Complement activation by neurofibrillary tangles in Alzheimer's disease

Yong Shen, Lih Fen Lue, Li Bang Yang, Alex Roher, Yu Min Kuo, Ronald Strohmeyer, Warren J. Goux, Virginia Lee, Gail V.W. Johnson, Scott D. Webster, Neil R. Cooper, Bonnie Bradt, Joseph Rogers

Research output: Contribution to journalArticlepeer-review

118 Scopus citations


Brain inflammation is widely documented to occur in Alzheimer's disease (AD), but its sources are still incompletely understood. Here, we present in vitro and in situ evidence that, like amyloid β peptide (Aβ), tau, the major protein constituent of the neurofibrillary tangle, is a potent, antibody-independent activator of the classical complement pathway. Complement activation, in turn, is known to drive numerous inflammatory responses, including scavenger cell activation and cytokine production. Because Aβ deposits and extracellular tangles are present from early preclinical to terminal stages of AD, their ability to activate complement provides a ready mechanism for initiating and sustaining chronic, low-level inflammatory responses that may cumulate over the disease course.

Original languageEnglish (US)
Pages (from-to)165-168
Number of pages4
JournalNeuroscience Letters
Issue number3
StatePublished - Jun 15 2001

Bibliographical note

Funding Information:
Supported by NIA AGO7367, the Alzheimer’s Association, and the Arizona Alzheimer’s Center.


  • Alzheimer's disease
  • Complement
  • Inflammation
  • Neurofibrillary tangles
  • Paired helical filaments
  • Tau

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