). Knockout of HtrA2 in mice also leads to mitochondrial dysfunction and to phenotypes that resemble those found in neurodegenerative disorders and, ultimately, lead to death of animals around postnatal day 30. Here, we show that Idebenone, a synthetic antioxidant of the coenzyme Q family, and Resveratrol, a bioactive compound extracted from grapes, are both able to ameliorate this phenotype. Feeding HtrA2 knockout mice with either compound extends lifespan and delays worsening of the motor phenotype. Experiments conducted in cell culture and on brain tissue of mice revealed that each compound has a different mechanism of action. While Idebenone acts by downregulating the integrated stress response, Resveratrol acts by attenuating apoptosis at the level of Bax. These activities can account for the delay in neuronal degeneration in the striata of these mice and illustrate the potential of these compounds as effective therapeutic approaches against neurodegenerative disorders such as HD or PD."],["dc.identifier.doi","10.1371/journal.pone.0028855"],["dc.identifier.isi","000298665600012"],["dc.identifier.pmid","22205977"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7784"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21336"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.title","Idebenone and Resveratrol Extend Lifespan and Improve Motor Function of HtrA2 Knockout Mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","6678"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Molecules"],["dc.bibliographiccitation.lastpage","6687"],["dc.bibliographiccitation.volume","15"],["dc.contributor.author","Liman, Jan"],["dc.contributor.author","Sroka, Kamila"],["dc.contributor.author","Dohm, Christoph Peter"],["dc.contributor.author","Deeg, Sebastian"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Kermer, Pawel"],["dc.date.accessioned","2017-09-07T11:45:18Z"],["dc.date.available","2017-09-07T11:45:18Z"],["dc.date.issued","2010"],["dc.description.abstract","Huntington's disease, one of the so-called poly-glutamine diseases, is a dominantly inherited movement disorder characterized by formation of cytosolic and nuclear inclusion bodies and progressive neurodegeneration. Recently, we have shown that Bcl-2-associated athanogene-1 (BAG1), a multifunctional co-chaperone, modulates toxicity, aggregation, degradation and subcellular distribution in vitro and in vivo of the disease-specific mutant huntingtin protein. Aiming at future small molecule-based therapeutical approaches, we further analysed structural demands for these effects employing the C-terminal deletion mutant BAG Delta C. We show that disruption of the BAG domain known to eliminate intracellular heat shock protein 70 (Hsp70) binding and activation also precludes binding of Siah-1 thereby leaving nuclear huntingtin translocation unaffected. At the same time BAG Delta C fails to induce increased proteasomal huntingtin turnover and does not inhibit intracellular huntingtin aggregation, a pre-requisite necessary for prevention of huntingtin toxicity."],["dc.identifier.doi","10.3390/molecules15106678"],["dc.identifier.gro","3142847"],["dc.identifier.isi","000283587400001"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6876"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/296"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: CMPB; High Q foundation; European Commission [MEST-CT-2004-504193]"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1420-3049"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Modulation of Huntingtin Toxicity by BAG1 is Dependent on an Intact BAG Domain"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","174"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Medical Case Reports"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Dohm, Christoph P."],["dc.contributor.author","Gröschel, Sonja"],["dc.contributor.author","Liman, Jan"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Kermer, Pawel"],["dc.date.accessioned","2018-03-08T09:22:12Z"],["dc.date.available","2018-03-08T09:22:12Z"],["dc.date.issued","2013"],["dc.description.abstract","Introduction ‘Dropped head sign’ relates to a severe disproportionate antecollis in parkinsonism. We present the first report of a rotigotine-induced dropped head sign in a patient with suspected idiopathic Parkinson’s disease, which was later defined as multiple system atrophy. The ‘dropped head sign’ is considered a rare symptom of unknown etiology in parkinsonian disorders, though a disproportionate antecollis is frequently observed in multiple system atrophy. It has also been described as a side effect of dopamine agonist medication with cabergoline and pramipexole. Rotigotine is a transdermally applied, non-ergot dopamine agonist, resulting in a continuous stimulation of dopamine receptors, which is widely used in the treatment of patients with Parkinson’s disease. Case presentation We report a case of a 64-year-old Caucasian woman with a rapidly progressive two-and-a-half-year history of a hypokinetic Parkinson’s syndrome with asymmetric development of symptoms and an initially good response to levodopa medication. Due to side effects of other dopamimetic medications the patient was switched to rotigotine medication five weeks before clinical admission. Progressive antecollis without muscle weakness and prominent paraspinal muscle contraction developed within two weeks of treatment and resolved within a week after discontinuation of rotigotine and initiation of levodopa/cabergoline medication. Conclusion While the pathophysiology still remains unresolved, this case supports the concept of a dopaminergic imbalance as a cause of certain axial dystonias like disproportionate antecollis including the ‘dropped head sign’. We believe this case is specifically useful for neurologists and general practitioners, as the easily recognizable symptom should prompt a thorough reevaluation of diagnosis and medication in patients with Parkinson’s disease."],["dc.identifier.doi","10.1186/1752-1947-7-174"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9137"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/12913"],["dc.language.iso","en"],["dc.notes.intern","GRO-Li-Import"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation.doi","10.1186/1752-1947-7-174"],["dc.relation.issn","1752-1947"],["dc.relation.issn","1752-1947"],["dc.rights","CC BY 2.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.0"],["dc.title","Dropped head sign induced by transdermal application of the dopamine agonist rotigotine in parkinsonian syndrome: a case report"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]