Meyer-Lühmann, Melanie 1974-
Overview
Works: | 17 works in 20 publications in 2 languages and 84 library holdings |
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Roles: | dgs, Author |
Publication Timeline
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Most widely held works by
Melanie Meyer-Lühmann
Dynamics of amyloid plaque formation in Alzheimer's Disease a study in transgenic mice by Joanna F McCarter(
)
1 edition published in 2014 in English and held by 30 WorldCat member libraries worldwide
1 edition published in 2014 in English and held by 30 WorldCat member libraries worldwide
Einfluss von Trächtigkeit auf die A[beta]-Aggregation und die adulte hippocampale Neurogenese in einem transgenen Mausmodell
für Morbus Alzheimer by
Karin Marksteiner(
)
1 edition published in 2018 in German and held by 14 WorldCat member libraries worldwide
Abstract: Der Morbus Alzheimer gehört zum Feld der neurodegenerativen Erkrankungen und äußert sich durch kognitive, vor allem Hippocampus-abhängige Fähigkeiten betreffende, Defizite. Als Ursache werden unter anderem die Amyloid-b-(Ab)-Plaqueablagerungen und eine Störung der adulten hippocampalen Neurogenese vermutet. Epidemiologischen Studien zufolge sind Frauen von einem höheren Morbus-Alzheimer- Erkrankungsrisiko betroffen als Männer. Hormonelle Schwankungen im Leben der Frau, z.B. während der Schwangerschaft, könnten dafür verantwortlich sein. In der vorliegenden Arbeit sollte durch die Beobachtung der Wechselwirkungen zwischen Trächtigkeit und A[beta]-Aggregation bzw. adulter Neurogenese ein möglicher Einfluss der Gravidität auf Morbus Alzheimer detektiert werden. Dazu wurden transgene 5xFAD-Mäuse verwendet, welche fünf Mutationen in den Genen für das Amyloid-Vorläufer-Protein (APP) und Präsenilin-1 (PS1) exprimieren. Um Aussagen über den Einfluss von Gravidität auf die A[beta]-Aggregation und die adulte Neurogenese machen zu können, wurden 13 bzw. 14 Wochen alte trächtige 5xFAD-Weibchen an Gestationstag 5 bzw. 10 getötet und untersucht. Zur Analyse des Einflusses mehrmaliger Gravidität auf die Morbus-Alzheimer-Pathologie wurden 10 Monate alte 5xFAD-Weibchen, die vier Mal, einmal oder nie trächtig gewesen waren, mit vier Mal und nie trächtig gewesenen Wildtyp-Weibchen ohne familiäre Morbus-Alzheimer-Mutationen verglichen. Zur Quantifizierung der Ab-Aggregation wurden Ab-Immunfloureszenz-Färbungen sowie Kresyl-Violett-Färbungen der Hirnschnitte angefertigt und ein repräsentativer Western-Blot für die in den Hippocampi abgelagerten Ab-Peptide durchgeführt. Die adulte Neurogenese wurde mittels Immunfloureszenz-Färbungen gegen Zellproliferationsmarker (Ki67) und Neurogenesemarker (Doublecortin, DCX) quantifiziert. Ergänzt wurden die Untersuchungen durch einen repräsentativen Western-Blot für das von Neuroblasten und unreifen Neuronen exprimierte DCX. In den jungen 13 bzw. 14 Wochen alten Tieren konnte eine vermehrte Ab-Plaquebildung und zudem eine tendenziell erhöhte Zellproliferation beobachtet werden. Dies spricht für das Vorhandensein modulierender Einflüsse auf die Morbus-Alzheimer-Pathologie während der ersten Hälfte der Trächtigkeit. In den 10 Monate alten Tieren konnten weder in der Ab- Aggregation noch in der adulten Neurogenese Unterschiede zwischen den Gruppen festgestel
1 edition published in 2018 in German and held by 14 WorldCat member libraries worldwide
Abstract: Der Morbus Alzheimer gehört zum Feld der neurodegenerativen Erkrankungen und äußert sich durch kognitive, vor allem Hippocampus-abhängige Fähigkeiten betreffende, Defizite. Als Ursache werden unter anderem die Amyloid-b-(Ab)-Plaqueablagerungen und eine Störung der adulten hippocampalen Neurogenese vermutet. Epidemiologischen Studien zufolge sind Frauen von einem höheren Morbus-Alzheimer- Erkrankungsrisiko betroffen als Männer. Hormonelle Schwankungen im Leben der Frau, z.B. während der Schwangerschaft, könnten dafür verantwortlich sein. In der vorliegenden Arbeit sollte durch die Beobachtung der Wechselwirkungen zwischen Trächtigkeit und A[beta]-Aggregation bzw. adulter Neurogenese ein möglicher Einfluss der Gravidität auf Morbus Alzheimer detektiert werden. Dazu wurden transgene 5xFAD-Mäuse verwendet, welche fünf Mutationen in den Genen für das Amyloid-Vorläufer-Protein (APP) und Präsenilin-1 (PS1) exprimieren. Um Aussagen über den Einfluss von Gravidität auf die A[beta]-Aggregation und die adulte Neurogenese machen zu können, wurden 13 bzw. 14 Wochen alte trächtige 5xFAD-Weibchen an Gestationstag 5 bzw. 10 getötet und untersucht. Zur Analyse des Einflusses mehrmaliger Gravidität auf die Morbus-Alzheimer-Pathologie wurden 10 Monate alte 5xFAD-Weibchen, die vier Mal, einmal oder nie trächtig gewesen waren, mit vier Mal und nie trächtig gewesenen Wildtyp-Weibchen ohne familiäre Morbus-Alzheimer-Mutationen verglichen. Zur Quantifizierung der Ab-Aggregation wurden Ab-Immunfloureszenz-Färbungen sowie