Schmidt, Christian D.

[["dc.bibliographiccitation.firstpage","210"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Prion"],["dc.bibliographiccitation.lastpage","214"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Schmidt, Christian D."],["dc.contributor.author","Becker, Harry"],["dc.contributor.author","Peter, Christoph"],["dc.contributor.author","Lange, Katharina"],["dc.contributor.author","Friede, Tim"],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-11-07T09:42:43Z"],["dc.date.available","2018-11-07T09:42:43Z"],["dc.date.issued","2014"],["dc.description.abstract","Background/Objective: Recently, PrPc has been linked to AD pathogenesis. Second, a relation of PrPc plasma levels with cognitive status and decline of healthy elderly subjects has been reported. Therefore, we hypothesized baseline plasma levels of PrPc to be associated with AD progression in cognitive and functional domains. Methods: AD patients (n = 84) were included into an observational study at time of diagnosis. Baseline plasma PrPc levels were determined. Decline was assessed annually (mean follow-up time 3 years) with the aid of different standardized tests (MMSE, iADL, bADL, GDS, UPDRSIII). Multiple regression analyses were used to uncover potential associations between decline and PrPc levels. Results: No association of PrPc and decline could be established. Presence of diabetes mellitus was linked to slower deterioration. Intake of neuroleptic drugs or memantine was associated with faster progression. Conclusion: Plasma PrPc at baseline could not be shown to be related to AD progression in this study. An interesting association of diabetes mellitus and decline warrants further investigation."],["dc.identifier.doi","10.4161/pri.27964"],["dc.identifier.isi","000343228900010"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34021"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Landes Bioscience"],["dc.relation.issn","1933-690X"],["dc.relation.issn","1933-6896"],["dc.title","Plasma prion protein concentration and progression of 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","371"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Dementia and Geriatric Cognitive Disorders"],["dc.bibliographiccitation.lastpage","378"],["dc.bibliographiccitation.volume","29"],["dc.contributor.author","Schmidt, Christian D."],["dc.contributor.author","Redyk, Katharina"],["dc.contributor.author","Meissner, Bettina"],["dc.contributor.author","Krack, Lennart A."],["dc.contributor.author","von Ahsen, Nico"],["dc.contributor.author","Roeber, Sigrun"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-11-07T08:47:31Z"],["dc.date.available","2018-11-07T08:47:31Z"],["dc.date.issued","2010"],["dc.description.abstract","Objective: To characterize clinical features, CSF biomarkers and genetic polymorphisms of patients suffering from a rapidly progressing subtype of Alzheimer's dementia (rpAD). Methods: Retrospective analyses of 32 neuropathologically confirmed cases differentially diagnosed as AD out of a group with rapidly progressive dementia. CSF biomarkers (14-3-3, tau, beta-amyloid 1-42) and genetic markers (PRNP codon 129, apolipoprotein E, ApoE, polymorphism) were determined. Results: Median survival was 26 months, age at onset 73 years. Biomarkers: mean beta-amyloid 1-42: 266 pg/ml, median tau: 491 pg/ml, 14-3-3 positive: 31%. Genetic polymorphisms showed a predominance of methionine homozygosity at PRNP codon 129 and a low frequency of ApoE4 (38%, no homozygous patients). Thirty-five symptoms were studied. Frequent symptoms were myoclonus (75%), disturbed gait (66%) and rigidity (50%). Discussion: rpAD is associated with a diversity of neurological signs even able to mimic Creutz feldt-Jakob disease. Biomarkers and genetic profile differ from those seen in classical AD. The findings on biomarkers, symptomatology and genetics may aid the differential diagnostic process. Copyright (C) 2010 S. Karger AG, Basel"],["dc.identifier.doi","10.1159/000278692"],["dc.identifier.isi","000278130700012"],["dc.identifier.pmid","20453509"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9103"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20975"],["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","Clinical Features of Rapidly Progressive Alzheimer's Disease"],["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","189"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Alzheimer s Disease"],["dc.bibliographiccitation.lastpage","196"],["dc.bibliographiccitation.volume","48"],["dc.contributor.author","Schmidt, Christian