Wiltfang, Jens

[["dc.bibliographiccitation.firstpage","1651"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Journal of Neural Transmission"],["dc.bibliographiccitation.lastpage","1659"],["dc.bibliographiccitation.volume","115"],["dc.contributor.author","Kessler, Holger"],["dc.contributor.author","Pajonk, Frank-Gerald"],["dc.contributor.author","Bach, Daniela"],["dc.contributor.author","Schneider-Axmann, Thomas"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Herrmann, Wolfgang"],["dc.contributor.author","Multhaup, Gerd"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Schäfer, Stephanie"],["dc.contributor.author","Wirths, Oliver"],["dc.contributor.author","Bayer, Thomas"],["dc.date.accessioned","2019-07-09T11:52:23Z"],["dc.date.available","2019-07-09T11:52:23Z"],["dc.date.issued","2008"],["dc.description.abstract","A plethora of reports suggest that copper (Cu) homeostasis is disturbed in Alzheimer’s disease (AD). In the present report we evaluated the efficacy of oral Cu supplementation on Cp. biomarkers for AD. In a prospective, randomized, double-blind, placebo-controlled phase 2 clinical trial (12 months long) patients with mild AD received either Cu-(II)-orotate-dihydrate (verum group; 8 mg Cu daily) or placebo (placebo group). The primary outcome measures in CSF were Aβ42, Tau and Phospho-Tau. The clinical trial demonstrates that long-term oral intake of 8 mg Cu can be excluded as a risk factor for AD based on CSF biomarker analysis. Cu intake had no effect on the progression of Tau and Phospho-Tau levels in CSF. While Aβ42 levels declined by 30% in the placebo group (P = 0.001), they decreased only by 10% (P = 0.04) in the verum group. Since decreased CSF Aβ42 is a diagnostic marker for AD, this observation may indicate that Cu treatment had a positive effect on a relevant AD biomarker. Using mini-mental state examination (MMSE) and Alzheimer disease assessment scale-cognitive subscale (ADAS-cog) we have previously demonstrated that there are no Cu treatment effects on cognitive performance, however. Finally, CSF Aβ42 levels declined significantly in both groups within 12 months supporting the notion that CSF Aβ42 may be valid not only for diagnostic but also for prognostic purposes in AD."],["dc.identifier.doi","10.1007/s00702-008-0136-2"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?goescholar/3561"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60172"],["dc.notes.intern","Merged from goescholar"],["dc.publisher","Springer"],["dc.publisher.place","Vienna"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","Effect of copper intake on CSF parameters in patients with mild Alzheimer’s disease: a pilot phase 2 clinical trial"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e01401"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Brain and Behavior"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Abdel‐Hamid, Mona"],["dc.contributor.author","Niklewski, Franziska"],["dc.contributor.author","Heßmann, Philipp"],["dc.contributor.author","Guberina, Nika"],["dc.contributor.author","Kownatka, Melanie"],["dc.contributor.author","Kraemer, Markus"],["dc.contributor.author","Scherbaum, Norbert"],["dc.contributor.author","Dziobek, Isabel"],["dc.contributor.author","Bartels, Claudia"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Kis, Bernhard"],["dc.date.accessioned","2019-12-02T10:36:20Z"],["dc.date.accessioned","2021-10-27T13:21:41Z"],["dc.date.available","2019-12-02T10:36:20Z"],["dc.date.available","2021-10-27T13:21:41Z"],["dc.date.issued","2019"],["dc.description.abstract","OBJECTIVE: The cognitive capacity to change perspective is referred to as theory of mind (ToM). ToM deficits are detectable in a variety of psychiatric and neurological disorders. Since executive abilities are closely associated with ToM skills, we suspected that due to a common neuropsychological basis, ToM deficits exist in treatment-naïve adults with attention-deficit/hyperactivity disorder (ADHD). METHODS: Performance of treatment-naïve adults with ADHD (N = 30) in tasks assessing executive functions (Trail Making Test, Stroop color-word test, and Test Battery for Attentional Performance), empathy skills (Cambridge Behaviour Scale), and ToM (Movie for Assessment of Social Cognition) was compared with that of a healthy control group (N = 30) matched according to basic demographic variables. RESULTS: Compared to healthy controls, treatment-naïve adults