“…Because the fusion activity of MFN1-MFN2 heterotypic oligomers is comparable to those of homo-oligomers of MFN1 or MFN2 (Detmer and Chan, 2007), overexpression of appoptosin might interfere with the fusion machinery by impairing the interaction between MFN1 and MFN2, thus leading to mitochondrial fragmentation. Interestingly, considerable efforts have been devoted to studying the fission machinery deficits in Alzheimer's disease, with a focus on DRP1, and findings show that excessive ROS increases DRP1 activity (Iqbal and Hood, 2014;Wu et al, 2011), that Aβ interacts with DRP1 and increases its activity (Manczak et al, 2011), that S-nitrosylation of DRP1 enhances its activity (Cho et al, 2009) and that phosphorylation of DRP1 at specific sites promotes its activity (Chang and Blackstone, 2007;Cribbs and Strack, 2007;Merrill et al, 2011;Meuer et al, 2007;Rambold et al, 2011;Rehman et al, 2012;Taguchi et al, 2007). In contrast, research on the fusion machinery during Alzheimer's disease is limited.…”