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Neuroinflammation and Tauopathies
Marie-Noel Zeenny, Ingrid Salame, Lynn Maatouk, Elias Akoury. Molecular biology reports, 2026-06-30
Topic: Inflammation, microglia and astrocytes
Alzheimer's disease (AD) and related Tauopathies are neurodegenerative disorders characterized by the accumulation of hyperphosphorylated Tau protein in neurofibrillary tangles and frequently accompanied by amyloid-β (Aβ) pathology.1 While Tau aggregation has long been considered a primary driver of neurodegeneration, growing evidence highlights neuroinflammation as a central and early contributor to disease onset and progression. This review combines current knowledge on the molecular and cellular mechanisms linking Tau pathology to chronic neuroinflammatory signaling, with a particular focus on microglia- and astrocyte-mediated responses. We discuss how dysregulated kinase-phosphatase balance, impaired proteostasis, and oxidative stress promote Tau hyperphosphorylation and aggregation, and how these processes are amplified by innate immune pathways, including TREM2-DAP12, toll-like receptors, GPCR signaling, the PI3K-Akt/PTEN axis, Wnt/β-catenin signaling, and the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome. Special emphasis is placed on the transition from early protective glial responses to chronic inflammation, which fosters prion-like propagation of Tau and accelerates synaptic dysfunction and neuronal loss. Finally, we evaluate emerging therapeutic strategies aimed at modulating neuroinflammatory pathways and restoring signaling homeostasis, highlighting their potential to slow or halt disease progression. Collectively, this review positions neuroinflammation as a critical mechanistic link between Tau pathology and neurodegeneration, underscoring its relevance as a therapeutic target in AD and other Tauopathies.
Key findings
- This review combines current knowledge on the molecular and cellular mechanisms linking Tau pathology to chronic neuroinflammatory signaling, with a particular focus on microglia- and astrocyte-mediated responses.
- We discuss how dysregulated kinase-phosphatase balance, impaired proteostasis, and oxidative stress promote Tau hyperphosphorylation and aggregation, and how these processes are amplified by innate immune pathways, including TREM2-DAP12, toll-like receptors, GPCR signaling, the PI3K-Akt/PTEN axis, Wnt/β-catenin signaling, and the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome.
- Special emphasis is placed on the transition from early protective glial responses to chronic inflammation, which fosters prion-like propagation of Tau and accelerates synaptic dysfunction and neuronal loss.
- Finally, we evaluate emerging therapeutic strategies aimed at modulating neuroinflammatory pathways and restoring signaling homeostasis, highlighting their potential to slow or halt disease progression.
- Collectively, this review positions neuroinflammation as a critical mechanistic link between Tau pathology and neurodegeneration, underscoring its relevance as a therapeutic target in AD and other Tauopathies.
Study details
- Evidence strengthLow
How this study scored 45/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it. We have no data on journal's citation record, times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record, multi-centre collaboration and free to read, so those were left out: it earned 25 of the 56 points we could judge it on, which is 45 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Molecular biology reports) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 5 / 5 | 2026 — within 1 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | — / 7 | No citation count (not found in OpenAlex) — left out of this score |
| Citations per year | — / 5 | No citation count or no year — left out of this score |
| Impact for its field and year | — / 6 | No field-weighted citation impact (OpenAlex has none yet) — left out of this score |
| Cited by studies here | — / 6 | Not yet checked against this library's citation graph — left out of this score |
| Still being cited | — / 4 | No yearly citation counts — left out of this score |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | — / 3 | No institution listed in OpenAlex — left out of this score |
| Multi-centre collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 42377782) |
| Free to read | — / 2 | Access not recorded — left out of this score |
| Points | 25 / 56 | Scored on 10 of 20 parts. We have no data for the rest, so they are left out: 25 of the 56 points we could judge it on is 45 out of 100. |
| Total | 45 / 100 | — |
What each of these 20 components measures, and what this score is not →
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Cite this study APA, Vancouver, BibTeX · download .bib or .ris
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APA 7th
Zeenny, M.-N., Salame, I., Maatouk, L., & Akoury, E. (2026). Neuroinflammation and Tauopathies. Molecular biology reports. https://doi.org/10.1007/s11033-026-12253-4
Vancouver
Zeenny M.-N, Salame I, Maatouk L, Akoury E. Neuroinflammation and Tauopathies. Molecular biology reports. 2026. doi:10.1007/s11033-026-12253-4. PMID: 42377782.
BibTeX
@article{zeenny2026-42377782,
author = {Zeenny, Marie-Noel and Salame, Ingrid and Maatouk, Lynn and Akoury, Elias},
title = {{Neuroinflammation and Tauopathies}},
journal = {Molecular biology reports},
year = {2026},
doi = {10.1007/s11033-026-12253-4},
pmid = {42377782},
url = {https://doi.org/10.1007/s11033-026-12253-4}
}
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