Title |
Glutaminyl cyclase-mediated toxicity of pyroglutamate-beta amyloid induces striatal neurodegeneration
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Published in |
BMC Neuroscience, October 2013
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DOI | 10.1186/1471-2202-14-108 |
Pubmed ID | |
Authors |
Andreas Becker, Stephanie Kohlmann, Anca Alexandru, Wolfgang Jagla, Fabio Canneva, Christoph Bäuscher, Holger Cynis, Reinhard Sedlmeier, Sigrid Graubner, Stephan Schilling, Hans-Ulrich Demuth, Stephan von Hörsten |
Abstract |
Posttranslational modifications of beta amyloid (Aβ) have been shown to affect its biophysical and neurophysiological properties. One of these modifications is N-terminal pyroglutamate (pE) formation. Enzymatic glutaminyl cyclase (QC) activity catalyzes cyclization of truncated Aβ(3-x), generating pE3-Aβ. Compared to unmodified Aβ, pE3-Aβ is more hydrophobic and neurotoxic. In addition, it accelerates aggregation of other Aβ species. To directly investigate pE3-Aβ formation and toxicity in vivo, transgenic (tg) ETNA (E at the truncated N-terminus of Aβ) mice expressing truncated human Aβ(3-42) were generated and comprehensively characterized. To further investigate the role of QC in pE3-Aβ formation in vivo, ETNA mice were intercrossed with tg mice overexpressing human QC (hQC) to generate double tg ETNA-hQC mice. |
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