J
J. Michael Salbaum
Researcher at Heidelberg University
Publications - 5
Citations - 1308
J. Michael Salbaum is an academic researcher from Heidelberg University. The author has contributed to research in topics: Amyloid & BACE1-AS. The author has an hindex of 3, co-authored 5 publications receiving 1297 citations.
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Journal ArticleDOI
Identification, biogenesis, and localization of precursors of Alzheimer's disease A4 amyloid protein
Andreas Weidemann,G. König,D. Bunke,Peter Fischer,J. Michael Salbaum,Colin L. Masters,Konrad Beyreuther +6 more
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.
Journal ArticleDOI
Promoter of alzheimer??s disease amyloid a4 precursor gene
TL;DR: Findings suggest that four mechanisms may participate in the regulation of the PAD gene and could be of relevance for the progression of amyloid deposition in Alzheimer's disease.
Identification, transmembrane orientation andbiogenesis oftheamyloid A4 precursorofAlzheimer's disease
TL;DR: The precursor of the Alzheimer's disease-specific amyloid A4 protein is an integral, glycosylated membrane protein which spans the bilayer once as discussed by the authors, and the carboxy-terminal domain of 47 residues was located at the cytoplasmic site of the membrane.
Journal ArticleDOI
Molecular pathology of the amyloid a4 precursor of alzheimer??s disease
Thomas Dyrks,Andreas Weidemann,Gerd Multhaup,J. Michael Salbaum,Colin L. Masters,Konrad Beyreuther +5 more
TL;DR: It is suggested that besides proteolytic cleavage, other events, such as membrane damage are primary events that precede the release of the small, aggregating amyloid A4 subunit.
Book ChapterDOI
Regulation of the Amyloid Gene of Alzheimer’s Disease
TL;DR: Alzheimer’s disease (AD) is a progressive degenerative disorder of the human central nervous system that is accompanied by neuronal dysfunction, reduced synaptic density, gliosis, and neuronal loss, some of which are also observed in the normal aging process, however to a much lesser extent.