Wiltfang, Jens

[["dc.bibliographiccitation.firstpage","2114"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Human Brain Mapping"],["dc.bibliographiccitation.lastpage","2132"],["dc.bibliographiccitation.volume","37"],["dc.contributor.author","Marchitelli, Rocco"],["dc.contributor.author","Minati, Ludovico"],["dc.contributor.author","Marizzoni, Moira"],["dc.contributor.author","Bosch, Beatriz"],["dc.contributor.author","Bartrés-Faz, David"],["dc.contributor.author","Müller, Bernhard W."],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Fiedler, Ute"],["dc.contributor.author","Roccatagliata, Luca"],["dc.contributor.author","Picco, Agnese"],["dc.contributor.author","Nobili, Flavio"],["dc.contributor.author","Blin, Oliver"],["dc.contributor.author","Bombois, Stephanie"],["dc.contributor.author","Lopes, Renaud"],["dc.contributor.author","Bordet, Régis"],["dc.contributor.author","Sein, Julien"],["dc.contributor.author","Ranjeva, Jean-Philippe"],["dc.contributor.author","Didic, Mira"],["dc.contributor.author","Gros-Dagnac, Hélène"],["dc.contributor.author","Payoux, Pierre"],["dc.contributor.author","Zoccatelli, Giada"],["dc.contributor.author","Alessandrini, Franco"],["dc.contributor.author","Beltramello, Alberto"],["dc.contributor.author","Bargalló, Núria"],["dc.contributor.author","Ferretti, Antonio"],["dc.contributor.author","Caulo, Massimo"],["dc.contributor.author","Aiello, Marco"],["dc.contributor.author","Cavaliere, Carlo"],["dc.contributor.author","Soricelli, Andrea"],["dc.contributor.author","Parnetti, Lucilla"],["dc.contributor.author","Tarducci, Roberto"],["dc.contributor.author","Floridi, Piero"],["dc.contributor.author","Tsolaki, Magda"],["dc.contributor.author","Constantinidis, Manos"],["dc.contributor.author","Drevelegas, Antonios"],["dc.contributor.author","Rossini, Paolo Maria"],["dc.contributor.author","Marra, Camillo"],["dc.contributor.author","Schönknecht, Peter"],["dc.contributor.author","Hensch, Tilman"],["dc.contributor.author","Hoffmann, Karl-Titus"],["dc.contributor.author","Kuijer, Joost P."],["dc.contributor.author","Visser, Pieter Jelle"],["dc.contributor.author","Barkhof, Frederik"],["dc.contributor.author","Frisoni, Giovanni B."],["dc.contributor.author","Jovicich, Jorge"],["dc.date.accessioned","2017-09-07T11:44:25Z"],["dc.date.available","2017-09-07T11:44:25Z"],["dc.date.issued","2016"],["dc.description.abstract","Understanding how to reduce the influence of physiological noise in resting state fMRI data is important for the interpretation of functional brain connectivity. Limited data is currently available to assess the performance of physiological noise correction techniques, in particular when evaluating longitudinal changes in the default mode network (DMN) of healthy elderly participants. In this 3T harmonized multisite fMRI study, we investigated how different retrospective physiological noise correction (rPNC) methods influence the within-site test-retest reliability and the across-site reproducibility consistency of DMN-derived measurements across 13 MRI sites. Elderly participants were scanned twice at least a week apart (five participants per site). The rPNC methods were: none (NPC), Tissue-based regression, PESTICA and FSL-FIX. The DMN at the single subject level was robustly identified using ICA methods in all rPNC conditions. The methods significantly affected the mean z-scores and, albeit less markedly, the cluster-size in the DMN; in particular, FSL-FIX tended to increase the DMN z-scores compared to others. Within-site test-retest reliability was consistent across sites, with no differences across rPNC methods. The absolute percent errors were in the range of 5–11% for DMN z-scores and cluster-size reliability. DMN pattern overlap was in the range 60–65%. In particular, no rPNC method showed a significant reliability improvement relative to NPC. However, FSL-FIX and Tissue-based physiological correction methods showed both similar and significant improvements of reproducibility consistency across the consortium (ICC = 0.67) for the DMN z-scores relative to NPC. Overall these findings support the use of rPNC methods like tissue-based or FSL-FIX to characterize multisite longitudinal changes of intrinsic functional connectivity."],["dc.identifier.doi","10.1002/hbm.23157"],["dc.identifier.gro","3151645"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8461"],["dc.language.iso","en"],["dc.notes.status","public"],["dc.notes.submitter","chake"],["dc.relation.issn","1065-9471"],["dc.title","Test-retest reliability of the default mode network in a multi-centric fMRI study of healthy elderly: Effects of data-driven physiological noise correction techniques"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Frontiers in Psychiatry"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Hansen, Niels"],["dc.contributor.author","Hirschel, Sina"],["dc.contributor.author","Stöcker, Winfried"],["dc.contributor.author","Manig, Anja"],["dc.contributor.author","Falk, Hannah Sönne"],["dc.contributor.author","Ernst, Marielle"],["dc.contributor.author","Vukovich, Ruth"],["dc.contributor.author","Zerr, Inga"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Bartels, Claudia"],["dc.date.accessioned","2021-04-14T08:23:48Z"],["dc.date.available","2021-04-14T08:23:48Z"],["dc.date.issued","2020"],["dc.description.abstract","Background IgLON5 disease is an autoimmune disorder that shares neuropathological aspects with a tauopathy. Its clinical spectrum is heterogeneous, and figural memory impairment as an initial phenomenon of IgLON5 syndrome has not yet been described. The rationale of this report is to highlight symptoms related to IgLON5 disease that have not been reported to date. This case report will thereby emphasize how important it is to initiate thorough diagnostic methods including cerebrospinal fluid analysis (CSF) before starting early immunotherapy. Methods We examined a 65-year-old Caucasian male via neuropsychological tests, magnetic resonance imaging (MRI), electroencephalography (EEG), neurography and polysomnography. He also underwent two lumbar punctures from which we determined specific autoantibodies in cerebrospinal (CSF) and peripheral blood (PB). Results The patient presented initially complaining of memory loss, gradual dysphagia and sleeping dysfunction. Neuropsychological testing at first presentation and follow-up revealed subtle figural and working memory impairment. At onset and at his 6-month follow-up, we detected IgLON5 antibodies in CSF and PB. Furthermore, we identified in the CSF a blood–brain barrier disturbance at disease onset and follow-up, and markers of neuroaxonal damage such as mildly elevated phosphorylated Tau-181 protein with 86 pg/ml (normal range ≤ 61 pg/ml) at onset. Three months after his initial presentation, he was suffering from axonal neuropathy and transient ataxia in the extremities. Assuming a definitive autoimmune encephalitis-associated with anti-IgLON5 antibodies, we applied high-dose steroids monthly (1g methylprednisolone i.v. for five consecutive days) and his memory complaints, ataxia of extremities and peripheral neuropathy as well as sleeping dysfunction decreased. Conclusions Our findings broaden IgLON5 disease’s clinical spectrum to include predominant and discrete figural memory impairment together with sleeping dysfunction at disease onset. In addition, our report illustrates how important taking an elaborated diagnostic approach is to assuring an accurate diagnosis and the appropriate therapy if a patient presents with a persisting figural memory impairment and sleeping abnormalities so as to avoid overlooking IgLON5 disease and a potentially poor outcome."],["dc.identifier.doi","10.3389/fpsyt.2020.00576"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17685"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81054"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.notes.intern","Merged from goescholar"],["dc.publisher","Frontiers Media