with ADHD showed deficits in various executive functions and the ability to empathize (all p < .05). However, no performance differences were found with regard to ToM (all n.s.). CONCLUSIONS: Since studies in juveniles with ADHD often show impaired ToM performance, it is conceivable that ToM deficits may become attenuated due to neuronal development in adolescence. Furthermore, our findings imply that ToM impairments, even when present in adult ADHD, appear to be independent of executive deficits and might be explained by comorbid disorders."],["dc.identifier.doi","10.1002/brb3.1401"],["dc.identifier.eissn","2162-3279"],["dc.identifier.issn","2162-3279"],["dc.identifier.pmid","31475781"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16781"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/92040"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.relation.eissn","2162-3279"],["dc.relation.issn","2162-3279"],["dc.relation.issn","2162-3279"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","Impaired empathy but no theory of mind deficits in adult attention deficit hyperactivity disorder"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Human Mutation"],["dc.bibliographiccitation.lastpage","13"],["dc.bibliographiccitation.volume","41"],["dc.contributor.author","Karsak, Meliha"],["dc.contributor.author","Glebov, Konstantin"],["dc.contributor.author","Scheffold, Marina"],["dc.contributor.author","Bajaj, Thomas"],["dc.contributor.author","Kawalia, Amit"],["dc.contributor.author","Karaca, Ilker"],["dc.contributor.author","Rading, Sebastian"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Peters, Oliver"],["dc.contributor.author","Diez‐Fairen, Monica"],["dc.contributor.author","Frölich, Lutz"],["dc.contributor.author","Hüll, Michael"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Scherer, Martin"],["dc.contributor.author","Riedel‐Heller, Steffi"],["dc.contributor.author","Schneider, Anja"],["dc.contributor.author","Heneka, Michael T."],["dc.contributor.author","Fliessbach, Klaus"],["dc.contributor.author","Sharaf, Ahmed"],["dc.contributor.author","Thiele, Holger"],["dc.contributor.author","Lennarz, Martina"],["dc.contributor.author","Jessen, Frank"],["dc.contributor.author","Maier, Wolfgang"],["dc.contributor.author","Kubisch, Christian"],["dc.contributor.author","Ignatova, Zoya"],["dc.contributor.author","Nürnberg, Peter"],["dc.contributor.author","Pastor, Pau"],["dc.contributor.author","Walter, Jochen"],["dc.contributor.author","Ramirez, Alfredo"],["dc.date.accessioned","2019-12-02T14:18:33Z"],["dc.date.accessioned","2021-10-27T13:21:45Z"],["dc.date.available","2019-12-02T14:18:33Z"],["dc.date.available","2021-10-27T13:21:45Z"],["dc.date.issued","2019"],["dc.description.abstract","Rare coding variants in the triggering receptor expressed on myeloid cells-2 (TREM2) gene have been associated with Alzheimer disease (AD) and homozygous TREM2 loss-of-function variants have been reported in families with monogenic frontotemporal-like dementia with/without bone abnormalities. In a whole-exome sequencing study of a family with probable AD-type dementia without pathogenic variants in known autosomal dominant dementia disease genes and negative for the apolipoprotein E (APOE) ε4 allele, we identified an extremely rare TREM2 coding variant, that is, a glycine-to-tryptophan substitution at amino acid position 145 (NM_018965.3:c.433G>T/p.[Gly145Trp]). This alteration is found in only 1 of 251,150 control alleles in gnomAD. It was present in both severely affected as well as in another putatively affected and one 61 years old as yet unaffected family member suggesting incomplete penetrance and/or a variable age of onset. Gly145 maps to an intrinsically disordered region (IDR) of TREM2 between the immunoglobulin-like and transmembrane domain. Subsequent cellular studies showed that the variant led to IDR shortening and structural changes of the mutant protein resulting in an impairment of cellular responses upon receptor activation. Our results, suggest that a p.