Mechanisms linking apolipoprotein E isoforms with cardiovascular and neurological diseases
Yadong Huang. Current opinion in lipidology, 2010-08
Topic: Genetics and APOE
PURPOSE OF REVIEW: The purpose of this review is to provide insights into recent advances in mechanisms linking apolipoprotein (apo) E isoforms to cardiovascular and neurological diseases. RECENT FINDINGS: Human apoE has three common isoforms (apoE2, apoE3, and apoE4) with different structural and biophysical properties and different effects on lipid and neuronal homeostasis. ApoE is a protein constituent of different plasma lipoproteins and serves as a high-affinity ligand for several receptors. By interacting with its receptors, apoE mediates the clearance of different lipoproteins from the circulation. Absence or structural mutations of apoE cause significant disorders in lipid metabolism and cardiovascular disease. ApoE also has significant roles in neurobiology. ApoE4 is the major known genetic risk factor for Alzheimer's disease. It increases the occurrence and lowers the age of onset of Alzheimer's disease. ApoE4 carriers account for 65-80% of all Alzheimer's disease cases, highlighting the importance of apoE4 in Alzheimer's disease pathogenesis. ApoE4 has both amyloid beta-dependent and amyloid beta-independent roles in Alzheimer's disease pathogenesis. SUMMARY: Emerging data suggest that apoE isoforms, with their multiple cellular origins and multiple structural and biophysical properties, contribute to cardiovascular and neurological diseases by interacting with different factors through various pathways.
Key findings
- Absence or structural mutations of apoE cause significant disorders in lipid metabolism and cardiovascular disease.
- ApoE also has significant roles in neurobiology.
- SUMMARY: Emerging data suggest that apoE isoforms, with their multiple cellular origins and multiple structural and biophysical properties, contribute to cardiovascular and neurological diseases by interacting with different factors through various pathways.
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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. 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 21 of the 56 points we could judge it on, which is 38 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Current opinion in lipidology) |
| 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 | 1 / 5 | 2010 — within 20 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 20531185) |
| Free to read | — / 2 | Access not recorded — left out of this score |
| Points | 21 / 56 | Scored on 10 of 20 parts. We have no data for the rest, so they are left out: 21 of the 56 points we could judge it on is 38 out of 100. |
| Total | 38 / 100 | — |
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APA 7th
Huang, Y. (2010). Mechanisms linking apolipoprotein E isoforms with cardiovascular and neurological diseases. Current opinion in lipidology. https://doi.org/10.1097/mol.0b013e32833af368
Vancouver
Huang Y. Mechanisms linking apolipoprotein E isoforms with cardiovascular and neurological diseases. Current opinion in lipidology. 2010. doi:10.1097/mol.0b013e32833af368. PMID: 20531185.
BibTeX
@article{huang2010-20531185,
author = {Huang, Yadong},
title = {{Mechanisms linking apolipoprotein E isoforms with cardiovascular and neurological diseases}},
journal = {Current opinion in lipidology},
year = {2010},
doi = {10.1097/mol.0b013e32833af368},
pmid = {20531185},
url = {https://doi.org/10.1097/mol.0b013e32833af368}
}