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Rock inhibitors in Alzheimer’s disease
Chao Zheng, Weiming Xia, Jianhua Zhang. Frontiers in Aging, 2025-03-20
Topic: Amyloid, tau and blood-test diagnosis
Alzheimer's disease (AD) is the most common age-related neurodegenerative disease and cause of dementia. AD pathology primarily involves the formation of amyloid β (Aβ) plaques and neurofibrillary tangles containing hyperphosphorylated tau (p-tau). While Aβ targeted treatments have shown clinical promise, other aspects of AD pathology such as microgliosis, astrocytosis, synaptic loss, and hypometabolism may be viable targets for treatment. Among notable novel therapeutic approaches, the Ras homolog (Rho)-associated kinases (ROCKs) are being investigated as targets for AD treatment, based on the observations that ROCK1/2 levels are elevated in AD, and activation or inhibition of ROCKs changes dendritic/synaptic structures, protein aggregate accumulation, inflammation, and gliosis. This review will highlight key findings on the effects of ROCK inhibition in Aβ and ptau pathologies, as well as its effects on neuroinflammation, synaptic density, and potentially metabolism and bioenergetics.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Zheng, C., Xia, W., & Zhang, J. (2025). Rock inhibitors in Alzheimer’s disease. Frontiers in Aging. https://doi.org/10.3389/fragi.2025.1547883
Vancouver
Zheng C, Xia W, Zhang J. Rock inhibitors in Alzheimer’s disease. Frontiers in Aging. 2025. doi:10.3389/fragi.2025.1547883. PMID: 40182055.
BibTeX
@article{zheng2025-40182055,
author = {Zheng, Chao and Xia, Weiming and Zhang, Jianhua},
title = {{Rock inhibitors in Alzheimer’s disease}},
journal = {Frontiers in Aging},
year = {2025},
doi = {10.3389/fragi.2025.1547883},
pmid = {40182055},
url = {https://doi.org/10.3389/fragi.2025.1547883}
}
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.
Key findings
- Alzheimer's disease (AD) is the most common age-related neurodegenerative disease and cause of dementia.
- AD pathology primarily involves the formation of amyloid β (Aβ) plaques and neurofibrillary tangles containing hyperphosphorylated tau (p-tau).
- While Aβ targeted treatments have shown clinical promise, other aspects of AD pathology such as microgliosis, astrocytosis, synaptic loss, and hypometabolism may be viable targets for treatment.
- Among notable novel therapeutic approaches, the Ras homolog (Rho)-associated kinases (ROCKs) are being investigated as targets for AD treatment, based on the observations that ROCK1/2 levels are elevated in AD, and activation or inhibition of ROCKs changes dendritic/synaptic structures, protein aggregate accumulation, inflammation, and gliosis.
- This review will highlight key findings on the effects of ROCK inhibition in Aβ and ptau pathologies, as well as its effects on neuroinflammation, synaptic density, and potentially metabolism and bioenergetics.
Why it matters
This review discusses ROCK inhibition as a possible approach for Alzheimer's disease, based on observations that ROCK1/2 levels are elevated in the disease and that ROCK activity changes synapses, protein aggregates and inflammation. It summarizes findings rather than reporting a proven treatment, cure or prevention.
Study details
- Evidence strengthLow
How this study scored 39/100
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.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Frontiers in Aging) |
| Journal's citation record | 0 / 4 | Frontiers in Aging: journal h-index 43 (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 9 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 3.0 citations a year over 3 year(s) since 2025 |
| Impact for its field and year | 3 / 6 | Cited 4.9× 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 9 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 1 / 4 | Last-listed author Jianhua Zhang: h-index 9 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | University of Toronto: institution h-index 1,923 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 7 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 40182055) |
| Free to read | 2 / 2 | Free to read |
| Total | 39 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.3389/fragi.2025.1547883
- PubMed: 40182055
- Original source →
- Free full text: Frontiers in Aging →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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