| First Author | Meißner JN | Year | 2015 |
| Journal | J Alzheimers Dis | Volume | 45 |
| Issue | 2 | Pages | 471-82 |
| PubMed ID | 25547635 | Mgi Jnum | J:284911 |
| Mgi Id | MGI:6392396 | Doi | 10.3233/JAD-142868 |
| Citation | Meissner JN, et al. (2015) Neuron Loss and Behavioral Deficits in the TBA42 Mouse Model Expressing N-Truncated Pyroglutamate Amyloid-beta3-42. J Alzheimers Dis 45(2):471-82 |
| abstractText | Pyroglutamate-modified amyloid-beta (Abeta) at amino acid position three (Abeta(pE3-42)) is gaining considerable attention as a potential key player in the pathogenesis of Alzheimer's disease (AD). Abeta(pE3-42) is abundant in AD brain and has a high aggregation propensity, stability, and cellular toxicity. The aim of the present work was to study the effect of Abeta(pE3-42) expression on neuron loss and associated behavioral deficits using the TBA42 transgenic mouse model. Expression of pyroglutamate Abeta(3-42) triggers hippocampal CA1 neuron loss and behavioral deficits in the TBA42 mouse model. Mice elicited significant neuron death (-35% at the age of 12 months), deficits in the spatial reference memory, working memory, loss of anxiety, and severe motor deficits in an age-dependent manner. These results support a major pathological function of pyroglutamate Abeta in AD. |
