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Related Experiment Video

Updated: Jul 1, 2026

In Vitro Aggregation Assays Using Hyperphosphorylated Tau Protein
09:22

In Vitro Aggregation Assays Using Hyperphosphorylated Tau Protein

Published on: January 2, 2015

Neuroinflammation and Tauopathies.

Marie-Noel Zeenny1, Ingrid Salame2, Lynn Maatouk1

  • 1Department of Biology, Holy Spirit University of Kaslik, Kaslik, Lebanon.

Molecular Biology Reports
|June 30, 2026
PubMed
Summary

Neuroinflammation is a key driver in Alzheimer's disease (AD) and Tauopathies, linking Tau pathology to neurodegeneration. Targeting these inflammatory pathways offers promising therapeutic strategies for AD and related disorders.

Keywords:
BiomarkersMicrogliaNeurodegenerative diseasesNeuroinflammationTauopathies

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Last Updated: Jul 1, 2026

In Vitro Aggregation Assays Using Hyperphosphorylated Tau Protein
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Published on: January 2, 2015

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An In Vitro Model for Studying Tau Aggregation Using Lentiviral-mediated Transduction of Human Neurons

Published on: May 23, 2019

Area of Science:

  • Neuroscience
  • Immunology
  • Pathology

Background:

  • Alzheimer's disease (AD) and Tauopathies involve Tau protein aggregation and amyloid-β (Aβ) pathology.
  • Neuroinflammation is increasingly recognized as an early and central factor in neurodegenerative disease progression.

Purpose of the Study:

  • To review molecular and cellular mechanisms linking Tau pathology to chronic neuroinflammatory signaling.
  • To emphasize the role of microglia and astrocytes in AD pathogenesis.
  • To evaluate therapeutic strategies targeting neuroinflammation.

Main Methods:

  • Literature review synthesizing current knowledge on Tau pathology and neuroinflammation.
  • Focus on innate immune pathways (e.g., TREM2, TLRs, NLRP3 inflammasome).
  • Analysis of glial responses and their transition to chronic inflammation.

Main Results:

  • Dysregulated cellular processes (kinase-phosphatase balance, proteostasis, oxidative stress) promote Tau hyperphosphorylation and aggregation.
  • Innate immune pathways amplify Tau pathology and neuroinflammation.
  • Chronic inflammation facilitates Tau propagation, synaptic dysfunction, and neuronal loss.

Conclusions:

  • Neuroinflammation is a critical mechanistic link between Tau pathology and neurodegeneration in AD and Tauopathies.
  • Modulating neuroinflammatory pathways is a promising therapeutic approach.
  • Restoring signaling homeostasis may slow or halt disease progression.