Lewczuk, Piotr

[["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","379"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Neurology"],["dc.bibliographiccitation.lastpage","386"],["dc.bibliographiccitation.volume","78"],["dc.contributor.author","Wagner, M."],["dc.contributor.author","Wolf, S."],["dc.contributor.author","Reischies, Friedel M."],["dc.contributor.author","Daerr, M."],["dc.contributor.author","Wolfsgruber, S."],["dc.contributor.author","Jessen, Frank"],["dc.contributor.author","Popp, J."],["dc.contributor.author","Maier, Wolfgang"],["dc.contributor.author","Huell, Michael"],["dc.contributor.author","Froelich, Lutz"],["dc.contributor.author","Hampel, Harald"],["dc.contributor.author","Perneczky, Robert"],["dc.contributor.author","Peters, Oliver"],["dc.contributor.author","Jahn, Holger"],["dc.contributor.author","Luckhaus, C."],["dc.contributor.author","Gertz, H.-J."],["dc.contributor.author","Schroeder, J."],["dc.contributor.author","Pantel, Johannes"],["dc.contributor.author","Lewczuk, Piotr"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Wiltfang, J."],["dc.date.accessioned","2018-11-07T09:13:50Z"],["dc.date.available","2018-11-07T09:13:50Z"],["dc.date.issued","2012"],["dc.description.abstract","Objective: To compare cued recall measures with other memory and nonmemory tests regarding their association with a biomarker profile indicative of Alzheimer disease (AD) in CSF among patients with mild cognitive impairment (MCI). Methods: Data were obtained by the German Dementia Competence Network. A total of 185 memory clinic patients fulfilling broad criteria for MCI (1 SD deficit in memory tests or in nonmemory tests) were assessed with an extended neuropsychological battery, which included the Free and Cued Selective Reminding Test (FCSRT), the word list learning task from the Consortium to Establish a Registry for Alzheimer's Disease neuropsychological battery (CERAD-NP), and the Logical Memory (LM) paragraph recall test from the Wechsler Memory Scale-Revised. CSF was obtained from all patients. Results: A total of 74 out of 185 subjects with MCI (40%) had a CSF profile consistent with AD (A beta(1-42)/tau ratio; CSF AD + group). FCSRT measures reflecting both free and cued recall discriminated best between CSF AD + and CSF AD - patients, and significantly improved CSF AD classification accuracy, as compared with CERAD delayed recall and LM delayed recall. Conclusions: Cued recall deficits are most closely associated with CSF biomarkers indicative of AD in subjects with MCI. This novel finding complements results from prospective clinical studies and provides further empirical support for cued recall as a specific indicator of prodromal AD, in line with recently proposed research criteria. Neurology (R) 2012; 78: 379-386"],["dc.identifier.doi","10.1212/WNL.0b013e318245f447"],["dc.identifier.isi","000300392000007"],["dc.identifier.pmid","22238414"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27260"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","1526-632X"],["dc.relation.issn","0028-3878"],["dc.title","Biomarker validation of a cued recall memory deficit in prodromal Alzheimer disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","68"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Neuroscience Letters"],["dc.bibliographiccitation.lastpage","71"],["dc.bibliographiccitation.volume","440"],["dc.contributor.author","Koelsch, Heike"],["dc.contributor.author","Jessen, Frank"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Lewczuk, Piotr"],["dc.contributor.author","Dichgans, Martin"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Froelich, Lutz"],["dc.contributor.author","Heuser, Isabella"],["dc.contributor.author","Peters, Oliver"],["dc.contributor.author","Schulz, Joerg B."],["dc.contributor.author","Schwab, Sibylle G."],["dc.contributor.author","Maier, Wolfgang"],["dc.date.accessioned","2018-11-07T11:12:54Z"],["dc.date.available","2018-11-07T11:12:54Z"],["dc.date.issued","2008"],["dc.description.abstract","SORL1 gene variants were described as risk factors of Alzheimer's disease (AD). We investigated the association of four SORL1 variants with CSF levels of A beta(42) and A beta(40) in 153 AD patients recruited from a multicenter study of the German Competence Net Dementias. Only one SORL1 SNP was associated with altered A beta(42) levels in the single marker analysis (SNP21: p = 0.011), the other SNPs did not show an association with A beta(42) orA beta(40) CSF levels. Haplotype analysis identified a three marker SORL1 haplotype consisting of SNP19 T-allele, SNP21 G-allele and SNP23 A-allele (T/G/A) which was associated with reduced A beta(42) CSF levels in AD patients (p = 0.003). A beta(40) levels were also lower in carriers of this haplotype; however, this