| First Author | Bouter Y | Year | 2013 |
| Journal | Acta Neuropathol | Volume | 126 |
| Issue | 2 | Pages | 189-205 |
| PubMed ID | 23685882 | Mgi Jnum | J:275188 |
| Mgi Id | MGI:6306781 | Doi | 10.1007/s00401-013-1129-2 |
| Citation | Bouter Y, et al. (2013) N-truncated amyloid beta (Abeta) 4-42 forms stable aggregates and induces acute and long-lasting behavioral deficits. Acta Neuropathol 126(2):189-205 |
| abstractText | N-truncated Abeta4-42 is highly abundant in Alzheimer disease (AD) brain and was the first Abeta peptide discovered in AD plaques. However, a possible role in AD aetiology has largely been neglected. In the present report, we demonstrate that Abeta4-42 rapidly forms aggregates possessing a high aggregation propensity in terms of monomer consumption and oligomer formation. Short-term treatment of primary cortical neurons indicated that Abeta4-42 is as toxic as pyroglutamate Abeta3-42 and Abeta1-42. In line with these findings, treatment of wildtype mice using intraventricular Abeta injection induced significant working memory deficits with Abeta4-42, pyroglutamate Abeta3-42 and Abeta1-42. Transgenic mice expressing Abeta4-42 (Tg4-42 transgenic line) developed a massive CA1 pyramidal neuron loss in the hippocampus. The hippocampus-specific expression of Abeta4-42 correlates well with age-dependent spatial reference memory deficits assessed by the Morris water maze test. Our findings indicate that N-truncated Abeta4-42 triggers acute and long-lasting behavioral deficits comparable to AD typical memory dysfunction. |
