Fig. (3).

The ABAD decoy peptide approach. Left: Levels of Aβ are elevated in the AD mouse model (and the human AD brain), increasing its binding to loop D in ABAD. Endophilin-1 and peroxiredoxin-2 expression levels are increased in the AD mouse model as a result of the ABAD-Aβ interaction, which also causes neuronal cellular stress (increased ROS production, impaired metabolism, resulting in reduced plasma membrane integrity and LDH-release and apoptosis). Right: Administration of modified peptides based to the loop D amino acid sequence of ABAD are able to disrupt the ABAD-Aβ interaction in the AD mouse model in vivo, decrease the expression of endophilin-1 and peroxiredoxin-2 and restore cellular function and memory performance.