did not reach statistical significance (p = 0.15). We found a SORL1 haplotype which was associated with CSF levels of amyloid-P cleavage products, measured as altered levels of A beta(42). Thus our data suggest that: SORL1 gene variants might influence AD pathology. (C) 2008 Elsevier Ireland Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.neulet.2008.05.049"],["dc.identifier.isi","000257640200016"],["dc.identifier.pmid","18541377"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53768"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Ireland Ltd"],["dc.relation.issn","0304-3940"],["dc.title","Influence of SORL1 gene variants: Association with CSF amyloid-beta products in probable Alzheimer's disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","4044"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Proceedings of the National Academy of Sciences of the United States of America"],["dc.bibliographiccitation.lastpage","4049"],["dc.bibliographiccitation.volume","98"],["dc.contributor.author","Sirén, Anna-Leena"],["dc.contributor.author","Fratelli, Maddalena"],["dc.contributor.author","Brines, Michael"],["dc.contributor.author","Goemans, Christoph"],["dc.contributor.author","Casagrande, Simona"],["dc.contributor.author","Lewczuk, Pjotr"],["dc.contributor.author","Keenan, Sonja"],["dc.contributor.author","Gleiter, Christoph H."],["dc.contributor.author","Pasquali, Claudio"],["dc.contributor.author","Capobianco, Annalisa"],["dc.contributor.author","Mennini, Tiziana"],["dc.contributor.author","Heumann, Rolf"],["dc.contributor.author","Cerami, Anthony"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Ghezzi, Pietro"],["dc.date.accessioned","2018-03-08T09:22:11Z"],["dc.date.available","2018-03-08T09:22:11Z"],["dc.date.issued","2001"],["dc.description.abstract","Erythropoietin (EPO) promotes neuronal survival after hypoxia and other metabolic insults by largely unknown mechanisms. Apoptosis and necrosis have been proposed as mechanisms of cellular demise, and either could be the target of actions of EPO. This study evaluates whether antiapoptotic mechanisms can account for the neuroprotective actions of EPO. Systemic administration of EPO (5,000 units/kg of body weight, i.p.) after middle-cerebral artery occlusion in rats dramatically reduces the volume of infarction 24 h later, in concert with an almost complete reduction in the number of terminal deoxynucleotidyltransferase-mediated dUTP nick-end labeling of neurons within the ischemic penumbra. In both pure and mixed neuronal cultures, EPO (0.1–10 units/ml) also inhibits apoptosis induced by serum deprivation or kainic acid exposure. Protection requires pretreatment, consistent with the induction of a gene expression program, and is sustained for 3 days without the continued presence of EPO. EPO (0.3 units/ml) also protects hippocampal neurons against hypoxia-induced neuronal death through activation of extracellular signal-regulated kinases and protein kinase Akt-1/protein kinase B. The action of EPO is not limited to directly promoting cell survival, as EPO is trophic but not mitogenic in cultured neuronal cells. These data suggest that inhibition of neuronal apoptosis underlies short latency protective effects of EPO after cerebral ischemia and other brain injuries. The neurotrophic actions suggest there may be longer-latency effects as well. Evaluation of EPO, a compound established as clinically safe, as neuroprotective therapy in acute brain injury is further supported."],["dc.identifier.doi","10.1073/pnas.051606598"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/12910"],["dc.language.iso","en"],["dc.notes.intern","GRO-Li-Import"],["dc.notes.status","final"],["dc.relation.doi","10.1073/pnas.051606598"],["dc.relation.issn","0027-8424"],["dc.relation.issn","1091-6490"],["dc.title","Erythropoietin prevents neuronal apoptosis after cerebral ischemia and metabolic stress"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","601"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Neurobiology of Aging"],["dc.bibliographiccitation.lastpage","607"],["dc.bibliographiccitation.volume","36"],["dc.contributor.author","Popp, Julius"],["dc.contributor.author","Wolfsgruber, Steffen"],["dc.contributor.author","Heuser, Isabella"],["dc.contributor.author","Peters, Oliver"],["dc.contributor.author","Hüll, Michael"],["dc.contributor.author","Schröder, Johannes"],["dc.contributor.author","Möller, Hans-Jürgen"],["dc.contributor.author","Lewczuk, Piotr"],["dc.contributor.author","Schneider, Anja"],["dc.contributor.author","Jahn, Holger"],["dc.contributor.author","Luckhaus, Christian"],["dc.contributor.author","Perneczky, Robert"],["dc.contributor.author","Frölich, Lutz"],["dc.contributor.author","Wagner, Michael"],["dc.contributor.author","Maier, Wolfgang"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Jessen, Frank"],["dc.date.accessioned","2017-09-07T11:44:32Z"],["dc.date.available","2017-09-07T11:44:32Z"],["dc.date.issued","2015"],["dc.description.abstract","Increased