Amyloid beta protein dimer-containing human CSF disrupts synaptic plasticity: prevention by systemic passive immunization.

摘要: The current development of immunotherapy for Alzheimer's disease is based on the assumption that human-derived amyloid β protein (Aβ) can be targeted in a similar manner to animal cell-derived or synthetic Aβ. Because structure Aβ depends its source and presence cofactors, it great interest determine whether oligomeric species impair brain function and, if so, not their disruptive effects prevented using antibodies. We report untreated ex vivo human CSF contains dimers rapidly inhibits hippocampal long-term potentiation acute systemic infusion an anti-Aβ monoclonal antibody prevent this disruption synaptic plasticity. monomer isolated from did affect potentiation. These results strongly support strategy passive immunization against soluble oligomers early disease.