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Glutaminyl cyclase-mediated toxicity of pyroglutamate-beta amyloid induces striatal neurodegeneration

 
: Becker, Andreas; Kohlmann, Stephanie; Alexandru, Anca; Jagla, Wolfgang; Canneva, Fabio; Bäuscher, Christoph; Cynis, Holger; Sedlmeier, Reinhard; Graubner, Sigrid; Schilling, Stephan; Demuth, Hans-Ulrich; Hörsten, Stephan von

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Postprint (2.3 MByte; PDF; )

BMC neuroscience. Online journal 14 (2013), Art. 108, 18 pp.
http://www.biomedcentral.com/1471-2202/
ISSN: 1471-2202
English
Journal Article, Electronic Publication
Fraunhofer IZI ()
This ultimately resulted in astrocytosis, loss of DARPP-32 immunoreactivity, and neuronal loss at the sites of pE3-Aβ formation. Neuropathology in ETNA mice was associated with behavioral alterations. In particular, hyperactivity and impaired acoustic sensorimotor gating were detected. Double tg ETNA-hQC mice showed similar Aβ levels and expression sites, while pE3-Aβ were significantly increased, entailing increased astrocytosis and neuronal loss.
Conclusions
ETNA and ETNA-hQC mice represent novel mouse models for QC-mediated toxicity of truncated and pE-modified Aβ. Due to their significant striatal neurodegeneration these mice can also be used for analysis of striatal regulation of basal locomotor activity and sensorimotor gating, and possibly for DARPP-32-dependent neurophysiology and neuropathology. The spatio-temporal correlation of pE3-Aβ and neuropathology strongly argues for an important role of this Aβ species in neurodegenerative processes in these models.
ETNA; Pyroglutamate Aß; Glutaminyl cyclase; Alzheimer's disease; TBA; Neurodegeneration; Neuroinflammation; Striatum

: http://publica.fraunhofer.de/documents/N-281750.html