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- Title
Amyloid β Protein Dimer-Containing Human CSF Disrupts Synaptic Plasticity: Prevention by Systemic Passive Immunization.
- Authors
Klyubin, Igor; Betts, Vicki; Welzel, Alfred T.; Blennow, Kaj; Zetterberg, Henrik; Wallin, Anders; Lemere, Cynthia A.; Cullen, William K.; Ying Peng; Wisniewski, Thomas; Selkoe, Dennis J.; Anwyl, Roger; Walsh, Dominic M.; Rowan, Michael J.
- Abstract
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 the structure of Aβ depends on its source and the presence of cofactors, it is of great interest to determine whether human-derived oligomeric Aβ species impair brain function and, if so, whether or not their disruptive effects can be prevented using antibodies. We report that untreated ex vivo human CSF that contains Aβ dimers rapidly inhibits hippocampal long-term potentiation in vivo and that acute systemic infusion of an anti-Aβ monoclonal antibody can prevent this disruption of synaptic plasticity. Aβ monomer isolated from human CSF did not affect long-term potentiation. These results strongly support a strategy of passive immunization against soluble Aβ oligomers in early Alzheimer's disease.
- Subjects
AMYLOID beta-protein; CEREBROSPINAL fluid; NEUROPLASTICITY; ALZHEIMER'S disease; IMMUNIZATION
- Publication
Journal of Neuroscience, 2008, Vol 28, Issue 16, p4231
- ISSN
0270-6474
- Publication type
Article
- DOI
10.1523/JNEUROSCI.5161-07.2008