Kresyl-Violett-Färbungen der Hirnschnitte angefertigt und ein repräsentativer Western-Blot für die in den Hippocampi abgelagerten Ab-Peptide durchgeführt. Die adulte Neurogenese wurde mittels Immunfloureszenz-Färbungen gegen Zellproliferationsmarker (Ki67) und Neurogenesemarker (Doublecortin, DCX) quantifiziert. Ergänzt wurden die Untersuchungen durch einen repräsentativen Western-Blot für das von Neuroblasten und unreifen Neuronen exprimierte DCX. In den jungen 13 bzw. 14 Wochen alten Tieren konnte eine vermehrte Ab-Plaquebildung und zudem eine tendenziell erhöhte Zellproliferation beobachtet werden. Dies spricht für das Vorhandensein modulierender Einflüsse auf die Morbus-Alzheimer-Pathologie während der ersten Hälfte der Trächtigkeit. In den 10 Monate alten Tieren konnten weder in der Ab- Aggregation noch in der adulten Neurogenese Unterschiede zwischen den Gruppen festgestel
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Melanie Meyer-Luehmann(
)
2 editions published in 2011 in English and held by 4 WorldCat member libraries worldwide
2 editions published in 2011 in English and held by 4 WorldCat member libraries worldwide
The role of glial cells and synapse loss in mouse models of Alzheimer's disease by
Stephanie Ziegler-Waldkirch(
)
1 edition published in 2018 in English and held by 3 WorldCat member libraries worldwide
1 edition published in 2018 in English and held by 3 WorldCat member libraries worldwide
Mechanisms of pathogenic tau and A[Beta] protein spreading in Alzheimer's disease by
Paolo d' Errico(
)
1 edition published in 2020 in English and held by 3 WorldCat member libraries worldwide
1 edition published in 2020 in English and held by 3 WorldCat member libraries worldwide
Different effects of constitutive and induced microbiota modulation on microglia in a mouse model of Alzheimer's disease by
Charlotte Mezö(
)
1 edition published in 2020 in English and held by 3 WorldCat member libraries worldwide
1 edition published in 2020 in English and held by 3 WorldCat member libraries worldwide
Environmental enrichment reverses A[beta] pathology during pregnancy in a mouse model of Alzheimer's disease by
Stephanie Ziegler-Waldkirch(
)
1 edition published in 2018 in English and held by 3 WorldCat member libraries worldwide
1 edition published in 2018 in English and held by 3 WorldCat member libraries worldwide
The ratio of ADP- to TRAP-induced platelet aggregation quantifies P2Y12-dependent platelet inhibition independently of the
platelet count by
Christoph Olivier(
)
2 editions published in 2016 in English and held by 3 WorldCat member libraries worldwide
Abstract: Objective This study aimed to assess the association of clinical factors with P2Y 12 -dependent platelet inhibition as monitored by the ratio of ADP- to TRAP-induced platelet aggregation and conventional ADP-induced aggregation, respectively. BackgroundControversial findings to identify and overcome high platelet reactivity (HPR) after coronarystent-implantation and to improve clinical outcome by tailored anti-platelet therapy exist. Monitoring anti-platelet therapy ex vivo underlies several confounding parameters causing that ex vivo platelet aggregation might not reflect in vivoplatelet inhibition.MethodsIn a single centre observational study, multiple electrode aggregometry was performed in whole blood of patients after recent coronary stent-implantation. Relative ADP-induced aggregation (r-ADP-agg) was defined as the ratio of ADP- to TRAP- induced aggregation reflecting the individual degree of P2Y 12-mediated platelet reactivity. ResultsPlatelet aggregation was assessed in 359 patients. Means (±SD) of TRAP-, ADP-induced aggregation and r-ADP-agg were 794±239 AU*min, 297±153 AU*min and 37±14%,respectively. While ADP- and TRAP-induced platelet aggregation correlated significantly with platelet count (ADP: r = 0.302; p<0.001; TRAP: r = 0.509 p <0.001), r-ADP-agg values did not (r = -0.003; p = 0.960). These findings were unaltered in multivariate analysesadjusting for a range of factors potentially influencing platelet aggregation. The presence of an acute coronary syndrome and body weight were found to correlate with both ADP-induced platelet aggregation and r-ADP-agg.ConclusionThe ratio of ADP- to TRAP-induced platelet aggregation quantifies P2Y 12 -dependent plate-let inhibition independently of the platelet count in contrast to conventional ADP-induced aggregation. Furthermore, r-ADP-agg was associated with the presence of an acute coronary syndrome and body weight as well as ADP-induced aggregation. Thus, the r-ADP-aggis a more valid reflecting platelet aggregation and potentially prognosis after coronary stent-implantation in P2Y12-mediated HPR than conventional ADP-induced platelet aggregation
2 editions published in 2016 in English and held by 3 WorldCat member libraries worldwide