D."],["dc.contributor.author","Gerlach, Nicole"],["dc.contributor.author","Schmitz, Matthias"],["dc.contributor.author","Thom, Tobias"],["dc.contributor.author","Kramer, Katharina"],["dc.contributor.author","Friede, Tim"],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-11-07T10:02:58Z"],["dc.date.available","2018-11-07T10:02:58Z"],["dc.date.issued","2015"],["dc.description.abstract","Background/Objective: Apolipoprotein E (ApoE) has an active part in the pathogenesis of Alzheimer's disease (AD). Cerebrospinal fluid (CSF) and plasma level alterations have been reported in AD patients. In search of a biomarker potentially predictive of cognitive, functional, or motor decline, we analyzed the CSF to serum ratios of ApoE levels (CSF/serum ApoE) in AD patients in this regard. Methods: Subjects with newly diagnosed AD were followed within a longitudinal observational study (rpAD study). Annual neuropsychological testing and physical examination were performed. Multiple regression analyses were used to determine possible associations of the ApoE CSF/serum concentration ratios and velocity of decline on a variety of cognitive, functional and motor scales (MMSE, iADL, bADL, GDS, UPDRSIII) adjusted for relevant co-variables. Results: CSF/serum ratios of ApoE levels were associated with progression on the UPDRSIII (change of UPDRSIII slope [pt/yr] per unit of ApoE CSF/serum = -0.06, p < 0.01) and instrumental ADL scale (change of iADL slope [pt/yr] per unit of ApoE CSF/serum = 0.01, p = 0.01) (\"the lower the ratio, the faster the deterioration\" and vice versa). Secondarily, higher age at onset was associated with faster UPDRSIII progression, antidepressant use with faster iADL decline, and better baseline function with more rapid decline on either MMSE, iADL, or GDS scale. Conclusion: Here, CSF/serum ApoE at time of AD diagnosis was shown to be inversely associated with medium-term functional and motor progression. Whether this ratio qualifies for the use as a predictive biomarker must be validated in larger cohort studies over the long term."],["dc.description.sponsorship","Bundesministerium fur Bildung und Forschung (BMBF) [01GI1010C, KNDD-2]"],["dc.identifier.doi","10.3233/JAD-150286"],["dc.identifier.isi","000360931700017"],["dc.identifier.pmid","26401939"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/38342"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Ios Press"],["dc.relation.issn","1875-8908"],["dc.relation.issn","1387-2877"],["dc.title","Baseline CSF/Serum-Ratio of Apolipoprotein E and Rate of Differential Decline in 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","229"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Prion"],["dc.bibliographiccitation.lastpage","234"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Schmidt, Christian D."],["dc.contributor.author","Artjomova, Svetlana"],["dc.contributor.author","Hoeschel, Martin"],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-11-07T09:24:49Z"],["dc.date.available","2018-11-07T09:24:49Z"],["dc.date.issued","2013"],["dc.description.abstract","Background/Objective: PrPc has been suggested to play a role in AD pathophysiology. CSF concentrations of PrPc have been shown to be reduced in AD compared with healthy controls. Furthermore, serum levels of PrPc have recently been reported to be associated with the cognitive status of healthy elderly subjects. Therefore, we hypothesized that CSF levels of PrPc could be associated with cognitive function of AD patients at the time of diagnosis. Results: No association of CSF PrPc and cognitive status could be established, while other factors (i.e., use of antipsychotic drugs, use of anti-dementia drugs, female sex, pre-progression time) were related to worse cognitive function in some domains. Methods: AD patients (n = 114) included into an observational study underwent CERAD testing and lumbar puncture at time of diagnosis / study inclusion. CSF PrPc was determined. Generalized linear models were fitted to assess the associations of PrPc plus a variety of possible confounding factors and CERAD subscale measures. Conclusion: CSF PrPc appears not to be a useful biochemical surrogate of cognitive status in AD at the time of diagnosis. Follow-up analyses will examine possible associations with the speed of cognitive decline."],["dc.identifier.doi","10.4161/pri.23904"],["dc.identifier.isi","000326510900007"],["dc.identifier.pmid","23406922"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29917"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Landes