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LDL oxidation and cerebrovascular aging: mechanisms of endothelial dysfunction, inflammation, and vascular cognitive impairment and dementia
Jennifer Ihuoma, Madison Milan, Sharon Negri, Eva Troyano‐Rodriguez, Rakesh Rudraboina, Aleksandra Kosmider, Shantipriya Awasthi, Anna Csiszar et al.. Redox Biology, 2026-03-10
Topic: Brain proteins, microglia and lab models
Plain-language summary
Vascular cognitive impairment and dementia (VCID) is increasingly recognized as one of the leading causes of cognitive decline in aging populations. VCID is driven by the interplay of endothelial dysfunction, chronic inflammation, oxidative stress, and metabolic dysregulation. Aging exacerbates cerebrovascular damage by impairing endothelial function, compromising the blood-brain barrier (BBB), and promoting neuroinflammation, all of which contribute to the progression of small vessel disease (SVD) and white matter hyperintensities (WMHs), which are hallmarks of VCID. Epidemiological evidence suggests that aging is associated with modifications in circulating low-density lipoprotein (LDL) and high-density lipoproteins (HDL), particularly oxidation, which further accelerates neurovascular pathology. Oxidized LDL (oxLDL) disrupts endothelial homeostasis, enhances leukocyte adhesion, and triggers chronic inflammatory signaling through microglial and astrocytic activation. Additionally, oxLDL-mediated oxidative stress exacerbates mitochondrial dysfunction and epigenetic alterations in cerebrovascular cells, reinforcing a cycle of vascular injury and neurodegeneration. These mechanisms contribute to neurovascular uncoupling, cerebral hypoperfusion, and cognitive decline in aging individuals. This review examines the pathophysiological role of oxLDL in VCID, with a focus on its impact on endothelial integrity, BBB function, neuroinflammation, and lipid-mediated neurodegenerative processes. Furthermore, we discuss emerging therapeutic strategies targeting LDL oxidation, inflammation, and endothelial dysfunction as potential interventions to mitigate the burden of VCID in aging populations.
What this study adds
Evidence grade: Low
This review discusses how oxidized LDL may contribute to blood vessel damage, inflammation and cognitive decline in vascular cognitive impairment and dementia. It outlines mechanisms rather than testing a treatment.
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
Ihuoma, J., Milan, M., Negri, S., Troyano‐Rodriguez, E., Rudraboina, R., Kosmider, A., et al. (2026). LDL oxidation and cerebrovascular aging: mechanisms of endothelial dysfunction, inflammation, and vascular cognitive impairment and dementia. Redox Biology. https://doi.org/10.1016/j.redox.2026.104118
Vancouver
Ihuoma J, Milan M, Negri S, Troyano‐Rodriguez E, Rudraboina R, Kosmider A, et al. LDL oxidation and cerebrovascular aging: mechanisms of endothelial dysfunction, inflammation, and vascular cognitive impairment and dementia. Redox Biology. 2026. doi:10.1016/j.redox.2026.104118. PMID: 41831270.
BibTeX
@article{ihuoma2026-41831270,
author = {Ihuoma, Jennifer and Milan, Madison and Negri, Sharon and Troyano‐Rodriguez, Eva and Rudraboina, Rakesh and Kosmider, Aleksandra and Awasthi, Shantipriya and Csiszar, Anna and others},
title = {{LDL oxidation and cerebrovascular aging: mechanisms of endothelial dysfunction, inflammation, and vascular cognitive impairment and dementia}},
journal = {Redox Biology},
year = {2026},
doi = {10.1016/j.redox.2026.104118},
pmid = {41831270},
url = {https://doi.org/10.1016/j.redox.2026.104118}
}
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
- Epidemiological evidence suggests that aging is associated with modifications in circulating low-density lipoprotein (LDL) and high-density lipoproteins (HDL), particularly oxidation, which further accelerates neurovascular pathology.
Why it matters
This review discusses how oxidized LDL may contribute to blood vessel damage, inflammation and cognitive decline in vascular cognitive impairment and dementia. It outlines mechanisms rather than testing a treatment.
Study details
- Evidence strengthLow
How this study scored 43/100
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 (Redox Biology) |
| Journal's citation record | 2 / 4 | Redox Biology: journal h-index 209 (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 | 5 / 5 | 2026 — within 1 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 | 2 / 7 | Cited 12 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 6.0 citations a year over 2 year(s) since 2026 |
| Impact for its field and year | 5 / 6 | Cited 30.3× 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 12 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Stefano Tarantini: h-index 63 (OpenAlex, whole career) |
| Institution's track record | 0 / 3 | University of Oklahoma Health Sciences Center: institution h-index 557 (OpenAlex) |
| Multicenter collaboration | 1 / 3 | OpenAlex lists 3 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 41831270) |
| Free to read | 2 / 2 | Free to read |
| Total | 43 / 100 | — |
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