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Role of apolipoprotein E in neurodegenerative diseases
Giau VV, Bagyinszky E, An SS, Kim SY.. Neuropsychiatric disease and treatment, 2015-07-16
Topic: Brain proteins, microglia and lab models
Apolipoprotein E (APOE) is a lipid-transport protein abundantly expressed in most neurons in the central nervous system. APOE-dependent alterations of the endocytic pathway can affect different functions. APOE binds to cell-surface receptors to deliver lipids and to the hydrophobic amyloid-β peptide, regulating amyloid-β aggregations and clearances in the brain. Several APOE isoforms with major structural differences were discovered and shown to influence the brain lipid transport, glucose metabolism, neuronal signaling, neuroinflammation, and mitochondrial function. This review will summarize the updated research progress on APOE functions and its role in Alzheimer's disease, Parkinson's disease, cardiovascular diseases, multiple sclerosis, type 2 diabetes mellitus, Type III hyperlipoproteinemia, vascular dementia, and ischemic stroke. Understanding the mutations in APOE, their structural properties, and their isoforms is important to determine its role in various diseases and to advance the development of therapeutic strategies. Targeting APOE may be a potential approach for diagnosis, risk assessment, prevention, and treatment of various neurodegenerative and cardiovascular diseases in humans.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Giau, V. V., Bagyinszky, E., An, S. S., & Kim, S. Y. (2015). Role of apolipoprotein E in neurodegenerative diseases. Neuropsychiatric disease and treatment. https://doi.org/10.2147/ndt.s84266
Vancouver
Giau VV, Bagyinszky E, An SS, Kim SY. Role of apolipoprotein E in neurodegenerative diseases. Neuropsychiatric disease and treatment. 2015. doi:10.2147/ndt.s84266. PMID: 26213471.
BibTeX
@article{giau2015-26213471,
author = {Giau, V. V. and Bagyinszky, E. and An, S. S. and Kim, S. Y.},
title = {{Role of apolipoprotein E in neurodegenerative diseases}},
journal = {Neuropsychiatric disease and treatment},
year = {2015},
doi = {10.2147/ndt.s84266},
pmid = {26213471},
url = {https://doi.org/10.2147/ndt.s84266}
}
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Key findings
- APOE binds to cell-surface receptors to deliver lipids and to the hydrophobic amyloid-β peptide, regulating amyloid-β aggregations and clearances in the brain.
- Several APOE isoforms with major structural differences were discovered and shown to influence the brain lipid transport, glucose metabolism, neuronal signaling, neuroinflammation, and mitochondrial function.
- This review will summarize the updated research progress on APOE functions and its role in Alzheimer's disease, Parkinson's disease, cardiovascular diseases, multiple sclerosis, type 2 diabetes mellitus, Type III hyperlipoproteinemia, vascular dementia, and ischemic stroke.
- Understanding the mutations in APOE, their structural properties, and their isoforms is important to determine its role in various diseases and to advance the development of therapeutic strategies.
- Targeting APOE may be a potential approach for diagnosis, risk assessment, prevention, and treatment of various neurodegenerative and cardiovascular diseases in humans.
Why it matters
This review describes how apolipoprotein E binds amyloid-beta and regulates its aggregation and clearance, and how different APOE isoforms influence brain lipid transport, glucose metabolism, neuronal signaling, neuroinflammation, and mitochondrial function. It suggests that targeting APOE may be a potential approach for diagnosis, risk assessment, prevention, and treatment, but no treatment is tested here.
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Study details
- Evidence strengthLow
How this study scored 45/100
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 (Neuropsychiatric disease and treatment) |
| Journal's citation record | 1 / 4 | Neuropsychiatric Disease and Treatment: journal h-index 126 (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 | 1 / 5 | 2015 — 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) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 5 / 7 | Cited 173 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 13.3 citations a year over 13 year(s) since 2015 |
| Impact for its field and year | 4 / 6 | Cited 9.7× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 4 other studies in this library |
| Still being cited | 2 / 4 | Cited 38 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author SangYun Kim: h-index 53 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | Seoul National University: institution h-index 1,053 (OpenAlex) |
| Multicenter collaboration | 1 / 3 | OpenAlex lists 3 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 26213471) |
| Free to read | 2 / 2 | Free to read |
| Total | 45 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.2147/ndt.s84266
- PubMed: 26213471
- Original source →
- Free full text: Neuropsychiatric Disease and Treatment →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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