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Early Insulin Signaling Abnormalities and Oxidative Stress Responses in PS19 Tau Transgenic Mice
Elahi M, Burd I, Yang P, Shen W.. bioRxiv, 2026-10-22
Topic: Disease mechanisms in lab and animal studies
Pathological tau accumulation is a hallmark of Alzheimer’s disease (AD), yet its relationship with impaired insulin signaling remains unclear. Previously, we reported altered IRS1 phosphorylation reduced p-IRβ, and GLUT3 expression in young AD transgenic mice prior to overt pathology. Here, we investigated insulin signaling and oxidative stress pathways in the Tau P301S (PS19) mouse model. We found that alterations in phospho-IRS1, phospho-IRβ, and the glucose transporters GLUT3 and GLUT4 occur before pathogenic tau deposition. In stable tau-expressing human neuronal cell lines, tau expression was similarly associated with impaired insulin signaling. Concurrent dysregulation of insulin signaling and activation of oxidative stress-responsive kinases, accompanied by increased microglial abundance, were evident in 2- month-old PS19 mice and persisted into adulthood. Together, these findings demonstrate that insulin signaling abnormalities and oxidative stress kinase activation are early and sustained features of PS19 tauopathy, preceding the onset of overt neuropathology. Graphical Abstract
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Elahi, M., Burd, I., Yang, P., & Shen, W. (2026). Early Insulin Signaling Abnormalities and Oxidative Stress Responses in PS19 Tau Transgenic Mice. bioRxiv. https://doi.org/10.64898/2026.10.16.759692
Vancouver
Elahi M, Burd I, Yang P, Shen W. Early Insulin Signaling Abnormalities and Oxidative Stress Responses in PS19 Tau Transgenic Mice. bioRxiv. 2026. doi:10.64898/2026.10.16.759692.
BibTeX
@article{elahi2026-5cb25560,
author = {Elahi, M. and Burd, I. and Yang, P. and Shen, W.},
title = {{Early Insulin Signaling Abnormalities and Oxidative Stress Responses in PS19 Tau Transgenic Mice}},
journal = {bioRxiv},
year = {2026},
doi = {10.64898/2026.10.16.759692},
url = {https://doi.org/10.64898/2026.10.16.759692}
}
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Key findings
- We found that alterations in phospho-IRS1, phospho-IRβ, and the glucose transporters GLUT3 and GLUT4 occur before pathogenic tau deposition.
- In stable tau-expressing human neuronal cell lines, tau expression was similarly associated with impaired insulin signaling.
- Together, these findings demonstrate that insulin signaling abnormalities and oxidative stress kinase activation are early and sustained features of PS19 tauopathy, preceding the onset of overt neuropathology.
Study details
- Evidence strengthLow
How this study scored 16/100
Preprint — not yet peer-reviewed. It scored 21 on the same rubric, but non-peer-reviewed sources are capped at 16, so it shows as 16. Scored zero for study design, sample size, effect reported and randomised / blinded because the record does not state it. We have no data on 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 and multi-centre collaboration, so those were left out: it earned 13 of the 62 points we could judge it on, which is 21 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 2 / 10 | Tier 4 — not a peer-reviewed journal (bioRxiv) |
| Journal's citation record | 0 / 4 | Not a journal article, so the journal's record does not count |
| 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 | 4 / 10 | Preprint — not yet peer-reviewed. Hosted on a preprint server. |
| 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 | Laboratory or animal study (title names “transgenic”) — scores zero |
| 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 | 1 / 2 | Not in PubMed, but has a DOI |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 13 / 62 | Scored on 12 of 20 parts. We have no data for the rest, so they are left out: 13 of the 62 points we could judge it on is 21 out of 100. |
| Total | 21 / 100 | Capped to 16 because this is not a peer-reviewed article. |
What each of these 20 components measures, and what this score is not →
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