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Pathological angiogenesis was associated with cerebrovascular lesion and neurodegeneration in Alzheimer's disease
Gao F, Zhan Y, Wang Q, Zhang M, Dai L, Shen Y.. Alzheimer's & dementia : the journal of the Alzheimer's Association, 2025-01-08
Topic: Amyloid, tau and blood-test diagnosis
Introduction We investigated the specific factors driving abnormal angiogenesis in Alzheimer's disease (AD) and its role in cerebrovascular lesions and neurodegeneration. Methods We assessed cerebrovascular pathologies, amyloid-beta (Aβ), and tau pathologies in post mortem human brains and detected 12 angiogenic factors in cerebrospinal fluid (CSF) from the China Aging and Neurodegenerative Disease Initiative (CANDI) cohort. Results We observed severe blood-brain barrier damage and elevated levels of the vascular marker CD31 in human AD brains, which had a stronger correlation with tau pathology than Aβ pathology. Consistently, only CSF pTau181 showed positive associations with CSF angiogenesis factors (soluble vascular endothelial growth factor receptor 2 [sVEGFR2], VEGF-C, VEGF-D, placental growth factor [PLGF], Angiopoietin2, and Serpin E1), but not CSF Aβ42/40. Additionally, higher levels of CSF sVEGFR1, soluble Tyrosine-protein kinase receptor 2 [sTIE2], PLGF, and interleukin 8 [IL8], as well as lower levels of CSF urokinase-type plasminogen activator [uPA], were associated with worsen cerebrovascular pathologies and neurodegeneration. Discussion Our findings indicate that tau pathology may play a critical role in pathological angiogenesis, contributing to cerebrovascular lesions and neurodegeneration in AD. Highlights BBB damage and elevated vascular marker CD31 in human AD brains had a stronger correlation with tau pathology than Aβ pathology. CSF pTau181 mediated the effect of CSF Aβ42/40 on CSF sVEGFR1 and sTIE2. Only CSF pTau181 showed positive associations with sVEGFR2, VEGF-C, VEGF-D, PLGF, Angiopoietin2, and Serpin E1. Higher sVEGFR1, sTIE2, PLGF, and IL8, and lower uPA in CSF, were associated with cerebrovascular pathologies and neurodegeneration.
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APA 7th
Gao, F., Zhan, Y., Wang, Q., Zhang, M., Dai, L., & Shen, Y. (2025). Pathological angiogenesis was associated with cerebrovascular lesion and neurodegeneration in Alzheimer's disease. Alzheimer's & dementia : the journal of the Alzheimer's Association. https://doi.org/10.1002/alz.14521
Vancouver
Gao F, Zhan Y, Wang Q, Zhang M, Dai L, Shen Y. Pathological angiogenesis was associated with cerebrovascular lesion and neurodegeneration in Alzheimer's disease. Alzheimer's & dementia : the journal of the Alzheimer's Association. 2025. doi:10.1002/alz.14521. PMID: 39777972.
BibTeX
@article{gao2025-39777972,
author = {Gao, F. and Zhan, Y. and Wang, Q. and Zhang, M. and Dai, L. and Shen, Y.},
title = {{Pathological angiogenesis was associated with cerebrovascular lesion and neurodegeneration in Alzheimer's disease}},
journal = {Alzheimer's \& dementia : the journal of the Alzheimer's Association},
year = {2025},
doi = {10.1002/alz.14521},
pmid = {39777972},
url = {https://doi.org/10.1002/alz.14521}
}
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Key findings
- Results We observed severe blood-brain barrier damage and elevated levels of the vascular marker CD31 in human AD brains, which had a stronger correlation with tau pathology than Aβ pathology.
- Additionally, higher levels of CSF sVEGFR1, soluble Tyrosine-protein kinase receptor 2 [sTIE2], PLGF, and interleukin 8 [IL8], as well as lower levels of CSF urokinase-type plasminogen activator [uPA], were associated with worsen cerebrovascular pathologies and neurodegeneration.
- Discussion Our findings indicate that tau pathology may play a critical role in pathological angiogenesis, contributing to cerebrovascular lesions and neurodegeneration in AD.
- Higher sVEGFR1, sTIE2, PLGF, and IL8, and lower uPA in CSF, were associated with cerebrovascular pathologies and neurodegeneration.
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Study details
- Evidence strengthModerate
How this study scored 52/100
Published in a leading specialty 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 journal's citation record, times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record and multi-centre collaboration, so those were left out: it earned 30 of the 58 points we could judge it on, which is 52 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 9 / 10 | Tier 2 — leading specialty journal (Alzheimer's & dementia : the journal of the Alzheimer's Association) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 3 / 5 | Rated “moderate” 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 | — / 7 | No citation count (not found in OpenAlex) — left out of this score |
| Citations per year | — / 5 | No citation count or no year — left out of this score |
| Impact for its field and year | — / 6 | No field-weighted citation impact (OpenAlex has none yet) — left out of this score |
| Cited by studies here | — / 6 | Not yet checked against this library's citation graph — left out of this score |
| Still being cited | — / 4 | No yearly citation counts — left out of this score |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | — / 3 | No institution listed in OpenAlex — left out of this score |
| Multi-centre collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 39777972) |
| Free to read | 2 / 2 | Free to read |
| Points | 30 / 58 | Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 30 of the 58 points we could judge it on is 52 out of 100. |
| Total | 52 / 100 | — |
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