Bioscience"],["dc.relation.issn","1933-690X"],["dc.relation.issn","1933-6896"],["dc.title","CSF prion protein concentration and cognition in patients with Alzheimer disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Prion"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Schmidt, Christian D."],["dc.contributor.author","Karch, Andre"],["dc.contributor.author","Korth, Carsten"],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-11-07T09:03:55Z"],["dc.date.available","2018-11-07T09:03:55Z"],["dc.date.issued","2012"],["dc.description.abstract","Results from recent experiments with rodents imply that Alzheimer disease might be inducible by seeding A beta peptides into recipient animals. In respect to this new experimental data, public health aspects as well as epidemiological data have to be reevaluated. In this article, the available experimental and epidemiological data are reviewed."],["dc.identifier.doi","10.4161/pri.22502"],["dc.identifier.isi","000311341100008"],["dc.identifier.pmid","23052009"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10653"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24999"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Landes Bioscience"],["dc.relation.issn","1933-6896"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","On the issue of transmissibility of Alzheimer disease A critical review"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Prion"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Stoeck, Katharina"],["dc.contributor.author","Schmitz, Matthias"],["dc.contributor.author","Schmidt, Christian D."],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-11-07T09:26:11Z"],["dc.date.available","2018-11-07T09:26:11Z"],["dc.date.issued","2013"],["dc.format.extent","58"],["dc.identifier.isi","000323217500134"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/30244"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Landes Bioscience"],["dc.publisher.place","Austin"],["dc.relation.issn","1933-6896"],["dc.title","Immune responses in rapid dementia: A comparative study on neuroinflammatory markers in CJD, AD, rpAD and MS patients"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1229"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of Alzheimer s Disease"],["dc.bibliographiccitation.lastpage","1236"],["dc.bibliographiccitation.volume","43"],["dc.contributor.author","Schmidt, Christian D."],["dc.contributor.author","Gerlach, Nicole"],["dc.contributor.author","Peter, Christoph"],["dc.contributor.author","Gherib, Kerim"],["dc.contributor.author","Lange, Katharina"],["dc.contributor.author","Friede, Tim"],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-11-07T10:04:02Z"],["dc.date.available","2018-11-07T10:04:02Z"],["dc.date.issued","2015"],["dc.description.abstract","Background/Objective: Apolipoprotein E plays a role in the pathogenesis of Alzheimer's disease (AD). Cerebrospinal fluid (CSF) and plasma level alterations have been reported in AD patients. In search of a potential biomarker, which would be predictive of cognitive, functional, or motor decline, we analyzed CSF apolipoprotein E (ApoE) levels of AD patients in this regard. Methods: Subjects with newly diagnosed AD enrolled into an observational study were followed up longitudinally. Neuropsychological testing and physical examination were performed annually. In a sub-cohort of patients, where baseline CSF ApoE concentration values were available, multiple regression analyses were used to determine possible associations of CSF ApoE concentration and speed of decline on different cognitive, functional, and motor scales (MMSE, iADL, bADL, GDS, UPDRSIII) adjusting for possible confounders. Results: No association of CSF ApoE levels and speed of decline on the various scales could be established (p = 0.09 to 0.88). Nevertheless, the use of neuroleptic drugs could be linked to higher velocity of global and extrapyramidal deterioration (p = 0.04 and 0.05 for GDS and UPDRSIII, respectively), but not to other outcomes (MMSE, bADL, and iADL). \\Conclusion: Herein, CSF ApoE at time of AD diagnosis could not be shown to be a viable biomarker for future cognitive, functional, or motor decline. Expectedly, the use of neuroleptic drugs was associated with detrimental effects."],["dc.identifier.doi","10.3233/JAD-141581"],["dc.identifier.isi","000346857400012"],["dc.identifier.pmid","25125466"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/38608"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Ios Press"],["dc.relation.issn","1875-8908"],["dc.relation.issn","1387-2877"],["dc.title","Cerebrospinal