 According to the Amyloid hypothesis, the accumulation of extracellular amyloid betapeptides (Aβ) into plaques via oligomerization leads to hallmark symptomatic conditions of AD through synaptic dysfunction and neurodegeneration.Immunotherapy via exogenous monoclonal antibody (MAB) administration has been known to treat various central nervous disorders, such as AD, by inhibiting Aβ-oligomerization thereby preventing neurotoxicity.However, MABs are large for passive protein channels and are therefore inefficient due to the blood-brain barrier preventing MAB passage into the brain.