peripheral and central nervous system cortisol levels have been reported in Alzheimer's disease (AD) and may reflect dysfunction of cerebral components of the hypothalamic-pituitary-adrenal (HPA) axis. However, brain exposure to high cortisol concentrations may also accelerate disease progression and cognitive decline. The objectives of this study were to investigate whether HPA-axis dysregulation occurs at early clinical stages of AD and whether plasma and CSF cortisol levels are associated with clinical disease progression. Morning plasma and CSF cortisol concentrations were obtained from the subjects with AD dementia, mild cognitive impairment of AD type (MCI-AD), MCI of other type (MCI-O), and controls with normal cognition included in a multicenter study from the German Dementia Competence Network. A clinical and neuropsychological follow-up was performed in a subgroup of participants with MCI-AD, MCI-O, and AD dementia. CSF cortisol concentrations were increased in the subjects with AD dementia or MCI-AD compared with subjects with MCI-O or normal cognition. After controlling for possible confounders including CSF measures of amyloid beta1–42 and total tau, higher baseline CSF cortisol levels were associated with faster clinical worsening and cognitive decline in MCI-AD. The findings suggest that HPA-axis dysregulation occurs at the MCI stage of AD and may accelerate disease progression and cognitive decline."],["dc.identifier.doi","10.1016/j.neurobiolaging.2014.10.031"],["dc.identifier.gro","3151692"],["dc.identifier.pmid","25435336"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8511"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","chake"],["dc.relation.issn","0197-4580"],["dc.title","Cerebrospinal fluid cortisol and clinical disease progression in MCI and dementia of Alzheimer's type"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","166"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Clinical and Experimental Medicine"],["dc.bibliographiccitation.lastpage","170"],["dc.bibliographiccitation.volume","2"],["dc.contributor.author","Lewczuk, P."],["dc.contributor.author","Kele, H."],["dc.contributor.author","Ehrenreich, H."],["dc.contributor.author","Söhnchen, N."],["dc.contributor.author","Reimers, C. D."],["dc.date.accessioned","2021-06-01T10:49:17Z"],["dc.date.available","2021-06-01T10:49:17Z"],["dc.date.issued","2003"],["dc.description.abstract","Endothelin-1 plays an important role as a paracrine factor in the regulation of regional blood flow. Plasma levels may represent the net result of spill-over from local stimulation/release and elimination of endothelin-1. In order to compare changes in the concentration of endothelin-1 in the plasma of subjects performing different types of sports exercises we measured immunoreactive endothelin-1 in healthy volunteers ( n=20) performing in random order jogging on a treadmill and cycling on a bicycle ergometer, for 30 min each. Plasma immunoreactive endothelin-1 increased significantly after jogging (2.13+/-0.8 pg/ml versus 2.6+/-0.8 pg/ml, before and after exercise, respectively, P<0.03), whereas it decreased after cycling (2.45+/-0.76 pg/ml versus 2.25+/-0.9 pg/ml, before and after exercise, respectively, P<0.03). We suggest that microtraumatizing effects on the endothelial lining are more pronounced during jogging than during cycling, resulting in a greater increase in plasma endothelin-1, which is too high to be immediately eliminated by the lung despite exercise-induced enhanced pulmonary perfusion. In contrast, similarly enhanced lung perfusion together with a relatively lower stimulation of endothelin-1 compared with jogging, may explain the net decrease in plasma after cycling."],["dc.identifier.doi","10.1007/s102380300001"],["dc.identifier.gro","3150435"],["dc.identifier.pmid","12624706"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86234"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.status","final"],["dc.relation.eissn","1591-9528"],["dc.relation.issn","1591-8890"],["dc.title","Endothelin-1 concentration in plasma is increased after jogging but decreased after cycling in healthy men"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","256"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Dementia and Geriatric Cognitive