Changes in mitochondrial dynamics during amyloid β-induced PC12 cell apoptosis.

Changes in mitochondrial morphology and dynamics influence mitochondrial function and ultimately damage neurons in Alzheimer's disease (AD). Amyloid β (Aβ) is a major factor in the pathogenesis of AD. Although it has been proved that Aβ can affect the dynamics of mitochondria, there is little known on the precise dynamic process. Thus, MTT, Hoechst 33342, and Annexin V/PI analysis were used to study Aβ(25-35) neurotoxity on PC12 cells, live cell station and image processing were applied to study the moving parameters and characters of mitochondria. We also studied changes of mitochondrial membrane potential and reactive oxygen species production. The results showed that long-term exposure of PC12 cells to Aβ(25-35) resulted in increase of mitochondrial number and decrease of mitochondrial length and size, which presented fluctuated during early time and dramatic changes occurred after 6 h. Low concentration exposure caused little mitochondrial changes before 24 h while short time exposure induced mitochondrial fragmentation that could be recovered to normal. Mitochondrial membrane potential dissipation and reactive oxygen species production were observed, as well as apparent cell apoptosis with significant morphological changes. These data suggest that mitochondrial fission can be reversed during Aβ(25-35)-induced PC12 cell apoptosis, depending on the concentration and exposure time of Aβ(25-35), which may be helpful in AD prevention and therapy.