Objective The loss of cortical and hippocampal synapses is a universal hallmark of
Alzheimer's disease, and probably underlies its effects on cognition. Synapses are formed
from the interaction of neurites projecting from “presynaptic” neurons with dendritic spines
projecting from “postsynaptic” neurons. Both of these structures are vulnerable to the toxic
effects of nearby amyloid plaques, and their loss contributes to the decreased number of
synapses that characterize the disease. A treatment that increased the formation of neurites …