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Intravenous immunoglobulin (IVIG) treatment exerts antioxidant and neuropreservatory effects in preclinical models of Alzheimer's disease.

Abstract
Intravenous immunoglobulin (IVIG) has shown limited promise so far in human clinical studies on Alzheimer's disease (AD), yet overwhelmingly positive preclinical work in animals and human brain cultures support the notion that the therapy remains potentially efficacious. Here, we elaborate on IVIG neuropreservation by demonstrating that IVIG protects human primary neurons against oxidative stress in vitro and that IVIG preserves antioxidant defense mechanisms in vivo. Based on these results, we propose the following translational impact: If the dosage and treatment conditions are adequately optimized, then IVIG treatment could play a significant role in preventing and/or delaying the progression of neurodegenerative diseases, such as AD. We suggest that IVIG warrants further investigation to fully exploit its potential as an anti-oxidant, neuroprotective and synapto-protecting agent.
AuthorsScott E Counts, Balmiki Ray, Elliott J Mufson, Sylvia E Perez, Bin He, Debomoy K Lahiri
JournalJournal of clinical immunology (J Clin Immunol) Vol. 34 Suppl 1 Pg. S80-5 (Jul 2014) ISSN: 1573-2592 [Electronic] Netherlands
PMID24760109 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't)
Chemical References
  • Amyloid beta-Protein Precursor
  • Immunoglobulins, Intravenous
  • Neuroprotective Agents
  • tau Proteins
  • Hydrogen Peroxide
Topics
  • Alzheimer Disease (immunology, therapy)
  • Amyloid beta-Protein Precursor (genetics)
  • Animals
  • Cell Survival (drug effects)
  • Cells, Cultured
  • Disease Models, Animal
  • Fetus
  • Humans
  • Hydrogen Peroxide (metabolism)
  • Immunoglobulins, Intravenous (administration & dosage)
  • Immunotherapy (methods)
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Neurogenic Inflammation (immunology, therapy)
  • Neurons (drug effects, physiology)
  • Neuroprotective Agents
  • Oxidative Stress (drug effects)
  • Primary Cell Culture
  • tau Proteins (genetics)

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