Absence of synaptophysin near cortical neurons containing oligomer Aβ in Alzheimer's disease brain

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Abstract
Soluble amyloid β protein (Aβ) oligomers have been considered recently to be responsible for the cognitive dysfunction that sets in prior to senile plaque formation in the Alzheimer's disease (AD) brain. By using the newly prepared antibody against oligomer Aβ, rather than fibrillar or monomer Aβ, we observed that oligomer Aβ in AD brains was localized as clusters ofdot‐likeimmunostains in the neurons in a manner different from that in senile plaques. The relationship of oligomer Aβ with synaptophysin, a synaptic molecular marker, was examined because oligomer Aβ is widely believed to be related to synaptic failure. We observed that immunostainings for synaptophysin were absent near neurons bearing clusters of oligomer Aβ. The present study provides morphological evidence to support the idea that accumulated oligomer Aβ, but not fibrillar Aβ, is closely associated with synaptic failure, which is the major cause of cognitive dysfunction.