The designed synthetic peptides have been shown to reduce the initial rate of Aβ fibrillization, inhibit the aggregation pathway of Aβ by reducing Aβ oligomer uptake and protect cultured hippocampal neurons from the oligomer-induced retraction of neurites and loss of cell membrane integrity [204] whereas D-peptide RD2D3 has been shown to be successful in interfering with the PrPC-Aβ oligomer assembly and has been proposed as a promising therapeutic agent in AD [223]. Here, PRNP is linked to Alzheimer disease.