Disorders"],["dc.bibliographiccitation.lastpage","265"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Bibl, Mirko"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Esselmann, Hermann"],["dc.contributor.author","Schneider, Michael"],["dc.contributor.author","Lewczuk, Piotr"],["dc.contributor.author","Welge, Volker"],["dc.contributor.author","Gross, Martin"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Wiltfang, Jens"],["dc.date.accessioned","2018-11-07T11:19:48Z"],["dc.date.available","2018-11-07T11:19:48Z"],["dc.date.issued","2008"],["dc.description.abstract","Background/Aims: The study evaluated the patterns of cerebrospinal fluid (CSF), amyloid-beta (A beta) peptides, total tau and phospho-tau among Alzheimer's disease (AD) and vascular dementias (VAD). Methods: A beta-SDS-PAGE immunoblot and commercially available ELISAs were applied to the CSF analysis of 52 patients with probable (n = 21) and possible (n = 16) VAD, AD with cerebrovascular disease (n = 15), 30 patients with probable AD and 30 nondemented disease controls. Results: AD and AD with cerebrovascular disease displayed a similar neurochemical phenotype in contrast to nondemented disease controls and probable VAD with regard to tau, p-tau, A beta-40(ox) and A beta 1-42%. Possible VAD displayed AD-like changes only for A beta 1-40(ox) and A beta 1-42%. Conclusion: CSF neurochemical phenotypes sufficiently discriminate probable AD and VAD from each other, but their diagnostic value is limited in case of no clear-cut clinical appearance, such as possible VAD. Conversely, CSF A beta peptides and p-tau levels may help estimate the involvement of AD-like pathophysiological pathways in VAD subgroups. Copyright (c) 2008 S. Karger AG, Basel."],["dc.identifier.doi","10.1159/000115975"],["dc.identifier.isi","000253777500009"],["dc.identifier.pmid","18270488"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9353"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55373"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.relation.issn","1420-8008"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Cerebrospinal fluid neurochemical phenotypes in vascular dementias: Original data and mini-review"],["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","238"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of Clinical Laboratory Analysis"],["dc.bibliographiccitation.lastpage","245"],["dc.bibliographiccitation.volume","26"],["dc.contributor.author","Bibl, Mirko"],["dc.contributor.author","Welge, Volker"],["dc.contributor.author","Schmidt, Holger"],["dc.contributor.author","Esselmann, Hermann"],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Lewczuk, Piotr"],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Wiltfang, Jens"],["dc.date.accessioned","2018-11-07T09:15:09Z"],["dc.date.available","2018-11-07T09:15:09Z"],["dc.date.issued","2012"],["dc.description.abstract","Background Blood-based tests for a rapid and valid diagnosis as well as outcome prognosis of acute stroke are desirable. Recently, plasma A beta 40 was suggested as an independent cerebrovascular risk factor candidate. Methods We investigated eight plasma samples of patients with clinical signs of acute cerebral ischemia for derangements of plasma amyloid-beta (A beta) peptide patterns as compared to 13 patients with other neuropsychiatric diseases. For the analysis of plasma, we used immunoprecipitation followed by the quantitative A beta-SDS-PAGE/immunoblot. Results The major outcome was a striking decrease of A beta 140 in plasma paralleled by an increase in the ratio of A beta 138/A beta 140 in two patients with acute stroke. Interestingly, these patients had an onset of symptoms within only 24 hr before venous puncture and there was a strong correlation of A beta 138/A beta 140 levels with the time span between onset of symptoms and venous puncture. Conclusion From these results, we suggest the ratio of plasma A beta 138/A beta 140 as a possible biomarker for the early diagnosis of acute stroke. J. Clin. Lab. Anal. 26:238-245, 2012. (c) 2012 Wiley Periodicals, Inc."],["dc.identifier.doi","10.1002/jcla.21511"],["dc.identifier.isi","000306511500004"],["dc.identifier.pmid","22811355"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27608"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","0887-8013"],["dc.title","Plasma Amyloid-BetaPeptides in Acute Cerebral Ischemia: A Pilot Study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","6644"],["dc.bibliographiccitation.issue","24"],["dc.bibliographiccitation.journal","Human Molecular Genetics"],["dc.bibliographiccitation.lastpage","6658"],["dc.bibliographiccitation.volume","23"],["dc.contributor.author","Ramirez, Alfredo"],["dc.contributor.author","van der Flier, Wiesje M."],["dc.contributor.author","Herold, Christine"],["dc.contributor.author","Ramonet, David"],["dc.contributor.author","Heilmann, Stefanie"],["dc.contributor.author","Lewczuk, Piotr"],["dc.contributor.author","Popp, Julius"],["dc.contributor.author","Lacour, André"],["dc.contributor.author","Drichel, Dmitriy"],["dc.contributor.author","Louwersheimer, Eva"],["dc.contributor.author","Kummer, Markus