(Gly145Trp)-induced structural disturbance and functional impairment of TREM2 may contribute to the pathogenesis of an AD-like form of dementia."],["dc.identifier.doi","10.1002/humu.23904"],["dc.identifier.eissn","1098-1004"],["dc.identifier.isbn","31464095"],["dc.identifier.issn","1059-7794"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16802"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/92042"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.relation.eissn","1098-1004"],["dc.relation.issn","1098-1004"],["dc.relation.issn","1059-7794"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","A rare heterozygous TREM2 coding variant identified in familial clustering of dementia affects an intrinsically disordered protein region and function of TREM2"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.journal","ASN Neuro"],["dc.bibliographiccitation.lastpage","8"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Vogelgsang, Jonathan"],["dc.contributor.author","Vukovich, Ruth"],["dc.contributor.author","Wedekind, Dirk"],["dc.contributor.author","Wiltfang, Jens"],["dc.date.accessioned","2019-07-09T11:51:28Z"],["dc.date.available","2019-07-09T11:51:28Z"],["dc.date.issued","2019"],["dc.description.abstract","Cerebrospinal fluid (CSF) biomarkers are widely used in the diagnosis of dementia. Even though there is a causal correlation between apolipoprotein E ( APOE) genotype and amyloid-beta (Aβ), the determination of APOE is currently not supported by national or international guidelines. We compared parallel measured CSF biomarkers of two independent laboratories from 126 patients who underwent clinical dementia diagnostics regarding the APOE genotype. APOE ε4 reduces Aβ1-42 (Aβ42) and Aβ42 to Aβ 1-40 ratio (Aβ42/40) but not total Tau or phospho-181 Tau CSF levels. Higher discordance rates were observed for Aβ42 and subsequently for Aβ42/40 in APOE ε4 carriers compared with noncarriers, and the correlation between the two laboratories was significantly lower for Aβ42 in APOE ε4 positive patients compared with patients without APOE ε4. These observations demonstrate that the evaluation of CSF Aβ biomarkers needs to be interpreted carefully in the clinical context. Different immunoassays, disparate cutoff values, and APOE should be respected."],["dc.identifier.doi","10.1177/1759091419845524"],["dc.identifier.pmid","31104469"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16133"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59953"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY-NC 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/4.0"],["dc.subject.ddc","610"],["dc.title","Higher Level of Mismatch in APOEε4 Carriers for Amyloid-Beta Peptide Alzheimer’s Disease Biomarkers in Cerebrospinal Fluid"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","International journal of Alzheimer's disease"],["dc.bibliographiccitation.volume","2010"],["dc.contributor.author","Bibl, Mirko"],["dc.contributor.author","Esselmann, Hermann"],["dc.contributor.author","Lewczuk, Piotr"],["dc.contributor.author","Trenkwalder, Claudia"],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Mollenhauer, Brit"],["dc.date.accessioned","2019-07-09T11:53:09Z"],["dc.date.available","2019-07-09T11:53:09Z"],["dc.date.issued","2010"],["dc.description.abstract","We studied the diagnostic value of CSF Aβ42/tau versus low Aβ1-42% and high Aβ1-40(ox)% levels for differential diagnosis of Alzheimer's disease (AD) and dementia with Lewy bodies (DLB), respectively. CSF of 45 patients with AD, 15 with DLB, 21 with Parkinson's disease dementia (PDD), and 40 nondemented disease controls (NDC) was analyzed by Aβ-SDS-PAGE/immunoblot and ELISAs (Aβ42 and tau). Aβ42/tau lacked specificity in discriminating AD from DLB and PDD. Best discriminating biomarkers were Aβ1-42% and Aβ1-40(ox)% for AD and DLB, respectively. AD and DLB could be differentiated by both Aβ1-42% and Aβ1-40(ox)% with an accuracy of 80% at minimum. Thus, we consider Aβ1-42% and Aβ1-40(ox)% to be useful biomarkers for AD and DLB, respectively. We propose further studies on the integration of Aβ1-42% and Aβ1-40(ox)% into conventional assay formats. Moreover, future studies should investigate the combination of Aβ1-40(ox)% and CSF alpha-synuclein for the diagnosis of DLB."],["dc.identifier.doi","10.4061/2010/761571"],["dc.identifier.fs","575758"],["dc.identifier.pmid","20862375"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6918"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60350"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","2090-0252"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","Combined Analysis of CSF Tau, Aβ42, Aβ1-42% and Aβ1-40% in Alzheimer's Disease, Dementia with Lewy Bodies and Parkinson's Disease Dementia."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]