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Intravenous immunoglobulins: a treatment for Alzheimer’s disease?

¹ Department of Immunopathology, Sanquin Research at CLB, Amsterdam
² Department of Neurology and Alzheimer Center, VU University Medical Center, 1007 HVAmsterdam, The Netherlands

Correspondence to:
Correspondence to:
Professor P Scheltens
Department of Neurology and Alzheimer Center, VU University Medical Center, PO Box 7057, Amsterdam, 1007 HV, the Netherlands; p.scheltens@vumc.nl

Abbreviations: AD, Alzheimer’s disease; APP, amyloid precursor protein; IG, immunoglobulins; SAP, serum amyloid P component

Keywords: Alzheimer’s disease; immunoglobulins; ageing; dementia; therapy

The first 150 words of the full text of this article appear below.

Aß-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 1-antichymotrypsin. Observations in mice carrying the human APP transgene support the importance of Aß-peptide as a driving force for intracerebral amyloid deposits in AD. The mechanisms leading to neurotoxicity and neurodegeneration induced by Aß-peptide are not yet clear. According to one scenario deposits of Aß-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 Aß-oligomers as mediators of neurotoxicity.¹ Clearance of intracerebral amyloid deposits is currently one of the therapeutic options under investigation for AD.

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