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Updated: Jul 8, 2025

Sensitive Detection of Proteopathic Seeding Activity with FRET Flow Cytometry
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Sensitive Detection of Proteopathic Seeding Activity with FRET Flow Cytometry

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Tau seeding without tauopathy.

Michael S LaCroix1, Efrosini Artikis2, Brian D Hitt3

  • 1Center for Alzheimer's and Neurodegenerative Diseases, Peter O'Donnell Jr. Brain Institute, University of Texas Southwestern Medical Center, Dallas, Texas, USA.

The Journal of Biological Chemistry
|December 10, 2023
PubMed
Summary

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This summary is machine-generated.

Healthy brains contain tau seeding activity, suggesting a normal function that may become pathogenic in Alzheimer's disease (AD). This prion-like tau propagation differs conformationally from AD tau.

Area of Science:

  • Neuroscience
  • Biochemistry

Background:

  • Neurodegenerative tauopathies, including Alzheimer's disease (AD), are characterized by the accumulation of tau protein assemblies in the brain.
  • Emerging evidence indicates tau may function as a prion, capable of self-propagation and transmission between cells and organisms.
  • This prion-like behavior suggests a cellular machinery for tau replication, potentially linked to a normal physiological role for tau seeds.

Purpose of the Study:

  • To investigate the presence of tau seeding activity in healthy human brain tissue.
  • To characterize the properties of tau seeds found in non-pathological brains.
  • To compare tau seeds from healthy controls with those found in Alzheimer's disease.

Main Methods:

  • Development and utilization of a novel monoclonal antibody (MD3.1) specific for tau seeds.
Keywords:
Alzheimer’s diseaseFRET biosensorhealthy brainpriontau seeding activitytauopathy

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  • Immunopurification of tau from the parietal and cerebellar cortices of healthy individuals (19-65 years old).
  • Detection of seeding activity using orthogonal assays, including real-time quaking-induced conversion (RT-QuIC) and antibody binding profiles.

    • Main Results:

    • Tau seeding activity was detected in the parietal cortex of healthy controls, but not in the cerebellum.
    • No seeding activity was observed in brain homogenates from wildtype or human tau knockin mice.
    • Seeding activity did not correlate with subject age or overall brain tau levels.
    • Conformational analysis revealed that control tau seeds differ from those in AD, suggesting distinct structural ensembles.

    Conclusions:

    • Healthy brains possess endogenous tau seeding activity, supporting the hypothesis of a normal physiological function for tau seeds.
    • The cellular and genetic context appears critical for the development of seed-competent tau.
    • The distinct conformational characteristics of tau seeds in controls versus AD suggest that a normal function may become aberrant in disease states.