Intravenous immunoglobulins: a treatment for Alzheimer’s disease?
- 1Department of Immunopathology, Sanquin Research at CLB, Amsterdam
- 2Department of Neurology and Alzheimer Center, VU University Medical Center, 1007 HVAmsterdam, The Netherlands
- Correspondence to: Professor P Scheltens Department of Neurology and Alzheimer Center, VU University Medical Center, PO Box 7057, Amsterdam, 1007 HV, the Netherlands; p.scheltensvumc.nl
- AD, Alzheimer’s disease
- APP, amyloid precursor protein
- IG, immunoglobulins
- SAP, serum amyloid P component
A novel therapeutic option for Alzheimer’s disease
Aβ-peptide is generally considered to play a central role in the pathogenesis of Alzheimer’s disease (AD). The peptide is cleaved from amyloid precursor protein (APP) by secretases and is a key component of the amyloid plaques. Amyloid plaques may also contain other proteins such as serum amyloid P component (SAP), activated complement proteins, clusterin, and α1-antichymotrypsin. Observations in mice carrying the human APP transgene support the importance of Aβ-peptide as a driving force for intracerebral amyloid deposits in AD. The mechanisms leading to neurotoxicity and neurodegeneration induced by Aβ-peptide are not yet clear. According to one scenario deposits of Aβ-fibrils, together with associated proteins, are toxic for neurones—either directly or indirectly—by recruitment and stimulation of microglial cells. An alternative scenario claims a major role of Aβ-oligomers as mediators of neurotoxicity.1 Clearance of intracerebral amyloid deposits is currently one of the therapeutic options under investigation for AD.
Recently it was found that vaccination with Aβ-peptide slowed down the amyloid accumulation in the brains of APP transgenic mice,2 the effect of which could be reproduced by administration of anti-Aβ antibodies.3 This has …
