Schneider, Anja

[["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Clinical and Translational Medicine"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Caldi Gomes, Lucas"],["dc.contributor.author","Roser, Anna‐Elisa"],["dc.contributor.author","Jain, Gaurav"],["dc.contributor.author","Pena Centeno, Tonatiuh"],["dc.contributor.author","Maass, Fabian"],["dc.contributor.author","Schilde, Lukas"],["dc.contributor.author","May, Caroline"],["dc.contributor.author","Schneider, Anja"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Lingor, Paul"],["dc.date.accessioned","2021-06-01T09:41:18Z"],["dc.date.available","2021-06-01T09:41:18Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1002/ctm2.357"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/84876"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.eissn","2001-1326"],["dc.relation.issn","2001-1326"],["dc.title","MicroRNAs from extracellular vesicles as a signature for Parkinson's disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","33"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Cell and Tissue Research"],["dc.bibliographiccitation.lastpage","47"],["dc.bibliographiccitation.volume","352"],["dc.contributor.author","Schneider, Anja"],["dc.contributor.author","Simons, Mikael"],["dc.date.accessioned","2019-07-09T11:39:48Z"],["dc.date.available","2019-07-09T11:39:48Z"],["dc.date.issued","2012"],["dc.description.abstract","The intercellular transfer of misfolded proteins has received increasing attention in various neurodegenerative diseases characterized by the aggregation of specific proteins, as observed in Alzheimer’s, Parkinson’s and Huntington’s disease. One hypothesis holds that intercellular dissemination of these aggregates within the central nervous system results in the seeded assembly of the cognate soluble protein in target cells, similar to that proposed for transmissible prion diseases. The molecular mechanisms underlying the intercellular transfer of these proteinaceous aggregates are poorly understood. Various transfer modes of misfolded proteins including continuous cell-cell contacts such as nanotubes, unconventional secretion or microvesicle/exosome-associated dissemination have been suggested. Cells can release proteins, lipids and nucleic acids by vesicular exocytosis pathways destined for horizontal transfer. Encapsulation into microvesicular/exosomal vehicles not only protects these molecules from degradation and dilution in the extracellular space but also facilitates delivery over large distances, e.g. within the blood flow or interstitial fluid. Specific surface ligands might allow the highly efficient and targeted uptake of these vesicles by recipient cells. In this review, we focus on the cell biology and function of neuronal microvesicles/exosomes and discuss the evidence for pathogenic intercellular protein transfer mediated by vesicular carriers."],["dc.identifier.doi","10.1007/s00441-012-1428-2"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10314"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58038"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.publisher","Springer"],["dc.publisher.place","Berlin/Heidelberg"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Exosomes: vesicular carriers for intercellular communication in neurodegenerative disorders"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","937"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","The Journal of Cell Biology"],["dc.bibliographiccitation.lastpage","948"],["dc.bibliographiccitation.volume","172"],["dc.contributor.author","Trajkovic, K."],["dc.contributor.author","Dhaunchak, A. S."],["dc.contributor.author","Goncalves, J. T."],["dc.contributor.author","Wenzel, D."],["dc.contributor.author","Schneider, Anja"],["dc.contributor.author","Bunt, Gertrude"],["dc.contributor.author","Nave, K. A."],["dc.contributor.author","Simons, Mikael"],["dc.date.accessioned","2018-11-07T10:06:22Z"],["dc.date.available","2018-11-07T10:06:22Z"],["dc.date.issued","2006"],["dc.description.abstract","During vertebrate brain development, axons are enwrapped by myelin, an insulating membrane produced by oligodendrocytes. Neuron-derived signaling molecules are temporally and spatially required to coordinate oligodendrocyte differentiation. In this study, we show that neurons regulate myelin membrane trafficking in oligodendrocytes. In the absence of