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Intravenous immunoglobulins containing antibodies against β-amyloid for the treatment of Alzheimer’s disease
  1. R C Dodel1,
  2. Y Du2,
  3. C Depboylu1,
  4. H Hampel3,
  5. L Frölich4,
  6. A Haag5,
  7. U Hemmeter6,
  8. S Paulsen7,
  9. S J Teipel3,
  10. S Brettschneider3,
  11. A Spottke1,
  12. C Nölker1,
  13. H J Möller3,
  14. X Wei2,
  15. M Farlow2,
  16. N Sommer5,
  17. W H Oertel5
  1. 1Department of Neurology, Friedrich-Wilhelms-University, Bonn, Germany
  2. 2Department of Neurology, Indiana University Medical School, Indianapolis, USA
  3. 3Department of Psychiatry, Ludwig-Maximilians-University, Munich, Germany
  4. 4Department of Psychiatry, Johann Wolfgang Goethe University, Frankfurt, Germany
  5. 5Department of Neurology, Philipps-University Marburg, Germany
  6. 6Department of Psychiatry, Philipps-University Marburg, Germany
  7. 7Department of Psychiatry, University of Giessen, Germany
  1. Correspondence to:
 R C Dodel
 Department of Neurology, Friedrich-Wilhelms-University, Sigmund-Freudstr. 25, 53105 Bonn, Germany;


Objective: Active or passive immunisation can mitigate plaque pathology in murine models of Alzheimer’s disease (AD). Recently, it has been shown that antibodies against β-amyloid (Aβ) are present in human immunoglobulin preparations (IVIgG), which specifically recognise and inhibit the neurotoxic effects of Aβ. This study reports the results from a pilot study using IVIgG in patients with AD.

Methods: Five patients with AD were enrolled and received monthly IVIgG over a 6 month period. Efficacy assessment included total Aβ/Aβ1–42 measured in the CSF/serum as well as effects on cognition (ADAS-cog; CERAD) at baseline and at 6 months following IVIgG.

Results: Following IVIgG, total Aβ levels in the CSF decreased by 30.1% (17.3–43.5%) compared to baseline (p<0.05). Total Aβ increased in the serum by 233% (p<0.05). No significant change was found in Aβ1–42 levels in the CSF/serum. Using ADAS-cog, an improvement of 3.7±2.9 points was detected. Scores in the MMSE were essentially unchanged (improved in four patients, stable in one patient) following IVIgG compared to baseline.

Conclusion: Although the sample size of this pilot study is too small to draw a clear conclusion, the results of this pilot study provide evidence for a more detailed investigation of IVIgG for the treatment of AD.

  • Aβ, β-amyloid
  • AD, Alzheimer’s disease
  • CSF, cerebrospinal fluid
  • IVlgG, human immunoglobulin preparations
  • MMSE, Mini-Mental State Examination
  • alzheimer
  • immunoglobulin
  • beta amyloid
  • immunisation

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  • Funding: This study was supported in part by the Alzheimer Forschungsinitiative (grant: 00806), Germany.

  • Competing interest: Octapharma (Lagenfeld, Germany) provided the intravenous immunoglobulins and Eli Lilly and Company (Indianapolis, USA) provided the Aβ antibodies for this study. Both companies had no impact on the design and the data analysis in this investigator driven study.

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