S.A."],["dc.relation.eissn","1664-0640"],["dc.relation.haserratum","/handle/2/83966"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Figural Memory Impairment in Conjunction With Neuropsychiatric Symptoms in IgLON5 Antibody-Associated Autoimmune Encephalitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","15"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Alzheimer's Disease"],["dc.bibliographiccitation.lastpage","35"],["dc.bibliographiccitation.volume","69"],["dc.contributor.author","Jovicich, Jorge"],["dc.contributor.author","Babiloni, Claudio"],["dc.contributor.author","Ferrari, Clarissa"],["dc.contributor.author","Marizzoni, Moira"],["dc.contributor.author","Moretti, Davide V."],["dc.contributor.author","Del Percio, Claudio"],["dc.contributor.author","Lizio, Roberta"],["dc.contributor.author","Lopez, Susanna"],["dc.contributor.author","Galluzzi, Samantha"],["dc.contributor.author","Albani, Diego"],["dc.contributor.author","Cavaliere, Libera"],["dc.contributor.author","Minati, Ludovico"],["dc.contributor.author","Didic, Mira"],["dc.contributor.author","Fiedler, Ute"],["dc.contributor.author","Forloni, Gianluigi"],["dc.contributor.author","Hensch, Tilman"],["dc.contributor.author","Molinuevo, José Luis"],["dc.contributor.author","Bartrés Faz, David"],["dc.contributor.author","Nobili, Flavio"],["dc.contributor.author","Orlandi, Daniele"],["dc.contributor.author","Parnetti, Lucilla"],["dc.contributor.author","Farotti, Lucia"],["dc.contributor.author","Costa, Cinzia"],["dc.contributor.author","Payoux, Pierre"],["dc.contributor.author","Rossini, Paolo Maria"],["dc.contributor.author","Marra, Camillo"],["dc.contributor.author","Schönknecht, Peter"],["dc.contributor.author","Soricelli, Andrea"],["dc.contributor.author","Noce, Giuseppe"],["dc.contributor.author","Salvatore, Marco"],["dc.contributor.author","Tsolaki, Magda"],["dc.contributor.author","Visser, Pieter Jelle"],["dc.contributor.author","Richardson, Jill C."],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Bordet, Régis"],["dc.contributor.author","Blin, Olivier"],["dc.contributor.author","Frisoniand, Giovanni B."],["dc.date.accessioned","2020-12-10T18:44:12Z"],["dc.date.available","2020-12-10T18:44:12Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.3233/JAD-180158"],["dc.identifier.eissn","1875-8908"],["dc.identifier.issn","1387-2877"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78361"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Two-Year Longitudinal Monitoring of Amnestic Mild Cognitive Impairment Patients with Prodromal Alzheimer’s Disease Using Topographical Biomarkers Derived from Functional Magnetic Resonance Imaging and Electroencephalographic Activity"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","7S_Part_1"],["dc.bibliographiccitation.journal","Alzheimer's & Dementia"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Franzmeier, Nicolai"],["dc.contributor.author","Wolfsgruber, Steffen"],["dc.contributor.author","Ramirez, Alfredo"],["dc.contributor.author","Wagner, Michael"],["dc.contributor.author","Buerger, Katharina"],["dc.contributor.author","Dichgans, Martin"],["dc.contributor.author","Heneka, Michael"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Teipel, Stefan J."],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Ewers, Michael"],["dc.date.accessioned","2021-12-08T12:27:22Z"],["dc.date.available","2021-12-08T12:27:22Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1016/j.jalz.2017.06.2302"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/95331"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-476"],["dc.relation.eissn","1552-5279"],["dc.relation.issn","1552-5260"],["dc.rights.uri","http://onlinelibrary.wiley.com/termsAndConditions#vor"],["dc.title","[IC‐P‐030]: Connectivity of the Left Frontal Cortex Attenuates Detrimental Effects of Csf‐Tau on Memory in Preclinical and Clinical Alzheimer's Disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Clinica Chimica Acta"],["dc.bibliographiccitation.lastpage","12"],["dc.bibliographiccitation.volume","292"],["dc.contributor.author","Smirnov, Alexander