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Neurosci Lett. 2001 Jun 15;305(3):165-8.

Complement activation by neurofibrillary tangles in Alzheimer's disease.

Author information

1
Sun Health Research Institute, 10515 West Santa Fe Drive, Sun City, AZ 85351, USA

Abstract

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 beta peptide (Abeta), 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 Abeta 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.

PMID:
11403931
DOI:
10.1016/s0304-3940(01)01842-0
[Indexed for MEDLINE]

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