Antibody-mediated immunotherapy for Alzheimer's disease

Research output: Contribution to journalReview articlepeer-review


Immunotherapy against β-amyloid (Aβ) peptide in transgenic mouse models of Alzheimer's disease alleviates the amyloid-associated pathology via three distinct mechanisms. First, antibodies directed against the N-terminal region of Aβ plaques leads to the dissolution of Aβ in the CNS. Second, opsonization of amyloid by an antibody occurs and is thus cleared via Fc-dependent phagocytosis. However, both of these mechanisms require the entry of antibodies into the CNS. Conversely, the third mechanism involves the sequestering of plasma Aβ by antibodies, establishing a gradient favoring the efflux of Aβ from the CNS, and is thus not dependent upon the translocation of antibodies across the blood-brain barrier. Clearly, future therapeutic approaches for Alzheimer's disease depend on increased research into the various mechanisms of immunotherapy to successfully clear Aβ peptides.

Original languageEnglish
Pages (from-to)519-524
Number of pages6
JournalCurrent Opinion in Investigational Drugs
Issue number7
StatePublished - Jul 2007


  • Alzheimer's disease
  • Amyloid plaque
  • Amyloid-β
  • Immunotherapy
  • Inflammation
  • Neuropathology


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