V."],["dc.contributor.author","Tumani, Hayrettin"],["dc.contributor.author","Henne, Sergej"],["dc.contributor.author","Barchfeld, Sandra"],["dc.contributor.author","Olgemöller, Ulrike"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Lange, Peter"],["dc.contributor.author","Mäder, Michael"],["dc.contributor.author","Nau, Roland"],["dc.date.accessioned","2017-09-07T11:45:22Z"],["dc.date.available","2017-09-07T11:45:22Z"],["dc.date.issued","2000"],["dc.description.abstract","Glutamine synthetase (GS) activity is higher in the neocortex but not in the hippocampal formation of rabbit brain during Streptococcus pneumoniae meningitis compared to the respective brain region of uninfected control animals. One-dimensional polyacrylamide gel electrophoresis (1D-SDS-PAGE) revealed an apparent molecular mass (Mr) of 44 000 Dalton (Da) for GS from rabbit brain. After two-dimensional gel electrophoresis (2D-PAGE), followed by Coomassie-blue staining, GS separated into three distinct spots (S1, S2, S3). One additional spot (S4) occurred on the immunoblot. All four GS spots exhibited the same Mr (44 000 Da), but differed in their isoelectric points. Densitometric evaluation of the two-dimensional maps revealed a strong increase of optical density (OD) of S3 in the frontal cortex of infected animals. The calculated OD ratio S3/S2 in the frontal cortex from rabbits with meningitis was 1.75±0.68 (mean±standard deviation). Compared to controls (0.85±0.39), this value was significantly increased (p=0.0006). In the hippocampal formation, the ratio S3/S2 was nearly unchanged during meningitis. It is suggested that the ratio S3/S2 may indicate a neuroprotective feature of rabbit brain during meningitis since neuronal apoptosis occurs only in the dentate gyrus and not in the frontal cortex."],["dc.identifier.doi","10.1016/s0009-8981(99)00180-1"],["dc.identifier.gro","3151752"],["dc.identifier.pmid","10686272"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8576"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","chake"],["dc.relation.issn","0009-8981"],["dc.title","Glutamine synthetase in experimental meningitis: increased ratio of the subunits 3 and 2 may indicate enhanced activity"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","The Journal of Clinical Psychiatry"],["dc.bibliographiccitation.volume","81"],["dc.contributor.author","Bartels, Claudia"],["dc.contributor.author","Belz, Michael"],["dc.contributor.author","Vogelgsang, Jonathan"],["dc.contributor.author","Hessmann, Philipp"],["dc.contributor.author","Bohlken, Jens"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Kostev, Karel"],["dc.date.accessioned","2021-04-14T08:32:26Z"],["dc.date.available","2021-04-14T08:32:26Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.4088/JCP.19m13205"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83919"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1555-2101"],["dc.title","To Be Continued? Long-Term Treatment Effects ofAntidepressant Drug Classes and Individual Antidepressants on the Risk of Developing Dementia"],["dc.title.alternative","A German Case-Control Study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","919"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Journal of Neural Transmission"],["dc.bibliographiccitation.lastpage","927"],["dc.bibliographiccitation.volume","114"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Bibl, Mirko"],["dc.contributor.author","Esselmann, Herrmann"],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Trenkwalder, Claudia"],["dc.contributor.author","Wiltfang, J."],["dc.contributor.author","Otto, Markus"],["dc.date.accessioned","2018-11-07T11:06:56Z"],["dc.date.available","2018-11-07T11:06:56Z"],["dc.date.issued","2007"],["dc.description.abstract","To evaluate variations in amyloid beta (A beta) peptide pattern in cerebrospinal fluid (CSF) in neurodegenerative disorders. A recently estabfished quantitative urea-based A beta-sodium-dodecylsulfate-polyacrylamide-gel-electrophoresis with western