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Bart De Strooper

Researcher at Katholieke Universiteit Leuven

Publications -  433
Citations -  56592

Bart De Strooper is an academic researcher from Katholieke Universiteit Leuven. The author has contributed to research in topics: Amyloid precursor protein & Presenilin. The author has an hindex of 117, co-authored 397 publications receiving 48516 citations. Previous affiliations of Bart De Strooper include Ghent University & Allen Institute for Brain Science.

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The discrepancy between presenilin subcellular localization and γ-secretase processing of amyloid precursor protein

TL;DR: It is concluded that γ-secretase cleavage of APP-C99 occurs in a specialized subcellular compartment where little or no PS1 is detected, which suggests that at least one other factor than PS1, located downstream of the ER, is required for theγ-cleavage ofAPP-C 99.
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Neurotoxicity and Memory Deficits Induced by Soluble Low-Molecular-Weight Amyloid-β1–42 Oligomers Are Revealed In Vivo by Using a Novel Animal Model

TL;DR: A novel mouse model provides evidence that small, soluble Aβ1–42 oligomers are able to induce extensive neuronal loss in vivo and initiate a cascade of events that mimic the key neuropathological hallmarks of AD.
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Role of Presenilins in Neuronal Calcium Homeostasis

TL;DR: Interestingly, it is discovered that presenilins play a major role in ER Ca2+ leak function in hippocampal but not in striatal neurons, and disruption of ER Ca1-mediated leak function of presenILins may play an important role in AD pathogenesis.
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The Neural Cell Adhesion Molecules L1 and CHL1 Are Cleaved by BACE1 Protease in Vivo

TL;DR: It is shown that L1 and CHL1 are cleaved by BACE1 under physiological conditions, and this work will help to predict or interpret possible side effects of Bace1 inhibitor drugs in current clinical trials.
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The thymic epithelial microRNA network elevates the threshold for infection-associated thymic involution via miR-29a mediated suppression of the IFN-α receptor

TL;DR: It is found that the microRNA network dependent on the endoribonuclease Dicer, and specifically microRNA miR-29a, was critical for diminishing the sensitivity of the thymic epithelium to simulated infection signals, protecting the thcyus against inappropriate involution.