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Stefan von Berg

Researcher at AstraZeneca

Publications -  48
Citations -  1902

Stefan von Berg is an academic researcher from AstraZeneca. The author has contributed to research in topics: GSK-3 & In vivo. The author has an hindex of 22, co-authored 48 publications receiving 1746 citations.

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Structural Insights and Biological Effects of Glycogen Synthase Kinase 3-specific Inhibitor AR-A014418

TL;DR: AR-A014418 is the first compound of a family of specific inhibitors of GSK3 that does not significantly inhibit closely related kinases such as cdk2 or cdk5 and may have important applications as a tool to elucidate the role of Gsk3 in cellular signaling and possibly in Alzheimer's disease.
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A zebrafish model of tauopathy allows in vivo imaging of neuronal cell death and drug evaluation

TL;DR: This transgenic zebrafish model may become a valuable tool for further studies of the neuropathology of dementia and be used to identify compounds targeting the TAU kinase glycogen synthase kinase 3beta (GSK3beta).
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Discovery of novel potent and highly selective glycogen synthase kinase-3β (GSK3β) inhibitors for Alzheimer's disease: design, synthesis, and characterization of pyrazines.

TL;DR: This work has developed highly potent and selective inhibitors of GSK3β showing cellular efficacy and blood-brain barrier penetrance that are suitable for in vivo efficacy testing and may serve as a new treatment strategy for Alzheimer's disease.
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Discovery of AZD3839, a Potent and Selective BACE1 Inhibitor Clinical Candidate for the Treatment of Alzheimer Disease *

TL;DR: Zhang et al. as mentioned in this paper reported the discovery and comprehensive preclinical characterization of AZD3839, a potent and selective inhibitor of human β-Site amyloid precursor protein cleaving enzyme1 (BACE1), which was identified using fragment-based screening and structure-based design.
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AZD1080, a novel GSK3 inhibitor, rescues synaptic plasticity deficits in rodent brain and exhibits peripheral target engagement in humans

TL;DR: Interestingly, subchronic but not acute administration with AZD1080 reverses MK‐801‐induced deficits, measured by long‐term potentiation in hippocampal slices and in a cognitive test in mice, suggesting that reversal of synaptic plasticity deficits in dysfunctional systems requires longer term modifications of proteins downstream of GSK3β signaling.