Fig. (2).

Synaptic dysfunction caused by the ABAD-Aβ interaction. Binding of Aβ affects the enzymatic function of ABAD, thereby causing unfavorable changes in lipid metabolism and mitochondrial respiration. This ultimately leads to increased reactive oxygen species (ROS) production and impaired calcium (Ca²⁺) retention and provokes the up-regulation of peroxiredoxin-2 (Prx-2) and endophilin-1 (Ep-1). 1) Prx-2 is able to degrade ROS but its function can be affected by elevated Ca²⁺ leading to its phosphorylation and inactivation and the accumulation of ROS. 2) Ep-1 plays a role in glutamatergic (glut) synaptic transmission by functioning in synaptic vesicle endocytosis, which is directly regulated by Ca²⁺ binding to Ep-1 [80]. Ep-1 can also be involved in 3) JNK-activation as well as 4) signaling events in the post-synapse leading to dendritogenesis. The correct balance of all of these events in the synapse, which is disturbed by the ABAD-Aβ interaction, is of crucial importance for synaptic plasticity and memory formation.