Fluid Apolipoprotein E Concentration and Progression of 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","451"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of Alzheimer s Disease"],["dc.bibliographiccitation.lastpage","454"],["dc.bibliographiccitation.volume","35"],["dc.contributor.author","Schmidt, Christian D."],["dc.contributor.author","Karch, Andre"],["dc.contributor.author","Artjomova, Svetlana"],["dc.contributor.author","Hoeschel, Martin"],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-11-07T09:30:00Z"],["dc.date.available","2018-11-07T09:30:00Z"],["dc.date.issued","2013"],["dc.description.abstract","Background: Pre-progression rates (PPR) in Alzheimer's disease (AD) have been reported to be associated with cognitive and functional decline. Objective: The objective was to reevaluate PPRs in a prospective cohort of AD patients. Methods: A prospective AD cohort was analyzed. Multiple regression was used to examine associations of PPRs with short term decline on different cognitive and functional scales (MMSE, instrumental and basic ADL, GDS, UPDRS III). Results: PPRs were only associated with first year instrumental ADL declines. Conclusion: The predictive abilities of PPRs could partially be confirmed. These findings can help to adapt patient care shortly after diagnosis."],["dc.identifier.doi","10.3233/JAD-130074"],["dc.identifier.isi","000318627800003"],["dc.identifier.pmid","23435410"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31196"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Ios Press"],["dc.relation.issn","1387-2877"],["dc.title","Pre-Progression Rates in Alzheimer's Disease Revisited"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","84"],["dc.bibliographiccitation.issue","2-3"],["dc.bibliographiccitation.journal","Dementia and Geriatric Cognitive Disorders"],["dc.bibliographiccitation.lastpage","89"],["dc.bibliographiccitation.volume","33"],["dc.contributor.author","Schmidt, Christian D."],["dc.contributor.author","Wolff, Martin"],["dc.contributor.author","von Ahsen, Nicolas"],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-11-07T09:15:14Z"],["dc.date.available","2018-11-07T09:15:14Z"],["dc.date.issued","2012"],["dc.description.abstract","Background/Aim: To investigate the influence of established genetic risk factors for Alzheimer's disease on the speed of disease progression. Methods: Polymorphisms (in ACE, ApoE, BIN1, CLU, CR1, CST3, EXOC3L2, GWA14q32.13, IL8, LDLR, PICALM, TNK1) of 40 Alzheimer's disease patients from a longitudinal study were analyzed. A standardized loss of Mini-Mental State Examination points was used as the progression parameter. Results: Polymorphisms in CST3 and EXOC3L2 as well as the absence of APOE4 were associated with more aggressive disease courses. A trend was observed for BIN1. Conclusion: In addition to being a risk factor for disease development, some of the polymorphisms investigated here are associated with higher rates of decline and disease progression and thus might act as prognostic disease markers. This effect needs to be considered in future treatment strategies. Copyright (C) 2012 S. Karger AG, Basel"],["dc.identifier.doi","10.1159/000336790"],["dc.identifier.isi","000305654800002"],["dc.identifier.pmid","22414550"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9085"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27631"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","S. Karger AG"],["dc.relation.eissn","1421-9824"],["dc.relation.issn","1420-8008"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Alzheimer's Disease: Genetic Polymorphisms and Rate of Decline"],["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","215"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","CNS Spectrums"],["dc.bibliographiccitation.lastpage","218"],["dc.bibliographiccitation.volume","15"],["dc.contributor.author","Schmidt, Christian D."],["dc.contributor.author","Plickert, Steffen"],["dc.contributor.author","Summers, David K."],["dc.contributor.author","Zerr, Inge"],["dc.date.accessioned","2018-11-07T08:44:26Z"],["dc.date.available","2018-11-07T08:44:26Z"],["dc.date.issued","2010"],["dc.identifier.isi","000276960400006"],["dc.identifier.pmid","20414170"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20193"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","M B L Communications, Inc"],["dc.relation.issn","1092-8529"],["dc.title","Pulvinar Sign in Wernicke's Encephalopathy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","letter_note"],["dspace.entity.type","Publication"]]