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

134 Citations (Scopus)


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
Pages (from-to)165-168
Number of pages4
JournalNeuroscience Letters
Issue number3
Publication statusPublished - 2001 Jun 15

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)


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