| First Author | Caillava C | Year | 2014 |
| Journal | Neurobiol Aging | Volume | 35 |
| Issue | 7 | Pages | 1570-81 |
| PubMed ID | 24495834 | Mgi Jnum | J:213881 |
| Mgi Id | MGI:5586777 | Doi | 10.1016/j.neurobiolaging.2014.01.011 |
| Citation | Caillava C, et al. (2014) Study on Abeta34 biology and detection in transgenic mice brains. Neurobiol Aging 35(7):1570-81 |
| abstractText | The beta-amyloid precursor protein undergoes cleavages by beta- and gamma-secretasses yielding amyloid-beta peptides (Abeta) that accumulate in Alzheimer's disease. Subsequently, Abeta peptides are targets of additional truncations or endoproteolytic cleavages explaining the diversity of Abeta-related fragments recovered in cell media or pathologic human fluids. Here, we focused on Abeta1-34 (Abeta34) that has been detected both in vitro and in vivo and that derives from the hydrolysis of Abeta by beta-secretase. We have obtained and fully characterized by immunologic and biochemical approaches, a polyclonal antibody that specifically recognizes the C-terminus of Abetax-34. We present immunohistochemical evidence for the presence of Abetax-34 in the brain of 3xTg mice and Alzheimer's disease-affected human brains. Finally, we demonstrate a neprilysin-mediated degradation process of Abeta34 and the ability of synthetic Abeta34 to protect HEK cells overexpressing either wild type or Swedish-mutated beta-amyloid precursor protein from apoptosis. |
