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Eckart Förster

Researcher at University of Freiburg

Publications -  47
Citations -  3902

Eckart Förster is an academic researcher from University of Freiburg. The author has contributed to research in topics: Reelin & DAB1. The author has an hindex of 27, co-authored 38 publications receiving 3719 citations. Previous affiliations of Eckart Förster include University of Basel & University of Hamburg.

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Reelin and apoE receptors cooperate to enhance hippocampal synaptic plasticity and learning

TL;DR: A role for Reelin is revealed in controlling synaptic plasticity in the adult brain and the impairment of apoE receptor-dependent neuromodulation may contribute to cognitive impairment and synaptic loss in Alzheimer disease.
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A role for Cajal–Retzius cells and reelin in the development of hippocampal connections

TL;DR: It is reported that ablation of Cajal–Retzius cells in organotypic slice cultures of hippocampus prevented the ingrowth of entorhinal but not of commissural afferents, and reelin is essential for the formation of layer-specific hippocampal connections.
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Fyn tyrosine kinase is a critical regulator of disabled-1 during brain development.

TL;DR: It is found that fyn is required for proper Dab1 levels and phosphorylation in vivo and in vitro, suggesting additional complexity in the Reelin signaling pathway.
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Reelin, Disabled 1, and β1 integrins are required for the formation of the radial glial scaffold in the hippocampus

TL;DR: It is shown that a regular glial scaffold fails to form in vivo in the dentate gyrus of mice deficient of Reelin or Disabled 1, a neuronal adaptor protein in the Reelin signaling pathway, and data suggest that Reelin affects glial differentiation via Disabled 1 and β1-class integrin-dependent signaling pathways.
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Laminating the hippocampus.

TL;DR: The hippocampus, with its clearly segregated cell and fibre layers, has become a major subject of studies on cortical lamination and the determinants of the laminated cortical architecture will contribute to the understanding of how cortical functions have evolved in phylogenetic and ontogenetic development.