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Cataract Aggravates Alzheimer-Like Pathologies and Cognitive Deficits in an APP/PS1 Mouse Model
Zhao Geng, Zhong-Yuan Yu, Jun Tan, Xuan-Yue Wang, Gui‐Hua Zeng, JL Li, Yu-Di Bai, Xiaoqin Zeng et al.. Neuroscience Bulletin, 2025-06-28
Topic: Amyloid, tau and blood-test diagnosis
Clinical investigations have suggested a potential link between cataracts and Alzheimer's disease (AD). However, whether cataract has an impact on the progression of AD remains unclear. The objective of this research was to determine the relationship between cataracts and AD. A cataract model was established in APP/PS1 [mutant amyloid precursor protein (APP) and a mutant presenilin-1 (PS1) gene] mice via lens puncture. Behavioural assays were used to evaluate cognitive function. Immunohistochemistry, immunofluorescence, and enzyme-linked immunosorbent assays (ELISA) were applied to detect AD-related pathology. Visual signals were markedly obstructed following surgery to induce cataracts, and these mice presented an increased cerebral amyloid-beta (Aβ) load, while no significant alterations in the levels of enzymes associated with Aβ metabolism were detected. In addition, compared with control mice, cataract model mice presented increased astrogliosis and microgliosis, along with elevated levels of proinflammatory factors. Moreover, cataract model mice presented more pronounced cognitive impairments than did control mice. Our study offers experimental confirmation that cataract considerably contributes to the pathogenesis of AD, thereby emphasizing the importance of visual signals in maintaining cognitive well-being.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Geng, Z., Yu, Z.-Y., Tan, J., Wang, X.-Y., Zeng, G., Li, J. L., et al. (2025). Cataract Aggravates Alzheimer-Like Pathologies and Cognitive Deficits in an APP/PS1 Mouse Model. Neuroscience Bulletin. https://doi.org/10.1007/s12264-025-01442-z
Vancouver
Geng Z, Yu Z.-Y, Tan J, Wang X.-Y, Zeng G, Li JL, et al. Cataract Aggravates Alzheimer-Like Pathologies and Cognitive Deficits in an APP/PS1 Mouse Model. Neuroscience Bulletin. 2025. doi:10.1007/s12264-025-01442-z. PMID: 40580389.
BibTeX
@article{geng2025-40580389,
author = {Geng, Zhao and Yu, Zhong-Yuan and Tan, Jun and Wang, Xuan-Yue and Zeng, Gui‐Hua and Li, JL and Bai, Yu-Di and Zeng, Xiaoqin and others},
title = {{Cataract Aggravates Alzheimer-Like Pathologies and Cognitive Deficits in an APP/PS1 Mouse Model}},
journal = {Neuroscience Bulletin},
year = {2025},
doi = {10.1007/s12264-025-01442-z},
pmid = {40580389},
url = {https://doi.org/10.1007/s12264-025-01442-z}
}
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. The record's author list ends in “et al.”, so not every author is named. Check the citation against the original before you use it.
Key findings
- Visual signals were markedly obstructed following surgery to induce cataracts, and these mice presented an increased cerebral amyloid-beta (Aβ) load, while no significant alterations in the levels of enzymes associated with Aβ metabolism were detected.
- In addition, compared with control mice, cataract model mice presented increased astrogliosis and microgliosis, along with elevated levels of proinflammatory factors.
Why it matters
In APP/PS1 mice, surgically induced cataracts led to increased cerebral Aβ load, more astrogliosis and microgliosis, higher proinflammatory factors, and more pronounced cognitive impairment than in control mice. These findings are from an animal model and suggest that visual signals may matter for cognitive well-being, but they do not establish a treatment or prevention for Alzheimer's disease in people.
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Study details
- Evidence strengthLow
How this study scored 35/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported 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 34 of the 96 points we could judge it on, which is 35 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Neuroscience Bulletin) |
| Journal's citation record | 1 / 4 | Neuroscience Bulletin: journal h-index 88 (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 | Laboratory or animal study (title names “app/ps1”) — scores zero |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 1 / 7 | Cited 3 times (OpenAlex, 2026-10-10) |
| Citations per year | 1 / 5 | 1.0 citations a year over 3 year(s) since 2025 |
| Impact for its field and year | 2 / 6 | Cited 1.6× 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 3 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | — / 4 | OpenAlex's profile for last-listed author Z. Li holds only 3 work(s), too few to judge a track record — left out of this score |
| Institution's track record | 0 / 3 | Army Medical University: institution h-index 478 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 4 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 40580389) |
| Free to read | 2 / 2 | Free to read |
| Points | 34 / 96 | Scored on 19 of 20 parts. We have no data for the rest, so they are left out: 34 of the 96 points we could judge it on is 35 out of 100. |
| Total | 35 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1007/s12264-025-01442-z
- PubMed: 40580389
- Original source →
- Free full text: Neuroscience Bulletin →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
Studies this one cites
Referenced by this study and also in the alzhub library, so you can read them here.
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