neurons, the major myelin membrane protein, the proteolipid protein (PLP), is internalized and stored in late endosomes/lysosomes (LEs/Ls) by a cholesterol-dependent and clathrin-independent endocytosis pathway that requires actin and the RhoA guanosine triphosphatase. Upon maturation, the rate of endocytosis is reduced, and a cAMP-dependent neuronal signal triggers the transport of PLP from LEs/Ls to the plasma membrane. These findings reveal a fundamental and novel role of LEs/Ls in oligodendrocytes: to store and release PLP in a regulated fashion. The release of myelin membrane from LEs/Ls by neuronal signals may represent a mechanism to control myelin membrane growth."],["dc.identifier.doi","10.1083/jcb.200509022"],["dc.identifier.isi","000235971900018"],["dc.identifier.pmid","16520383"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39080"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Rockefeller Univ Press"],["dc.relation.issn","0021-9525"],["dc.title","Neuron to glia signaling triggers myelin membrane exocytosis from endosomal storage sites"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","S6"],["dc.bibliographiccitation.journal","Alzheimer's & Dementia"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Miebach, Lisa"],["dc.contributor.author","Kleineidam, Luca"],["dc.contributor.author","Peters, Oliver"],["dc.contributor.author","Priller, Josef"],["dc.contributor.author","Buerger, Katharina"],["dc.contributor.author","Teipel, Stefan J."],["dc.contributor.author","Perneczky, Robert"],["dc.contributor.author","Laske, Christoph"],["dc.contributor.author","Schneider, Anja"],["dc.contributor.author","Heneka, Michael T."],["dc.contributor.author","Wagner, Michael"],["dc.date.accessioned","2021-12-08T12:29:51Z"],["dc.date.available","2021-12-08T12:29:51Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1002/alz.044744"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/96232"],["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","Awareness of cognitive decline and CSF‐biomarkers in memory clinic patients: Results from the DELCODE‐study"],["dc.title.alternative","Neuropsychology/Neuropsychological correlates of physiologic markers of cognitive decline/Dementia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","902"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Current Alzheimer Research"],["dc.bibliographiccitation.lastpage","912"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Vellas, B."],["dc.contributor.author","Hausner, Lucrezia"],["dc.contributor.author","Froelich, Lutz"],["dc.contributor.author","Cantet, C."],["dc.contributor.author","Gardette, V."],["dc.contributor.author","Reynish, E."],["dc.contributor.author","Gillette, S."],["dc.contributor.author","Agueera-Morales, E."],["dc.contributor.author","Auriacombe, S."],["dc.contributor.author","Boada, Merce"],["dc.contributor.author","Bullock, R."],["dc.contributor.author","Byrne, J."],["dc.contributor.author","Camus, V."],["dc.contributor.author","Cherubini, A."],["dc.contributor.author","Eriksdotter-Joenhagen, M."],["dc.contributor.author","Frisoni, Giovanni B."],["dc.contributor.author","Hasselbalch, S."],["dc.contributor.author","Jones, R. W."],["dc.contributor.author","Martinez-Lage, P."],["dc.contributor.author","Rikkert, M. O."],["dc.contributor.author","Tsolaki, Magda"],["dc.contributor.author","Ousset, P.-J."],["dc.contributor.author","Pasquier, F."],["dc.contributor.author","Ribera-Casado, J. M."],["dc.contributor.author","Rigaud, A. S."],["dc.contributor.author","Robert, P."],["dc.contributor.author","Rodriguez, G."],["dc.contributor.author","Salmon, E."],["dc.contributor.author","Salva, A."],["dc.contributor.author","Scheltens, Philip"],["dc.contributor.author","Schneider, Anja"],["dc.contributor.author","Sinclair, A."],["dc.contributor.author","Spiru, L."],["dc.contributor.author","Touchon, J."],["dc.contributor.author","Zekry, D."],["dc.contributor.author","Winblad, Bengt"],["dc.contributor.author","Andrieu, S."],["dc.date.accessioned","2018-11-07T09:05:07Z"],["dc.date.available","2018-11-07T09:05:07Z"],["dc.date.issued","2012"],["dc.description.abstract","The clinical progression of Alzheimer disease (AD) was studied in European subjects under treatment with AChE inhibitors (AChE-I) in relation to geographical location over a 2-years period. One thousand three hundred and six subjects from 11 European countries were clustered