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Brain Advance Access published online on June 23, 2003
Brain, doi:10.1093/brain/awg191
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© 2003 The Guarantors of Brain

Article

Human anti-{beta}-amyloid antibodies block {beta}-amyloid fibril formation and prevent {beta}-amyloid-induced neurotoxicity

Yansheng Du 1*, Xing Wei 1, Richard Dodel 2, Norbert Sommer 3, Harald Hampel 4, Feng Gao 1, Zhizhong Ma 1, Liming Zhao 1, Wolfgang H. Oertel 3, and Martin Farlow 1

1 Department of Neurology, Indiana University School of Medicine, Indianapolis, IN, USA
2 Department of Neurology, Friedrich-Wilhelms-University, Bonn, Germany
3 Department of Neurology, Philipps University, Marburg, Germany
4 Department of Psychiatry, Ludwig-Maximilian University, Munich, Germany

* Corresponding author. E-mail: ydu{at}iupui.edu.

Received 25 November 2002 ; revised 31 March 2003 ; accepted 7 April 2003

Abstract

The accumulation of {beta}-amyloid (A{beta}) in neuritic plaques is thought to be causative for the progression of Alzheimer's disease (AD). Recently, both active immunization and passive administration of A{beta} antibodies dramatically attenuated amyloid plaque deposition, neuritic dystrophy, astrogliosis and behaviour deficits in transgenic animals. In addition, we and others have found that titres of naturally occurring anti-A{beta} antibodies in the CSF of AD patients are significantly lower than those in age-matched controls. Treatment with intravenous immunoglobulins (a preparation that contained anti-A{beta} antibodies) significantly lowered CSF levels of A{beta} in non-demented patients. In this study, anti-A{beta} antibodies were isolated from immunoglobulin preparations and these anti-A{beta} antibodies strongly block fibril formation or disrupt formation of fibrilar structures. Furthermore, these antibodies almost completely prevented neurotoxicity of A{beta}. In contrast, immunoglobulins depleted of anti-A{beta} antibodies had little effect on A{beta} fibril formation or protection of neuronal cells. This study supports the findings that human anti-A{beta} antibodies may interfere with the pathogenesis of AD by more than one mechanism, and administration of polyclonal human anti-A{beta} antibodies isolated from plasma is a potential therapeutic agent to prevent or slow down disease progression.

Keywords: Alzheimer's disease; {beta}-amyloid; neurotoxicity; immunotherapy; A{beta} antibodies
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