Selective increase in cellular Aβ42 is related to apoptosis but not necrosis

Amyloid β protein ending at 42 (Aβ42) plays an important role in the pathology of Alzheimer's disease (AD). Here we show an increase in cellular Aβ42 in damaged neurons, with both ELISA and immunocytochemistry. The cellular Aβ42 increase was caused by 3-day treatments with H 2 O 2 , etoposide or melphalan, all of which induce genotoxic apoptosis, but not by treatment with sodium azide, which causes necrosis. Secreted Aβ was similarly decrease with all these treatments. The cellular Aβ42 increase appeared even with minimal damage (ELISA) and Aβ42-positive cells were TUNEL negative (double staining), indicating that nay early apoptosis mechanisms may induce the cellular Aβ42 increase may be linked in a way that contributes importantly to AD pathology.