into 3 regions (North, South, West) and investigated with biannual follow-up over 2 years. Primary outcomes were cognitive, functional and behavioral measures. Caregiver burden, hospital admission and admission to nursing home were also recorded. Participant cognitive function declined non-linearly over time (MMSE: -1.5 pts/first year, -2.5 pts/second year; ADAScog: + 3.5 pts/first year, + 4.8 pts/second year), while the progression of behavioral disturbances (NPI scale) was linear. Neither scale showed regional differences, and progression of the disease was similar across Europe despite different health care systems. Functional decline (ADL, IADL) tended to progress more rapidly in Southern Europe (p=0.09), while progression of caregiver burden (Zarit Burden Interview) was most rapid in Northern Europe (5.6 pts/y, p=0.04). Incidences of hospital admission (10.44, 95% CI: 8.13-12.75, p<0.001) and admission to nursing home (2.97, 95% CI: 1.83-4.11, p<0.001) were lowest in Southern Europe. In general cognitive and functional decline was slower than in former cohorts. European geographical location reflecting differences in culture and in health care system does not impact on the progression of AD but does influence the management of AD subjects and caregiver burden."],["dc.identifier.isi","000309510400003"],["dc.identifier.pmid","22742853"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/25253"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Bentham Science Publ Ltd"],["dc.relation.issn","1875-5828"],["dc.relation.issn","1567-2050"],["dc.title","Progression of Alzheimer Disease in Europe: Data from the European ICTUS Study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","481"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.lastpage","494"],["dc.bibliographiccitation.volume","139"],["dc.contributor.author","Stuendl, Anne"],["dc.contributor.author","Kunadt, Marcel"],["dc.contributor.author","Kruse, Niels"],["dc.contributor.author","Bartels, Claudia"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Danzer, Karin M."],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Schneider, Anja"],["dc.date.accessioned","2018-11-07T10:18:37Z"],["dc.date.available","2018-11-07T10:18:37Z"],["dc.date.issued","2016"],["dc.description.abstract","Extracellular alpha-synuclein has been proposed as a crucial mechanism for induction of pathological aggregate formation in previously healthy cells. In vitro, extracellular alpha-synuclein is partially associated with exosomal vesicles. Recently, we have provided evidence that exosomal alpha-synuclein is present in the central nervous system in vivo. We hypothesized that exosomal alpha-synuclein species from patients with alpha-synuclein related neurodegeneration serve as carriers for interneuronal disease transmission. We isolated exosomes from cerebrospinal fluid from patients with Parkinson's disease, dementia with Lewy bodies, progressive supranuclear palsy as a non-alpha-synuclein related disorder that clinically overlaps with Parkinson's disease, and neurological controls. Cerebrospinal fluid exosome numbers, alpha-synuclein protein content of cerebrospinal fluid exosomes and their potential to induce oligomerization of alpha-synuclein were analysed. The quantification of cerebrospinal fluid exosomal alpha-synuclein showed distinct differences between patients with Parkinson's disease and dementia with Lewy bodies. In addition, exosomal alpha-synuclein levels correlated with the severity of cognitive impairment in cross-sectional samples from patients with dementia with Lewy bodies. Importantly, cerebrospinal fluid exosomes derived from Parkinson's disease and dementia with Lewy bodies induce oligomerization of alpha-synuclein in a reporter cell line in a dose-dependent manner. Our data suggest that cerebrospinal fluid exosomes from patients with Parkinson's disease and dementia with Lewy bodies contain a pathogenic species of alpha-synuclein, which could initiate oligomerization of soluble alpha-synuclein in target cells and confer disease pathology."],["dc.identifier.doi","10.1093/brain/awv346"],["dc.identifier.isi","000370205100026"],["dc.identifier.pmid","26647156"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41483"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","1460-2156"],["dc.relation.issn","0006-8950"],["dc.title","Induction of alpha-synuclein aggregate formation