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This page is alzhub.org's plain-English summary of a published study, not the paper itself. It is generated from the record we hold for this study, sourced and linked below — check the original for the full text and methods.

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Disease mechanisms

Topic: Brain proteins, microglia and lab models

Tau, mainly expressed in neurons and less expressed in glial cells (astrocytes and oligodendrocytes) and peripheral tissues, is involved in the assembly and stabilization of microtubules, and other biological processes such as axonal transport, metal ion transport, etc. Dysfunction of tau, caused by mutations, hyperphosphorylation, aggregation, or reduced expression, is closely associated with tauopathies (e.g., Alzheimer disease) and psychiatric disorders. Tau-based biomarkers have emerged as predictive/diagnostic tools for these conditions. However, despite advancing to clinical trials, tau-targeted therapies have demonstrated limited efficacy in diseases. Therefore, this review aims to systematically summarize tau's physiological and pathological functions, the progress in tau-targeted therapies, and the development of tau as a disease biomarker, as well as to discuss critical gaps in understanding tau's pathophysiological roles and therapeutic translatability.

Key findings

Why it matters

This review notes that tau-targeted therapies have shown limited efficacy in diseases despite reaching clinical trials. It summarizes tau biology and biomarker development while pointing to critical gaps in understanding tau's role and the translatability of treatments.

Study details

How this study scored 36/100
How this study's score is builtJournal tier 7 of 10; Journal's citation record 0 of 4; Study design 0 of 12; Strength of evidence 1 of 5; Peer-review validation 10 of 10; How recent 4 of 5; Sample size 0 of 4; Effect reported 0 of 3; Studied in people 0 of 3; Randomised / blinded 0 of 2; Times cited 2 of 7; Citations per year 1 of 5; Impact for its field and year 2 of 6; Cited by studies here 0 of 6; Still being cited 1 of 4; Senior author's track record left out, no data; Institution's track record 1 of 3; Multi-centre collaboration 2 of 3; Indexed in PubMed 2 of 2; Free to read 2 of 2. 35 of the 96 points it could be judged on, which is 36 of 100. Total 36 of 100.35 of the 96 points we could judge = 36 of 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 senior author's track record, so that was left out: it earned 35 of the 96 points we could judge it on, which is 36 out of 100.

ComponentPointsWhy
Journal tier 7 / 10 Tier 3 — peer-reviewed journal (Genomic psychiatry :)
Journal's citation record 0 / 4 Genomic psychiatry :: journal h-index 5 (OpenAlex, 2026-10-29)
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 4 / 5 2025 — within 3 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 2 / 7 Cited 5 times (OpenAlex, 2026-10-10)
Citations per year 1 / 5 1.7 citations a year over 3 year(s) since 2025
Impact for its field and year 2 / 6 Cited 2.7× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here 0 / 6 No other study in this library cites it
Still being cited 1 / 4 Cited 5 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record — / 4 Senior author's record not available — left out of this score
Institution's track record 1 / 3 Sichuan University: institution h-index 720 (OpenAlex)
Multi-centre collaboration 2 / 3 OpenAlex lists 4 institution(s) in 2 countries
Indexed in PubMed 2 / 2 Indexed in PubMed (PMID 41488807)
Free to read 2 / 2 Free to read
Points 35 / 96 Scored on 19 of 20 parts. We have no data for the rest, so they are left out: 35 of the 96 points we could judge it on is 36 out of 100.
Total 36 / 100 —

What each of these 20 components measures, and what this score is not →

Read the original

Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).

Cite this study APA, Vancouver, BibTeX · download .bib or .ris

Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.

APA 7th

Tang, F., Wei, J., Wong, M.-L., & Lei, P. (2025). Tau protein: Physiological functions and multifaceted roles in neurodegenerative and psychiatric disorders. Genomic psychiatry :. https://doi.org/10.61373/gp025i.0122

Vancouver

Tang F, Wei J, Wong M.-L, Lei P. Tau protein: Physiological functions and multifaceted roles in neurodegenerative and psychiatric disorders. Genomic psychiatry :. 2025. doi:10.61373/gp025i.0122. PMID: 41488807.

BibTeX

@article{tang2025-41488807,
  author  = {Tang, Fei and Wei, Junfen and Wong, Ma-Li and Lei, Peng},
  title   = {{Tau protein: Physiological functions and multifaceted roles in neurodegenerative and psychiatric disorders}},
  journal = {Genomic psychiatry :},
  year    = {2025},
  doi     = {10.61373/gp025i.0122},
  pmid    = {41488807},
  url     = {https://doi.org/10.61373/gp025i.0122}
}

Studies this one cites

Referenced by this study and also in the alzhub library, so you can read them here. Showing 12 of 36.

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