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Amyloid- protein dimers isolated directly from Alzheimer's brains impair synaptic plasticity and memory
Application of antibodies to the N-terminus of amyloid prevented the LTP and LTD deficiencies. Antibodies directed against the midregion of the C-terminus were not as successful.
If instead of soluble amyloid, insoluble amyloid plaque cores were used, still taken from a Morbus Alzheimer cortex, LTP was not impaired. In case the plaques were solubised and thus released amyloid dimers, LTP was also effectively inhibited. The plaques, therefore, seem to be mostly inactive except for segregating synaptotoxic amyloid dimers.
The research group suggest that soluble amyloid oligomers that were extracted from Morbus Alzheimer brains can very effectively inhibit the structure and function of synapses. Amyloid dimers seem to be the smallest synaptotoxic unit.
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