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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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A presenilin-1-dependent gamma-secretase-like protease mediates release of Notch intracellular domain.

TL;DR: It is reported that, in mammalian cells, PS1 deficiency also reduces the proteolytic release of NICD from a truncated Notch construct, thus identifying the specific biochemical step of the Notch signalling pathway that is affected by PS1.
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The amyloid cascade hypothesis for Alzheimer's disease: an appraisal for the development of therapeutics.

TL;DR: It is timely to review the science underpinning the amyloid cascade hypothesis, consider what type of clinical trials will constitute a valid test of this hypothesis and explore whether amyloids-β-directed therapeutics will provide the medicines that are urgently needed by society for treating this devastating disease.
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Deficiency of presenilin-1 inhibits the normal cleavage of amyloid precursor protein

TL;DR: The results indicate that mutations in PS1 that manifest clinically cause a gain of function and that inhibition of PS1 activity is a potential target for anti-amyloidogenic therapy in Alzheimer's disease.
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The toxic Aβ oligomer and Alzheimer's disease: an emperor in need of clothes

TL;DR: The evidence supporting toxic Aβ oligomers as drivers of neurodegeneration is reviewed and some suggestions that might facilitate progress are made to facilitate progress in this complex field.
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OPA1 Controls Apoptotic Cristae Remodeling Independently from Mitochondrial Fusion

TL;DR: Evidence is provided that Optic Atrophy 1 (OPA1), a profusion dynamin-related protein of the inner mitochondrial membrane mutated in dominant optic atrophy, protects from apoptosis by preventing cytochrome c release independently from mitochondrial fusion.