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Andreas Weidemann

Researcher at Heidelberg University

Publications -  39
Citations -  5705

Andreas Weidemann is an academic researcher from Heidelberg University. The author has contributed to research in topics: Amyloid precursor protein & P3 peptide. The author has an hindex of 25, co-authored 37 publications receiving 5585 citations. Previous affiliations of Andreas Weidemann include Johns Hopkins University School of Medicine & University of Melbourne.

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Identification, biogenesis, and localization of precursors of Alzheimer's disease A4 amyloid protein

TL;DR: To study the putative precursor proteins of Alzheimer's disease A4 amyloid protein, polyclonal and monoclonal antibodies were raised against a recombinant bacterial PreA4(695) fusion protein to identify the precursors in different cell lines as well as in human brain homogenates and cerebrospinal fluid.
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Precursor of amyloid protein in Alzheimer disease undergoes fast anterograde axonal transport.

TL;DR: It is suggested that APP is synthesized in neurons and delivered to dystrophic nerve endings, where subsequent alterations of local processing of APP result in deposits of brain amyloid.
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Identification, transmembrane orientation and biogenesis of the amyloid A4 precursor of Alzheimer's disease.

TL;DR: The finding suggests that there is a precursor‐product relationship between precursor and amyloid A4 and it is concluded that besides proteolytic cleavage other events such as post‐translational modification and membrane injury are primary events that precede the release of the small aggregating amyloids A4 subunit.
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A Novel ε-Cleavage within the Transmembrane Domain of the Alzheimer Amyloid Precursor Protein Demonstrates Homology with Notch Processing†

TL;DR: Using C-terminally tagged APP derivatives, a novel cleavage site is identified, at Leu-49, distal to the gamma-secretase site, which shares similarities with site 3 cleavage of Notch-1: membrane topology, cleavage before a valine, dependence on presenilins, and inhibition profile.
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The amyloid precursor protein of Alzheimer's disease is released by human platelets.

TL;DR: A role in regulation of the coagulation cascade or in platelet aggregation is suggested, and material released by platelets in response to stimulation revealed that platelets release APP during degranulation.