Ulrike Zeitschel

TL;DR: It is concluded that ADAM10 is the physiologically relevant, constitutive α‐secretase of APP, and a novel pathway for APP processing is suggested, in which ADAM 10 can partially compete with γ‐secret enzyme for the cleavage of a C‐terminal APP fragment generated by β‐ secretase.

TL;DR: It is found that the N-terminal pE-formation is catalyzed by glutaminyl cyclase in vivo, and Aβ3(pE)–40/42 peptides seem to represent Aβ forms with exceptional potency for disturbing neuronal function.

TL;DR: The secretome protein enrichment with click sugars (SPECS) method, which allows proteome‐wide identification of shedding substrates and secreted proteins from primary cells, even in the presence of serum proteins, is developed.

TL;DR: To address the question whether astrocytic BACE1 expression is an event specifically triggered by β‐amyloid plaques or whether glial cell activation by other mechanisms also induces Bace1 expression, six different experimental strategies to activate brain glial cells acutely or chronically are used.

TL;DR: Evidence is presented demonstrating that astrocytes are an alternative source of BACE1 and therefore may contribute to β‐amyloid plaque formation, suggesting that therapeutic strategies that targetAstrocyte activation in brain may be beneficial for the treatment of AD.