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Amyloid- protein dimers isolated directly from Alzheimer's brains impair synaptic plasticity and memory

Scientists of Harvard University succeeded in extracting soluble amyloid-beta protein oligomers directly from the cerebral cortex of patients. The amyloid-beta oligomers effectively inhibited long-term potentiation (LTP), enhanced long-term depression (LTD) and reduced dendritic spine density in normal rodent hippocampus, the brain centre of long-term memory.

Soluble from the diseased brains blocked the memory of learned behaviour in healthy rats. Abeta dimers were especially potent. were required for the LTD enhancement, and were required for the spine loss.

Application of antibodies to the prevented the LTP and LTD deficiencies. Antibodies directed against the midregion of the were not as successful.

If instead of soluble amyloid, insoluble amyloid plaque cores were used, still taken from a 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 brains can very effectively inhibit the structure and function of synapses. dimers seem to be the smallest synaptotoxic unit.

Related antibodies on antibodies-online.com:

Amyloid, N-terminal

N-methyl D-aspartate receptors:



Glutamate Receptor, Ionotropic, N-methyl D-aspartate receptor 3a
Glutamate Receptor, Ionotropic, N-methyl D-aspartate receptor 3b

Metabotropic glutamate receptors:
Glutamate receptor, metabotropic 1
Glutamate receptor, metabotropic 2
Glutamate receptor, metabotropic 3

Glutamate receptor, metabotropic 7
Glutamate receptor, metabotropic 8

Antibodies for the research area Morbus Alzheimer:

Antibodies for the research area receptors: