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The interaction between dysfunction of vasculature and tauopathy in Alzheimer's disease and related dementias
Chuyao Huang, Zhenwen Wei, Ningxiang Zheng, Jingsi Yan, Jiayu Zhang, Xinyi Ye, Wei Zhao. Alzheimer s & Dementia, 2025-02-01
Topic: Amyloid, tau and blood-test diagnosis
Tauopathy is one of the pathological features of Alzheimer's disease and related dementias (ADRD). At present, there have been many studies on the formation, deposition, and intercellular transmission of tau in neurons and immune cells. The vasculature is an important component of the central nervous system. This review discusses the interaction between vasculature and tau in detail from three aspects. (1) The vascular risk factors (VRFs) discussed in this review include diabetes mellitus (DM), abnormal blood pressure (BP), and hypercholesterolemia. (2) In ADRD pathology, the hyperphosphorylation and deposition of tau interact with disrupted vasculature, such as different cells (endothelial cells, smooth muscular cells, and pericytes), the blood-brain barrier (BBB), and the cerebral lymphatic system. (3) The functions of vasculature are regulated by various signaling transductions. Endothelial nitric oxide synthase/nitric oxide, calcium signaling, Rho/Rho-associated coiled-coil containing Kinase, and receptors for advanced glycation end products are discussed in this review. Our findings indicate that the prevention and treatment of vascular health may be a potential target for ADRD combination therapy. HIGHLIGHTS: Persistent VRFs increase early disruption of vascular mechanisms and are strongly associated with tau pathology in ADRD. Cell dysfunction in the vasculature causes BBB leakage and drainage incapacity of the cerebral lymphatic system, which interacts with tau pathology. Signaling molecules in the vasculature regulate vasodilation and contraction, angiogenesis, and CBF. Abnormal signaling transduction is related to tau hyperphosphorylation and deposition.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Huang, C., Wei, Z., Zheng, N., Yan, J., Zhang, J., Ye, X., et al. (2025). The interaction between dysfunction of vasculature and tauopathy in Alzheimer's disease and related dementias. Alzheimer s & Dementia. https://doi.org/10.1002/alz.14618
Vancouver
Huang C, Wei Z, Zheng N, Yan J, Zhang J, Ye X, et al. The interaction between dysfunction of vasculature and tauopathy in Alzheimer's disease and related dementias. Alzheimer s & Dementia. 2025. doi:10.1002/alz.14618. PMID: 39998958.
BibTeX
@article{huang2025-39998958,
author = {Huang, Chuyao and Wei, Zhenwen and Zheng, Ningxiang and Yan, Jingsi and Zhang, Jiayu and Ye, Xinyi and Zhao, Wei},
title = {{The interaction between dysfunction of vasculature and tauopathy in Alzheimer's disease and related dementias}},
journal = {Alzheimer s \& Dementia},
year = {2025},
doi = {10.1002/alz.14618},
pmid = {39998958},
url = {https://doi.org/10.1002/alz.14618}
}
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 names 7 authors; APA and Vancouver show the first six, BibTeX and the downloads carry all of them. Check the citation against the original before you use it.
Key findings
- Our findings indicate that the prevention and treatment of vascular health may be a potential target for ADRD combination therapy.
- HIGHLIGHTS: Persistent VRFs increase early disruption of vascular mechanisms and are strongly associated with tau pathology in ADRD.
Why it matters
This review describes how vascular risk factors and blood vessel dysfunction interact with tau pathology in Alzheimer's disease and related dementias, suggesting vascular health as a possible target for combination therapy. It is a review of mechanisms, not proof that any treatment works.
Study details
- Evidence strengthLow
How this study scored 38/100
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 (Alzheimer s & Dementia) |
| Journal's citation record | 2 / 4 | Alzheimer s & Dementia: journal h-index 228 (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 11 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 3.7 citations a year over 3 year(s) since 2025 |
| Impact for its field and year | 3 / 6 | Cited 6.0× 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 11 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Wei Zhao: h-index 30 (OpenAlex, whole career) |
| Institution's track record | 0 / 3 | Guangzhou University of Chinese Medicine: institution h-index 248 (OpenAlex) |
| Multi-centre collaboration | 0 / 3 | OpenAlex lists 1 institution(s) in 1 country — scores zero (affiliation lists can be incomplete) |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 39998958) |
| Free to read | 2 / 2 | Free to read |
| Total | 38 / 100 | — |
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