by CSF exosomes from patients with Parkinson's disease and dementia with Lewy bodies"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","124"],["dc.bibliographiccitation.journal","Cortex"],["dc.bibliographiccitation.lastpage","135"],["dc.bibliographiccitation.volume","83"],["dc.contributor.author","Teipel, Stefan J."],["dc.contributor.author","Raiser, Theresa"],["dc.contributor.author","Riedl, Lina"],["dc.contributor.author","Riederer, Isabelle"],["dc.contributor.author","Schroeter, Matthias L."],["dc.contributor.author","Bisenius, Sandrine"],["dc.contributor.author","Schneider, Anja"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Fliessbach, Klaus"],["dc.contributor.author","Spottke, Annika"],["dc.contributor.author","Grothe, Michel J."],["dc.contributor.author","Prudlo, Johannes"],["dc.contributor.author","Kassubek, Jan"],["dc.contributor.author","Ludolph, Albert C."],["dc.contributor.author","Landwehrmeyer, Bernhard G."],["dc.contributor.author","Anderl-Straub, Sarah"],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Danek, Adrian"],["dc.date.accessioned","2018-11-07T10:07:28Z"],["dc.date.available","2018-11-07T10:07:28Z"],["dc.date.issued","2016"],["dc.description.abstract","Primary progressive aphasia (PPA) is characterized by profound destruction of cortical language areas. Anatomical studies suggest an involvement of cholinergic basal forebrain (BF) in PPA syndromes, particularly in the area of the nucleus subputaminalis (NSP). Here we aimed to determine the pattern of atrophy and structural covariance as a proxy of structural connectivity of BF nuclei in PPA variants. We studied 62 prospectively recruited cases with the clinical diagnosis of PPA and 31 healthy older control participants from the cohort study of the German consortium for frontotemporal lobar. degeneration (FTLD). We determined cortical and BF atrophy based on high-resolution magnetic resonance imaging (MRI) scans. Patterns of structural covariance of BF with cortical regions were determined using voxel-based partial least square analysis. We found significant atrophy of total BF and BF subregions in PPA patients compared with controls [F(1, 82) = 20.2, p < .001]. Atrophy was most pronounced in the NSP and the posterior BF, and most severe in the semantic variant and the nonfluent variant of PPA. Structural covariance analysis in healthy controls revealed associations of the BF nuclei, particularly the NSP, with left hemispheric predominant prefrontal, lateral temporal, and parietal cortical areas, including Broca's speech area (p < .001, permutation test). In contrast, the PPA patients showed preserved structural covariance of the BF nuclei mostly with right but not with left hemispheric cortical areas (p < .001, permutation test). Our findings agree with the neuroanatomically proposed involvement of the cholinergic BF, particularly the NSP, in PPA syndromes. We found a shift from a structural covariance of the BF with left hemispheric cortical areas in healthy aging towards right hemispheric cortical areas in PPA, possibly reflecting a consequence of the profound and early destruction of cortical language areas in PPA. (C) 2016 The Author(s). Published by Elsevier Ltd."],["dc.identifier.doi","10.1016/j.cortex.2016.07.004"],["dc.identifier.isi","000385599300011"],["dc.identifier.pmid","27509365"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14211"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39287"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.eissn","0010-9452"],["dc.relation.issn","1973-8102"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.title","Atrophy and structural covariance of the cholinergic basal forebrain in primary progressive aphasia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1118"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Annals of Neurology"],["dc.bibliographiccitation.lastpage","1131"],["dc.bibliographiccitation.volume","88"],["dc.contributor.author","Tetreault, Aaron M."],["dc.contributor.author","Phan, Tony"],["dc.contributor.author","Petersen, Kalen J."],["dc.contributor.author","Claassen, Daniel O."],["dc.contributor.author","Neth, Byran J."],["dc.contributor.author","Graff‐Radford, Jonathan"],["dc.contributor.author","Albrecht, Franziska"],["dc.contributor.author","Fliessbach, Klaus"],["dc.contributor.author","Schneider, Anja"],["dc.contributor.author","Synofzik, Matthis"],["dc.contributor.author","Diehl‐Schmid, Janine"],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Schroeter, Matthias