P."],["dc.contributor.author","Cruchaga, Carlos"],["dc.contributor.author","Hoffmann, Per"],["dc.contributor.author","Teunissen, Charlotte E."],["dc.contributor.author","Holstege, Henne"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Peters, Oliver"],["dc.contributor.author","Naj, Adam C."],["dc.contributor.author","Chouraki, Vincent"],["dc.contributor.author","Bellenguez, Céline"],["dc.contributor.author","Gerrish, Amy"],["dc.contributor.author","Heun, Reiner"],["dc.contributor.author","Frölich, Lutz"],["dc.contributor.author","Hüll, Michael"],["dc.contributor.author","Buscemi, Lara"],["dc.contributor.author","Herms, Stefan"],["dc.contributor.author","Kölsch, Heike"],["dc.contributor.author","Scheltens, Philip"],["dc.contributor.author","Breteler, Monique M."],["dc.contributor.author","Rüther, Eckart"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Goate, Alison"],["dc.contributor.author","Jessen, Frank"],["dc.contributor.author","Maier, Wolfgang"],["dc.contributor.author","Heneka, Michael T."],["dc.contributor.author","Becker, Tim"],["dc.contributor.author","Nöthen, Markus M."],["dc.date.accessioned","2017-09-07T11:44:26Z"],["dc.date.available","2017-09-07T11:44:26Z"],["dc.date.issued","2014"],["dc.description.abstract","Alzheimer’s disease (AD) is a complex disorder in which severalpathways contribute to pathology and clinical phenotype. Delineationof each pathological pathway and identification of thefactors which modulate them are crucial for the developmentof effective treatment. Information on individual pathologicalpathways is provided by biomarkers. In AD, cerebrospinalfluid (CSF) levels of Ab1–42 and phosphorylated Tau (pTau)reflect cerebral amyloid deposition and tau-related neurodegeneration,respectively. However, many of the biological factorsthat influence these core AD pathways remain elusive.Research has shown that AD risk genes contribute to CSFmarker variance (1–4). However, genes may also exist thataffect CSF markers without conferring disease susceptibility.These genes may be promising candidates for modulation ofthe disease process.The aim of the present study was to identify genetic factorsrelated to heterogeneity in pathological pathways involved inamyloid deposition and tau-related neurodegeneration—asmanifested through CSF Ab1–42 and pTau levels—and whichmight influence the clinical course of AD. To achieve this, weperformed a four-step investigation involving analysis andmeta-analysis of data from genome-wide association studies(GWASs) of these two CSF biomarkers; replication of our topfindings in an independent sample; and specific analyses andfunctional experiments to follow-up promising findings. In contrastto previous GWAS of CSF biomarkers (1,4,5), the presentGWAS was restricted to patients with dementia secondary toAD only in order to enrich for genetic effects occurring afterdisease onset."],["dc.identifier.doi","10.1093/hmg/ddu372"],["dc.identifier.gro","3151650"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8467"],["dc.language.iso","en"],["dc.notes.status","public"],["dc.notes.submitter","chake"],["dc.relation.issn","1460-2083"],["dc.title","SUCLG2 identified as both a determinator of CSF Aβ1–42 levels and an attenuator of cognitive decline in Alzheimer's disease"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","737"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of the American Geriatrics Society"],["dc.bibliographiccitation.lastpage","739"],["dc.bibliographiccitation.volume","57"],["dc.contributor.author","Alexopoulos, Panagiotis"],["dc.contributor.author","Günther, Florian"],["dc.contributor.author","Popp, Julius"],["dc.contributor.author","Jessen, Frank"],["dc.contributor.author","Peters, Oliver"],["dc.contributor.author","Wolf, Stefanie"],["dc.contributor.author","Kneib, Thomas"],["dc.contributor.author","Kurz, Alexander"],["dc.contributor.author","Richter-Schmidinger, Tanja"],["dc.contributor.author","Lewczuk, Piotr"],["dc.contributor.author","Bleich, Stefan"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Kornhuber, Johannes"],["dc.date.accessioned","2017-09-07T11:47:13Z"],["dc.date.available","2017-09-07T11:47:13Z"],["dc.date.issued","2009"],["dc.identifier.doi","10.1111/j.1532-5415.2009.02212.x"],["dc.identifier.gro","3149297"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/5958"],["dc.notes.intern","Kneib Crossref Import"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","chake"],["dc.publisher","Wiley-Blackwell"],["dc.relation.issn","0002-8614"],["dc.title","PLASMA HOMOCYSTEINE AND CEREBROSPINAL FLUID NEURODEGENERATION BIOMARKERS IN MILD COGNITIVE IMPAIRMENT AND DEMENTIA"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]