immunoblot (AP-SDS-PAGE/immunoblot) revealed a highly conserved A beta peptide (A beta 1-37, 1-38, 1-39, 1-40, 1-42) pattern in CSF. We asked whether the variation might be useful to further elucidate the overlap between or distinctions among neurodegenerative diseases in A beta-processing. We used the A beta-SDS-PAGE/immunoblot to investigate CSF for diseasespecific A beta peptide patterns. CSF samples from 96 patients with mainly clinically diagnosed Alzheimer's disease (n = 15), progressive supranuclear palsy (n = 20), corticobasal degeneration (n =: 12), Parkinson's disease (n = 11), multiple systems atrophy (n = 18), and dementia with Lewy-bodies (n = 20) were analysed as well a comparison group (n = 19). The A beta peptide patterns varied between tauopathies and synucleinopathies and between all diseases and the comparison group, possibly due to the influence of tau and a-synuctein on Ap-processing."],["dc.identifier.doi","10.1007/s00702-007-0629-4"],["dc.identifier.isi","000248001800007"],["dc.identifier.pmid","17318305"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/52433"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Wien"],["dc.relation.issn","0300-9564"],["dc.title","Tauopathies and synucleinopathies: Do cerebrospinal fluid beta-amyloid peptides reflect disease-specific pathogenesis?"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1229"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Schizophrenia Bulletin"],["dc.bibliographiccitation.lastpage","1239"],["dc.bibliographiccitation.volume","43"],["dc.contributor.author","Schiffer, Boris"],["dc.contributor.author","Pawliczek, Christina"],["dc.contributor.author","Müller, Bernhard W"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Brüne, Martin"],["dc.contributor.author","Forsting, Michael"],["dc.contributor.author","Gizewski, Elke R"],["dc.contributor.author","Leygraf, Norbert"],["dc.contributor.author","Hodgins, Sheilagh"],["dc.date.accessioned","2020-12-10T18:19:41Z"],["dc.date.available","2020-12-10T18:19:41Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1093/schbul/sbx012"],["dc.identifier.eissn","1745-1701"],["dc.identifier.issn","0586-7614"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/75337"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Neural Mechanisms Underlying Affective Theory of Mind in Violent Antisocial Personality Disorder and/or Schizophrenia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","366"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Experimental Neurology"],["dc.bibliographiccitation.lastpage","370"],["dc.bibliographiccitation.volume","223"],["dc.contributor.author","Lewczuk, Piotr"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Vanmechelen, Eugeen"],["dc.contributor.author","Peters, Oliver"],["dc.contributor.author","Heuser, Isabella"],["dc.contributor.author","Maier, Wolfgang"],["dc.contributor.author","Jessen, Frank"],["dc.contributor.author","Buerger, Katharina"],["dc.contributor.author","Hampel, Harald"],["dc.contributor.author","Froelich, Lutz"],["dc.contributor.author","Henn, Fritz A."],["dc.contributor.author","Falkai, Peter Gaston"],["dc.contributor.author","Ruether, Eckhart"],["dc.contributor.author","Jahn, Holger"],["dc.contributor.author","Luckhaus, C. H."],["dc.contributor.author","Perneczky, Robert"],["dc.contributor.author","Schmidtke, K."],["dc.contributor.author","Schroeder, J."],["dc.contributor.author","Kessler, H."],["dc.contributor.author","Pantel, Johannes"],["dc.contributor.author","Gertz, H.