L."],["dc.contributor.author","Darby, Richard Ryan"],["dc.date.accessioned","2021-04-14T08:32:24Z"],["dc.date.available","2021-04-14T08:32:24Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1002/ana.25901"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83907"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1531-8249"],["dc.relation.issn","0364-5134"],["dc.title","Network Localization of Alien Limb in Patients with Corticobasal Syndrome"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3752"],["dc.bibliographiccitation.issue","19"],["dc.bibliographiccitation.journal","The Journal of Neuroscience"],["dc.bibliographiccitation.lastpage","3769"],["dc.bibliographiccitation.volume","39"],["dc.contributor.author","Gong, Jing"],["dc.contributor.author","Szego, Éva M."],["dc.contributor.author","Leonov, Andrei"],["dc.contributor.author","Benito, Eva"],["dc.contributor.author","Becker, Stefan"],["dc.contributor.author","Fischer, Andre"],["dc.contributor.author","Zweckstetter, Markus"],["dc.contributor.author","Outeiro, Tiago"],["dc.contributor.author","Schneider, Anja"],["dc.date.accessioned","2020-12-10T18:42:35Z"],["dc.date.available","2020-12-10T18:42:35Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1523/JNEUROSCI.2070-18.2019"],["dc.identifier.pmid","30796158"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78015"],["dc.identifier.url","https://sfb1286.uni-goettingen.de/literature/publications/13"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.relation","SFB 1286: Quantitative Synaptologie"],["dc.relation","SFB 1286 | B06: Die Rolle von RNA in Synapsenphysiologie und Neurodegeneration"],["dc.relation.workinggroup","RG A. Fischer (Epigenetics and Systems Medicine in Neurodegenerative Diseases)"],["dc.relation.workinggroup","RG Outeiro (Experimental Neurodegeneration)"],["dc.title","Translocator Protein Ligand Protects against Neurodegeneration in the MPTP Mouse Model of Parkinsonism"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","4913"],["dc.bibliographiccitation.issue","13"],["dc.bibliographiccitation.journal","Journal of the American Chemical Society"],["dc.bibliographiccitation.lastpage","4919"],["dc.bibliographiccitation.volume","136"],["dc.contributor.author","Rezaei-Ghaleh, Nasrollah"],["dc.contributor.author","Amininasab, Mehriar"],["dc.contributor.author","Giller, Karin"],["dc.contributor.author","Kumar, Sathish"],["dc.contributor.author","Stuendl, Anne"],["dc.contributor.author","Schneider, Anja"],["dc.contributor.author","Becker, Stefan"],["dc.contributor.author","Walter, Jochen"],["dc.contributor.author","Zweckstetter, Markus"],["dc.date.accessioned","2018-11-07T09:41:25Z"],["dc.date.available","2018-11-07T09:41:25Z"],["dc.date.issued","2014"],["dc.description.abstract","Pathogenesis of Alzheimer's disease (AD) is associated with aggregation of the amyloid-beta (A beta) peptide into oligomeric and fibrillar assemblies; however, little is known about the molecular basis of aggregation of A beta into distinct assembly states. Here we demonstrate that phosphorylation at serine 26 (S26) impairs A beta fibrillization while stabilizing its monomers and nontoxic soluble assemblies of nonfibrillar morphology. NMR spectroscopy and replica-exchange molecular dynamics indicate that introduction of a phosphate group or phosphomimetic at position 26 diminishes A beta's propensity to form a beta-hairpin, rigidifies the region around the modification site, and interferes with formation of a fibril-specific salt bridge between aspartic acid 23 and lysine 28. The combined data demonstrate that phosphorylation of S26 prevents a distinct conformational rearrangement that is required for progression of A beta aggregation toward fibrils and provide a basis for a possible role of phosphorylation at serine 26 in AD."],["dc.description.sponsorship","DFG [ZW 71/2-2, ZW 71/3-2, WA1477/6-2]"],["dc.identifier.doi","10.1021/ja411707y"],["dc.identifier.isi","000333947900030"],["dc.identifier.pmid","24617810"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33723"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Chemical Soc"],["dc.relation.issn","0002-7863"],["dc.title","Turn Plasticity Distinguishes Different Modes of Amyloid-beta Aggregation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]