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Updated: Jul 1, 2026
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
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.
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.
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