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Christine L. Remmers

Researcher at Northwestern University

Publications -  12
Citations -  825

Christine L. Remmers is an academic researcher from Northwestern University. The author has contributed to research in topics: Dendritic spine & GABAergic. The author has an hindex of 9, co-authored 12 publications receiving 748 citations. Previous affiliations of Christine L. Remmers include Rockefeller University.

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Gamma-secretase activating protein is a therapeutic target for Alzheimer’s disease

TL;DR: It is demonstrated that imatinib, an anticancer drug previously found to inhibit amyloid-β formation without affecting Notch cleavage, achieves its amyloids-β-lowering effect by preventing GSAP interaction with the γ-secretase substrate, APP-CTF.
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Characterization of prefibrillar Tau oligomers in vitro and in Alzheimer disease.

TL;DR: In this paper, a photochemical cross-linking technique was employed to examine intermolecular interactions of full-length Tau in vitro and showed that dimerization is an early event in the Tau aggregation process and that these dimers self-associate to form larger oligomeric aggregates.
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Epac2 Mediates cAMP-Dependent Potentiation of Neurotransmission in the Hippocampus.

TL;DR: Examination of synaptic transmission during long sustained trains of activity suggested that the readily releasable pool of vesicles is reduced in Epac2−/− mice, and data suggest that cAMP elevation uses an Epac 2-dependent pathway to promote transmitter release, and thatEpac2 is required to maintain the readily RELEASable pool at MF synapses in the hippocampus.
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Delayed Maturation of Fast-Spiking Interneurons Is Rectified by Activation of the TrkB Receptor in the Mouse Model of Fragile X Syndrome.

TL;DR: Evidence is provided that the function of fast-spiking interneurons is disrupted due to a deficiency in neurotrophin signaling during early development in FXS, and the maturation of the GABAergic circuit in the sensory cortex is altered during a critical developmental period.
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Subchronic phencyclidine treatment in adult mice increases GABAergic transmission and LTP threshold in the hippocampus

TL;DR: The results suggest repeated PCP administration causes a long-lasting metaplastic change in the inhibitory circuits in the hippocampus that results in impaired LTP, and could contribute to the deficits in hippocampal-dependent memory in PCP-treated mice.