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45/100

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Disease mechanisms

Topic: Amyloid, tau and blood-test diagnosis

Plain-language summary

Abstract Pathological tau isoforms, including hyperphosphorylated tau at serine 396 (pS396-tau) and tau oligomers (Oligo-tau), are elevated in the retinas of patients with mild cognitive impairment (MCI) due to Alzheimer’s disease (AD) and AD dementia. These patients exhibit significant retinal ganglion cell (RGC) loss, however the presence of tau isoforms in RGCs and their impact on RGC integrity, particularly in early AD, have not been studied. Here, we analyzed retinal superior temporal cross-sections from 25 MCI or AD patients and 16 age- and sex-matched cognitively normal controls. Using the RGC marker ribonucleic acid binding protein with multiple splicing (RBPMS) and Nissl staining, we found a 46–56% reduction in RBPMS + RGCs and Nissl + neurons in the ganglion cell layer (GCL) of MCI and AD retinas ( P < 0.05–0.001). RGC loss was accompanied by soma hypertrophy (10–50% enlargement, P < 0.05–0.0001), nuclear displacement, apoptosis (30–50% increase, P < 0.05–0.01), and prominent expression of granulovacuolar degeneration (GVD) bodies and GVD-necroptotic markers. Both pS396-tau and Oligo-tau were identified in RGCs, including in hypertrophic cells. PS396-tau + and Oligo-tau + RGC counts were significantly increased by 2.1–3.5-fold in MCI and AD retinas versus control retinas ( P < 0.05–0.0001). Tauopathy-laden RGCs strongly inter-correlated ( r P =0.85, P < 0.0001) and retinal tauopathy associated with RGC reduction ( r P =-0.40–(-0.64), P < 0.05–0.01). Their abundance correlated with brain pathology and cognitive deficits, with higher tauopathy-laden RGCs in patients with Braak stages (V–VI), clinical dementia ratings (CDR = 3), and mini-mental state examination (MMSE ≤ 26) scores. PS396-tau + RGCs in the central and mid-periphery showed the closest associations with disease status, while Oligo-tau + RGCs in the mid-periphery exhibited the strongest correlations with brain pathology (NFTs, Braak stages, ABC scores; r S =0.78–0.81, P < 0.001–0.0001) and cognitive decline (MMSE; r S =-0.79, P = 0.0019). Overall, these findings identify a link between pathogenic tau in RGCs and RGC degeneration in AD, involving apoptotic and GVD-necroptotic cell death pathways. Future research should validate these results in larger and more diverse cohorts and develop RGC tauopathy as a potential noninvasive biomarker for early detection and monitoring of AD progression.

What this study adds

Evidence grade: Low

Retinas from people with mild cognitive impairment or Alzheimer's dementia showed loss of retinal ganglion cells along with accumulation of phosphorylated and oligomeric tau. This describes what happens in eye tissue during the disease but does not test any treatment, cure, or prevention.

Taken from this record’s own fields, not from reading the paper. The grade is assigned from the abstract’s wording; what that means.

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

APA 7th

Davis, M. R., Robinson, E., Koronyo, Y., Salobrar‐García, E., Rentsendorj, A., Gaire, B. P., et al. (2025). Retinal ganglion cell vulnerability to pathogenic tau in Alzheimer’s disease. Acta Neuropathologica Communications. https://doi.org/10.1186/s40478-025-01935-y

Vancouver

Davis MR, Robinson E, Koronyo Y, Salobrar‐García E, Rentsendorj A, Gaire BP, et al. Retinal ganglion cell vulnerability to pathogenic tau in Alzheimer’s disease. Acta Neuropathologica Communications. 2025. doi:10.1186/s40478-025-01935-y. PMID: 39955563.

BibTeX

@article{davis2025-39955563,
  author  = {Davis, Miyah R. and Robinson, Edward and Koronyo, Yosef and Salobrar‐García, Elena and Rentsendorj, Altan and Gaire, Bhakta Prasad and Mirzaei, Nazanin and Kayed, Rakez and others},
  title   = {{Retinal ganglion cell vulnerability to pathogenic tau in Alzheimer’s disease}},
  journal = {Acta Neuropathologica Communications},
  year    = {2025},
  doi     = {10.1186/s40478-025-01935-y},
  pmid    = {39955563},
  url     = {https://doi.org/10.1186/s40478-025-01935-y}
}

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How to read this study

Design: our record does not state a study design, so check the methods section of the original before weighing the result.
Size: the record gives no participant count. Look for one in the original before trusting a pattern.
Effect: the record gives no effect size, so the summary above cannot say how large any difference was.

What the evidence grade means here

This page is graded low. alzhub.org assigns the grade automatically from keywords in the abstract, not from reading the paper. Low means the abstract matched neither pattern. It is the default label, and it does not mean the work is poor; many sound lab and imaging papers land here. It can add at most 5 of the 100 points in the study score, and it is a label about design, not a verdict on whether the findings are true.

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Key findings

These patients exhibit significant retinal ganglion cell (RGC) loss, however the presence of tau isoforms in RGCs and their impact on RGC integrity, particularly in early AD, have not been studied.
Using the RGC marker ribonucleic acid binding protein with multiple splicing (RBPMS) and Nissl staining, we found a 46–56% reduction in RBPMS + RGCs and Nissl + neurons in the ganglion cell layer (GCL) of MCI and AD retinas ( P < 0.05–0.001).
PS396-tau + and Oligo-tau + RGC counts were significantly increased by 2.1–3.5-fold in MCI and AD retinas versus control retinas ( P < 0.05–0.0001).
Tauopathy-laden RGCs strongly inter-correlated ( r P =0.85, P < 0.0001) and retinal tauopathy associated with RGC reduction ( r P =-0.40–(-0.64), P < 0.05–0.01).
Overall, these findings identify a link between pathogenic tau in RGCs and RGC degeneration in AD, involving apoptotic and GVD-necroptotic cell death pathways.

Why it matters

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 randomized / blinded because the record does not state it.

Component	Points	Why
Journal tier	7 / 10	Tier 3 — peer-reviewed journal (Acta Neuropathologica Communications)
Journal's citation record	1 / 4	Acta Neuropathologica Communications: journal h-index 129 (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)
Randomized / blinded	0 / 2	No randomization or blinding stated — scores zero (not stated in the record — scored 0)
Times cited	3 / 7	Cited 34 times (OpenAlex, 2026-10-10)
Citations per year	3 / 5	11.3 citations a year over 3 year(s) since 2025
Impact for its field and year	4 / 6	Cited 17.5× 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	2 / 4	Cited 34 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	2 / 4	Last-listed author Maya Koronyo‐Hamaoui: h-index 42 (OpenAlex, whole career)
Institution's track record	2 / 3	University of California, Los Angeles: institution h-index 1,923 (OpenAlex)
Multicenter collaboration	2 / 3	OpenAlex lists 8 institution(s) in 2 countries
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 39955563)
Free to read	2 / 2	Free to read
Total	45 / 100	—

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

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