| First Author | Reinert J | Year | 2014 |
| Journal | J Alzheimers Dis | Volume | 39 |
| Issue | 4 | Pages | 871-81 |
| PubMed ID | 24305500 | Mgi Jnum | J:286212 |
| Mgi Id | MGI:6402358 | Doi | 10.3233/JAD-131373 |
| Citation | Reinert J, et al. (2014) Abeta38 in the brains of patients with sporadic and familial Alzheimer's disease and transgenic mouse models. J Alzheimers Dis 39(4):871-81 |
| abstractText | The pathogenesis of Alzheimer's disease (AD) is believed to be closely dependent on deposits of neurotoxic amyloid-beta peptides (Abeta), which become abundantly present throughout the central nervous system in advanced stages of the disease. The different Abeta peptides existing are generated by subsequent cleavage of the amyloid-beta protein precursor (AbetaPP) and may vary in length and differ at their C-terminus. Despite extensive studies on the most prevalent species Abeta40 and Abeta42, Abeta peptides with other C-termini such as Abeta38 have not received much attention. In the present study, we used a highly specific and sensitive antibody against Abeta38 to analyze the distribution of this Abeta species in cases of sporadic and familial AD, as well as in the brains of a series of established transgenic AD mouse models. We found Abeta38 to be present as vascular deposits in the brains of the majority of sporadic AD cases, whereas it is largely absent in non-demented control cases. Abeta38-positive extracellular plaques were virtually limited to familial cases. Interestingly we observed Abeta38-positive plaques not only among familial cases due to AbetaPP mutations, but also in cases of familial AD caused by presenilin (PSEN) mutations. Furthermore we demonstrate that Abeta38 deposits in the form of extracellular plaques are common in several AD transgenic mouse models carrying either only AbetaPP, or combinations of AbetaPP, PSEN1, and tau transgenes. |
