Apolipoprotein E, amyloid-beta, and blood-brain barrier permeability in Alzheimer disease
Donahue JE, Johanson CE.. Journal of neuropathology and experimental neurology, 2008-04-01
Topic: Amyloid, tau and blood-test diagnosis
There is increasing evidence for blood-brain barrier (BBB) compromise in Alzheimer disease (AD). The presence of the epsilon4 allele of the apolipoprotein E (apoE) gene is a risk factor for sporadic AD. Apolipoprotein E is essential both for maintenance of BBB integrity and for the deposition of fibrillar amyloid-beta (Abeta) that leads to the development of Abeta plaques in AD and to cerebral amyloid angiopathy. This review investigates the relationships between apoE, Abeta, and the BBB in AD. Alterations in the expression and distribution of the BBB Abeta transporters receptor for advanced glycation end-products and low-density lipoprotein receptor-related protein 1 in AD and the potential roles of apoE4 expression in adversely influencing Abeta burden and BBB permeability are also examined. Because both apoE and Abeta are ligands for low-density lipoprotein receptor-related protein 1, all 3 molecules are present in AD plaques, and most AD plaques are located close to the cerebral microvasculature. The interactions of these molecules at the BBB likely influence metabolism and clearance of Abeta and contribute to AD pathogenesis. Therapeutic alternatives targeting apoE/Abeta and sealing a compromised BBB are under development for the treatment of AD.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Donahue, J. E., & Johanson, C. E. (2008). Apolipoprotein E, amyloid-beta, and blood-brain barrier permeability in Alzheimer disease. Journal of neuropathology and experimental neurology. https://doi.org/10.1097/nen.0b013e31816a0dc8
Vancouver
Donahue JE, Johanson CE. Apolipoprotein E, amyloid-beta, and blood-brain barrier permeability in Alzheimer disease. Journal of neuropathology and experimental neurology. 2008. doi:10.1097/nen.0b013e31816a0dc8. PMID: 18379441.
BibTeX
@article{donahue2008-18379441,
author = {Donahue, J. E. and Johanson, C. E.},
title = {{Apolipoprotein E, amyloid-beta, and blood-brain barrier permeability in Alzheimer disease}},
journal = {Journal of neuropathology and experimental neurology},
year = {2008},
doi = {10.1097/nen.0b013e31816a0dc8},
pmid = {18379441},
url = {https://doi.org/10.1097/nen.0b013e31816a0dc8}
}
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Key findings
- This review investigates the relationships between apoE, Abeta, and the BBB in AD.
- Alterations in the expression and distribution of the BBB Abeta transporters receptor for advanced glycation end-products and low-density lipoprotein receptor-related protein 1 in AD and the potential roles of apoE4 expression in adversely influencing Abeta burden and BBB permeability are also examined.
- Because both apoE and Abeta are ligands for low-density lipoprotein receptor-related protein 1, all 3 molecules are present in AD plaques, and most AD plaques are located close to the cerebral microvasculature.
- The interactions of these molecules at the BBB likely influence metabolism and clearance of Abeta and contribute to AD pathogenesis.
- Therapeutic alternatives targeting apoE/Abeta and sealing a compromised BBB are under development for the treatment of AD.
Why it matters
This review examines how apolipoprotein E, amyloid-beta, and blood-brain barrier permeability are related in Alzheimer's disease. It notes that therapies targeting apoE/amyloid-beta and sealing a compromised blood-brain barrier are under development, but none are established treatments.
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Study details
- Evidence strengthLow
How this study scored 39/100
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.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Journal of neuropathology and experimental neurology) |
| Journal's citation record | 2 / 4 | Journal of Neuropathology & Experimental Neurology: journal h-index 239 (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 | 2008 — 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 | 4 / 7 | Cited 86 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 4.3 citations a year over 20 year(s) since 2008 |
| Impact for its field and year | 3 / 6 | Cited 5.4× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 1 / 6 | Cited by 1 other studies in this library |
| 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 Conrad E. Johanson: h-index 54 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | Brown University: institution h-index 1,120 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 3 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 18379441) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 39 / 100 | — |
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