APOE Lipoprotein Particles: Pathophysiology, Therapy, and the Crosstalk in Alzheimer's Disease and Cardiovascular Disease
Chan Liu, Juan Liu, Yan-Yang Wang, Shang-Fu Xu, Li-Mei Yu. Molecular neurobiology, 2025-12-23
Topic: Genetics and APOE
The APOE4 variant was the strongest genetic risk factor for sporadic Alzheimer's disease (AD). Individuals with APOE4 have an increased risk of developing the disease at an early age of onset. Similarly, APOE4 carriers are predisposed to high cholesterol levels and tend to have an increased risk of cardiovascular disease (CVD). The global allele frequency of APOE4 was 13.7%, underlining its widespread impact on global human health. Conversely, the relatively rare APOE2 allele was a genetic protective factor against AD and CVD. However, the mechanisms underlying this association remain to be elucidated. The apolipoprotein E (APOE) protein coats lipoprotein particles and mediates lipid transport and metabolism in the peripheral circulation and central nervous system (CNS). Although initial studies causally linked APOE lipoprotein particles (APOE particles) with lipid homeostasis, our understanding of the physiological and pathological effects of APOE particles has extended to amyloid-β (Aβ) accumulation, tau hyperphosphorylation and spread, as well as neuroinflammation in AD initiation and progression. Moreover, the most examined functions of APOE particles are reverse cholesterol transport, anti-inflammatory, anti-oxidation, and improvement of endothelial dysfunction in atherosclerotic CVD. This review outlines what is known about the structure and functions of APOE particles, emphasizing their involvement in AD and CVD pathogenesis, while also considering the crosstalk between the peripheral circulation and CNS. In addition, we discuss how these APOE particles act as therapeutic targets.
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APA 7th
Liu, C., Liu, J., Wang, Y.-Y., Xu, S.-F., & Yu, L.-M. (2025). APOE Lipoprotein Particles: Pathophysiology, Therapy, and the Crosstalk in Alzheimer's Disease and Cardiovascular Disease. Molecular neurobiology. https://doi.org/10.1007/s12035-025-05629-3
Vancouver
Liu C, Liu J, Wang Y.-Y, Xu S.-F, Yu L.-M. APOE Lipoprotein Particles: Pathophysiology, Therapy, and the Crosstalk in Alzheimer's Disease and Cardiovascular Disease. Molecular neurobiology. 2025. doi:10.1007/s12035-025-05629-3. PMID: 41436721.
BibTeX
@article{liu2025-41436721,
author = {Liu, Chan and Liu, Juan and Wang, Yan-Yang and Xu, Shang-Fu and Yu, Li-Mei},
title = {{APOE Lipoprotein Particles: Pathophysiology, Therapy, and the Crosstalk in Alzheimer's Disease and Cardiovascular Disease}},
journal = {Molecular neurobiology},
year = {2025},
doi = {10.1007/s12035-025-05629-3},
pmid = {41436721},
url = {https://doi.org/10.1007/s12035-025-05629-3}
}
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Key findings
- Individuals with APOE4 have an increased risk of developing the disease at an early age of onset.
- Similarly, APOE4 carriers are predisposed to high cholesterol levels and tend to have an increased risk of cardiovascular disease (CVD).
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Study details
- Effect size13.7%
- Evidence strengthLow
How this study scored 46/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, 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, multi-centre collaboration and free to read, so those were left out: it earned 26 of the 56 points we could judge it on, which is 46 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Molecular neurobiology) |
| 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 | 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 | 2 / 3 | Effect reported as a number, without an interval or test |
| 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 41436721) |
| Free to read | — / 2 | Access not recorded — left out of this score |
| Points | 26 / 56 | Scored on 10 of 20 parts. We have no data for the rest, so they are left out: 26 of the 56 points we could judge it on is 46 out of 100. |
| Total | 46 / 100 | — |
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