Peripheral clearance of amyloid β peptide by complement C3-dependent adherence to erythrocytes

Joseph Rogers, Rena Li, Diego Mastroeni, Andrew Grover, Brian Leonard, Geoffrey Ahern, Phillip Cao, Heather Kolody, Linda Vedders, William P. Kolb, Marwan Sabbagh

Research output: Contribution to journalArticle

118 Scopus citations

Abstract

Brain deposits of amyloid β peptide (Aβ) have been a diagnostic hallmark of Alzheimer's disease (AD) for nearly a century. Recent studies have demonstrated that Aβ is also present in peripheral blood. Here, we present evidence that circulating Aβ42 is subject to complement C3b-dependent adherence to complement receptor 1 (CR1) on erythrocytes, a classical set of mechanisms by which pathogens and proteins recognized as foreign are cleared from the bloodstream. Levels of Aβ42 targeted by this pathway differ significantly in AD compared to mild cognitive impairment and nondemented elderly controls.

Original languageEnglish (US)
Pages (from-to)1733-1739
Number of pages7
JournalNeurobiology of Aging
Volume27
Issue number12
DOIs
StatePublished - Dec 1 2006

Keywords

  • Alzheimer's disease
  • Amyloid β peptide
  • Blood
  • Clearance
  • Complement

ASJC Scopus subject areas

  • Neuroscience(all)
  • Aging
  • Clinical Neurology
  • Developmental Biology
  • Geriatrics and Gerontology

Fingerprint Dive into the research topics of 'Peripheral clearance of amyloid β peptide by complement C3-dependent adherence to erythrocytes'. Together they form a unique fingerprint.

  • Cite this

    Rogers, J., Li, R., Mastroeni, D., Grover, A., Leonard, B., Ahern, G., Cao, P., Kolody, H., Vedders, L., Kolb, W. P., & Sabbagh, M. (2006). Peripheral clearance of amyloid β peptide by complement C3-dependent adherence to erythrocytes. Neurobiology of Aging, 27(12), 1733-1739. https://doi.org/10.1016/j.neurobiolaging.2005.09.043