Abstract: Objective This study aimed to assess the association of clinical factors with P2Y 12 -dependent platelet inhibition as monitored by the ratio of ADP- to TRAP-induced platelet aggregation and conventional ADP-induced aggregation, respectively. BackgroundControversial findings to identify and overcome high platelet reactivity (HPR) after coronarystent-implantation and to improve clinical outcome by tailored anti-platelet therapy exist. Monitoring anti-platelet therapy ex vivo underlies several confounding parameters causing that ex vivo platelet aggregation might not reflect in vivoplatelet inhibition.MethodsIn a single centre observational study, multiple electrode aggregometry was performed in whole blood of patients after recent coronary stent-implantation. Relative ADP-induced aggregation (r-ADP-agg) was defined as the ratio of ADP- to TRAP- induced aggregation reflecting the individual degree of P2Y 12-mediated platelet reactivity. ResultsPlatelet aggregation was assessed in 359 patients. Means (±SD) of TRAP-, ADP-induced aggregation and r-ADP-agg were 794±239 AU*min, 297±153 AU*min and 37±14%,respectively. While ADP- and TRAP-induced platelet aggregation correlated significantly with platelet count (ADP: r = 0.302; p<0.001; TRAP: r = 0.509 p <0.001), r-ADP-agg values did not (r = -0.003; p = 0.960). These findings were unaltered in multivariate analysesadjusting for a range of factors potentially influencing platelet aggregation. The presence of an acute coronary syndrome and body weight were found to correlate with both ADP-induced platelet aggregation and r-ADP-agg.ConclusionThe ratio of ADP- to TRAP-induced platelet aggregation quantifies P2Y 12 -dependent plate-let inhibition independently of the platelet count in contrast to conventional ADP-induced aggregation. Furthermore, r-ADP-agg was associated with the presence of an acute coronary syndrome and body weight as well as ADP-induced aggregation. Thus, the r-ADP-aggis a more valid reflecting platelet aggregation and potentially prognosis after coronary stent-implantation in P2Y12-mediated HPR than conventional ADP-induced platelet aggregation
Detection of synaptic proteins in microglia by flow cytometry by
Simone Brioschi(
)
1 edition published in 2020 in English and held by 3 WorldCat member libraries worldwide
1 edition published in 2020 in English and held by 3 WorldCat member libraries worldwide
A[beta] oligomers trigger and accelerate A[beta] seeding by
Natalie Katzmarski(
)
1 edition published in 2020 in English and held by 3 WorldCat member libraries worldwide
1 edition published in 2020 in English and held by 3 WorldCat member libraries worldwide
A[beta] seeding as a tool to study cerebral amyloidosis and associated pathology by
Marina Friesen(
)
2 editions published in 2019 in English and held by 3 WorldCat member libraries worldwide
2 editions published in 2019 in English and held by 3 WorldCat member libraries worldwide
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Sabine Hellwig(
)
1 edition published in 2015 in English and held by 3 WorldCat member libraries worldwide
1 edition published in 2015 in English and held by 3 WorldCat member libraries worldwide
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Lea Neudel(
)
1 edition published in 2017 in German and held by 2 WorldCat member libraries worldwide
1 edition published in 2017 in German and held by 2 WorldCat member libraries worldwide
Loss of TREM2 function increases amyloid seeding but reduces plaque-associated ApoE by
Samira Parhizkar(
)
1 edition published in 2019 in English and held by 2 WorldCat member libraries worldwide
1 edition published in 2019 in English and held by 2 WorldCat member libraries worldwide
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Johannes Stoll(
)
1 edition published in 2020 in German and held by 2 WorldCat member libraries worldwide
1 edition published in 2020 in German and held by 2 WorldCat member libraries worldwide
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Stephanie Ziegler-Waldkirch(
)
1 edition published in 2016 in English and held by 2 WorldCat member libraries worldwide
1 edition published in 2016 in English and held by 2 WorldCat member libraries worldwide
A peephole into the brain: neuropathological features of Alzheimer's disease revealed by in vivo two-photon imaging by
Sabine Liebscher(
)
1 edition published in 2012 in English and held by 1 WorldCat member library worldwide
1 edition published in 2012 in English and held by 1 WorldCat member library worldwide
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General | Special |

- McCarter, Joanna F. Author
- Albert-Ludwigs-Universität Freiburg Medizinische Fakultät Degree grantor
- Marksteiner, Karin Author
- Ziegler-Waldkirch, Stephanie 1985- Author
- Albert-Ludwigs-Universität Freiburg Publisher
- Biber, Knut
- Friesen, Marina Author
- SpringerLink (Online service) Other
- Prinz, Marco 1970-
- Katzmarski, Natalie Author
Associated Subjects