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Updated: Jul 25, 2026
09:22
In Vitro Aggregation Assays Using Hyperphosphorylated Tau Protein
Published on: January 2, 2015
Complement activation by neurofibrillary tangles in Alzheimer's disease
1Sun Health Research Institute, 10515 West Santa Fe Drive, Sun City, AZ 85351, USA
Neuroscience Letters
|June 19, 2001
Summary
Tau protein, like amyloid beta, activates brain inflammation in Alzheimer's disease (AD) by triggering the complement pathway. This chronic inflammation may contribute to AD progression.
Area of Science:
- Neuroscience
- Immunology
- Pathology
Background:
- Brain inflammation is a known hallmark of Alzheimer's disease (AD).
- The precise sources initiating and sustaining this inflammation remain incompletely understood.
- Amyloid beta peptide (Abeta) is a known activator of inflammatory pathways in AD.
Purpose of the Study:
- To investigate the role of tau protein in activating complement-mediated inflammation in Alzheimer's disease.
- To determine if tau, similar to Abeta, can independently activate the classical complement pathway.
Main Methods:
- In vitro experiments to assess complement activation by tau.
- In situ studies to examine tau's role in the brain.
Main Results:
- Tau protein was identified as a potent activator of the classical complement pathway, independent of antibody presence.
- This activation mechanism is similar to that of amyloid beta peptide (Abeta).
- Complement activation by tau can drive inflammatory responses like scavenger cell activation and cytokine production.
Conclusions:
- Tau pathology, alongside Abeta, contributes to chronic neuroinflammation in Alzheimer's disease by activating the complement system.
- The presence of extracellular tau tangles provides a mechanism for sustained, low-level inflammatory responses throughout AD progression.
- Targeting tau-mediated complement activation may offer a novel therapeutic strategy for Alzheimer's disease.
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