Wittnam JL, Portelius E, Zetterberg H, Gustavsson MK, Schilling S, Koch B, Demuth HU, Blennow K, Wirths O, Bayer TA.
Pyroglutamate amyloid β (Aβ) aggravates behavioral deficits in transgenic amyloid mouse model for Alzheimer disease.
J Biol Chem. 2012 Mar 9;287(11):8154-62.
Please login to recommend the paper.
To make a comment you must login or register.
The TBA42 model produces human pyroglutamate Aβ3-42 in the CA1 region of the hippocampus. This peptide has received considerable attention in recent years, and has been hypothesized to be the Aβ species that seeds toxic aggregates, having prion-like features. The TBA42 model specifically expresses N-truncated human Aβ3-42 fused to a thyrotropin-releasing hormone backbone. Because these animals express no human APP, the effects of pyroglutamate Aβ3-42 are not confounded by other human APP products, such as sAPPα, sAPPβ, p3, and C-terminal fragments, which have a variety of biological activities, including neurotrophic and synaptotrophic effects. Another advantage to the TBA42 model is that it does not develop a severe plaque load. (Plaque levels do not correlate with cognitive decline in AD patients).