-J."],["dc.contributor.author","Vanderstichele, Hugo"],["dc.contributor.author","de Meyer, G."],["dc.contributor.author","Shapiro, F."],["dc.contributor.author","Wolf, S."],["dc.contributor.author","Bibl, Mirko"],["dc.contributor.author","Wiltfang, J."],["dc.date.accessioned","2018-11-07T08:42:36Z"],["dc.date.available","2018-11-07T08:42:36Z"],["dc.date.issued","2010"],["dc.description.abstract","We measured concentrations of to peptides 1-42 and 1-40, and their ratio in plasma of patients carefully categorized clinically and neurochemically as having AD or other dementias with a newly commercially available multiplexing assay, characterized by reasonable laboratory performance (intra-assay imprecision in the range of 1.3-3.8% for A beta 1-42, and 1.8-4.1% for A beta 1-40, inter-assay imprecision for A beta 1-42, A beta 1-40, and A beta 1-42/A beta 1-40 concentration ratio in the range of 2.3-11.5%, 2.2-10.4% and 42-9.7%, respectively). Patients with AD or mild cognitive impairment of AD type (MCI-AD) whose clinical diagnosis was supported with CSF biomarkers (n = 193) had significantly lower A beta 1-42 plasma concentrations (p<0.007), and A beta 1-42/1-40 ratios (p<0.003) compared to patients with other dementias and MCI of other types (n = 64). No significant differences between persons with MCI of AD type and patients with early AD were observed, or between MCI of other types versus patients with early dementia of other types. Our findings reconfirm the hypothesis that alterations of biomarker concentrations occur early in a preclinical AD stage and that these alterations are also reflected in plasma. (C) 2009 Published by Elsevier Inc."],["dc.identifier.doi","10.1016/j.expneurol.2009.07.024"],["dc.identifier.isi","000277743700015"],["dc.identifier.pmid","19664622"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19739"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Academic Press Inc Elsevier Science"],["dc.relation.issn","0014-4886"],["dc.title","Amyloid beta peptides in plasma in early diagnosis of Alzheimer's disease: A multicenter study with multiplexing"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","189"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Zeitschrift für Gerontologie und Geriatrie"],["dc.bibliographiccitation.lastpage","196"],["dc.bibliographiccitation.volume","36"],["dc.contributor.author","Diehl, J."],["dc.contributor.author","Staehelin, H."],["dc.contributor.author","Wiltfang, J."],["dc.contributor.author","Hampel, Harald"],["dc.contributor.author","Calabrese, P."],["dc.contributor.author","Monsch, Andreas U."],["dc.contributor.author","Schmid, R."],["dc.contributor.author","Romero, B."],["dc.contributor.author","Schunk, M."],["dc.contributor.author","Kuhlmann, P."],["dc.contributor.author","Wolter-Henseler, D. K."],["dc.contributor.author","Mauerer, C."],["dc.contributor.author","Stoppe, Gabriela"],["dc.contributor.author","Kurz, A."],["dc.date.accessioned","2018-11-07T10:38:51Z"],["dc.date.available","2018-11-07T10:38:51Z"],["dc.date.issued","2003"],["dc.description.abstract","The 7th annual meeting of the memory clinics of Germany, Switzerland and Austria in March 2002 in Gottingen, Germany was an optimal opportunity to make an inventory about the state of the art in diagnostic and therapy of dementia and mild cognitive impairment in German-speaking memory clinics. Several problems were discussed including difficulties in 1) diagnosis of-patients with aphasia or foreign patients, 2) handling of demented patients without a caregiver, 3) psychological support for patients, who have been diagnosed in a very early stage, 4) misunderstandings between general practitioners, neurologists and psychiatrists in private practice on the one hand and the memory clinics on the other hand, 5) recommendations for prevention of dementia, 6) recommendations concerning dementia and car driving and 7) questions of genetic counselling. The following paper is a summary of the results of a workshop in Gottingen and gives practical recommendations based on the experiences of the memory clinics."],["dc.identifier.doi","10.1007/s00391-003-0154-5"],["dc.identifier.isi","000184156300006"],["dc.identifier.pmid","12825136"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45909"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Dr Dietrich Steinkopff Verlag"],["dc.relation.issn","0948-6704"],["dc.title","German-speaking memory clinics: state of the art and practical recommendations"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]