Expression of human apolipoprotein E reduces amyloid-beta deposition in a mouse model of Alzheimer's disease
Holtzman DM, Bales KR, Wu S, Bhat P, Parsadanian M, Fagan AM, Chang LK, Sun Y et al.. The Journal of clinical investigation, 1999-03-01
Topic: Amyloid, tau and blood-test diagnosis
The epsilon4 allele of apolipoprotein E (apo E) is associated with an increased risk for developing Alzheimer's disease (AD). This may be due to interactions between apo E and the amyloid-beta protein (Abeta). To assess the effects of human apo E isoforms on Abeta deposition in vivo, we bred apo E3 and apo E4 hemizygous (+/-) transgenic mice expressing apo E by astrocytes to mice homozygous (+/+) for a mutant amyloid precursor protein (APPV717F) transgene that develop age-dependent AD neuropathology. All mice were on a mouse apo E null (-/-) background. By nine months of age, APPV717F+/-, apo E-/- mice had developed Abeta deposition, and, as reported previously, the quantity of Abeta deposits was significantly less than that seen in APPV717F+/- mice expressing mouse apo E. In contrast to effects of mouse apo E, similar levels of human apo E3 and apo E4 markedly suppressed early Abeta deposition at nine months of age in APPV717F+/- transgenic mice, even when compared with mice lacking apo E. These findings suggest that human apo E isoforms decrease Abeta aggregation or increase Abeta clearance relative to an environment in which mouse apo E or no apo E is present. The results may have important implications for understanding mechanisms underlying the link between apo E and AD.
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APA 7th
Holtzman, D. M., Bales, K. R., Wu, S., Bhat, P., Parsadanian, M., Fagan, A. M., et al. (1999). Expression of human apolipoprotein E reduces amyloid-beta deposition in a mouse model of Alzheimer's disease. The Journal of clinical investigation. https://doi.org/10.1172/jci6179
Vancouver
Holtzman DM, Bales KR, Wu S, Bhat P, Parsadanian M, Fagan AM, et al. Expression of human apolipoprotein E reduces amyloid-beta deposition in a mouse model of Alzheimer's disease. The Journal of clinical investigation. 1999. doi:10.1172/jci6179. PMID: 10079115.
BibTeX
@article{holtzman1999-10079115,
author = {Holtzman, D. M. and Bales, K. R. and Wu, S. and Bhat, P. and Parsadanian, M. and Fagan, A. M. and Chang, L. K. and Sun, Y. and others},
title = {{Expression of human apolipoprotein E reduces amyloid-beta deposition in a mouse model of Alzheimer's disease}},
journal = {The Journal of clinical investigation},
year = {1999},
doi = {10.1172/jci6179},
pmid = {10079115},
url = {https://doi.org/10.1172/jci6179}
}
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Key findings
- The epsilon4 allele of apolipoprotein E (apo E) is associated with an increased risk for developing Alzheimer's disease (AD).
- By nine months of age, APPV717F+/-, apo E-/- mice had developed Abeta deposition, and, as reported previously, the quantity of Abeta deposits was significantly less than that seen in APPV717F+/- mice expressing mouse apo E.
- In contrast to effects of mouse apo E, similar levels of human apo E3 and apo E4 markedly suppressed early Abeta deposition at nine months of age in APPV717F+/- transgenic mice, even when compared with mice lacking apo E.
- These findings suggest that human apo E isoforms decrease Abeta aggregation or increase Abeta clearance relative to an environment in which mouse apo E or no apo E is present.
- The results may have important implications for understanding mechanisms underlying the link between apo E and AD.
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Study details
- Evidence strengthLow
How this study scored 36/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported 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 and multi-centre collaboration, so those were left out: it earned 21 of the 58 points we could judge it on, which is 36 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (The Journal of clinical investigation) |
| 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 | 1999 — older than 20 years, still counted |
| 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 | Laboratory or animal study (title names “mouse”) — scores zero |
| 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 10079115) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 21 / 58 | Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 21 of the 58 points we could judge it on is 36 out of 100. |
| Total | 36 / 100 | — |
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