Apolipoprotein E isoforms in Alzheimer's disease pathology and etiology
L Baum, L Chen, H K Ng, C P Pang. Microscopy research and technique, 2000-08-15
Topic: Genetics and APOE
The apolipoprotein E (apoE) epsilon4 allele increases risk of Alzheimer's disease (AD), perhaps by accelerating plaque formation, or by impairing neuron repair. Considerable evidence supports both mechanisms. AD patients with epsilon4 have more and earlier amyloid deposits than do patients without epsilon4. The same is true of non-demented control subjects. In vitro, all apoE isoforms inhibit amyloid beta protein (Abeta) aggregation, but apoE4 less effectively than apoE3. Transgenic amyloid-producing mice expressing apoE3 or apoE4 develop less Abeta deposition than apoE knockout mice. These observations are consistent with an effect of apoE isoforms on Abeta aggregation in AD. ApoE is important for neurite maintenance since apoE knockout mice lose neurites and suffer behavioral deficits with aging or treatment with excitotoxins. ApoE4 mice show similar defects, but apoE3 mice are normal. AD patients with epsilon4 show more neuritic deficits than epsilon3 carriers. ApoE epsilon4 also worsens neurological impairment in head injury, stroke, and multiple sclerosis. Thus, apoE4 is less effective at neurite maintenance. Perhaps epsilon4 increases AD risk by both mechanisms: allowing amyloid deposition and failing to repair neurites. In either case, introducing apoE3 or apoE2 into the brain, for example by gene therapy or cell grafts, might delay AD progression.
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APA 7th
Baum, L., Chen, L., Ng, H. K., & Pang, C. P. (2000). Apolipoprotein E isoforms in Alzheimer's disease pathology and etiology. Microscopy research and technique. https://doi.org/10.1002/1097-0029(20000815)50:4<278::aid-jemt5>3.0.co;2-t
Vancouver
Baum L, Chen L, Ng HK, Pang CP. Apolipoprotein E isoforms in Alzheimer's disease pathology and etiology. Microscopy research and technique. 2000. doi:10.1002/1097-0029(20000815)50:4<278::aid-jemt5>3.0.co;2-t. PMID: 10936880.
BibTeX
@article{baum2000-10936880,
author = {Baum, L and Chen, L and Ng, H K and Pang, C P},
title = {{Apolipoprotein E isoforms in Alzheimer's disease pathology and etiology}},
journal = {Microscopy research and technique},
year = {2000},
doi = {10.1002/1097-0029(20000815)50:4<278::aid-jemt5>3.0.co;2-t},
pmid = {10936880},
url = {https://doi.org/10.1002/1097-0029(20000815)50:4<278::aid-jemt5>3.0.co;2-t}
}
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Key findings
- AD patients with epsilon4 show more neuritic deficits than epsilon3 carriers.
- ApoE epsilon4 also worsens neurological impairment in head injury, stroke, and multiple sclerosis.
- Thus, apoE4 is less effective at neurite maintenance.
- Perhaps epsilon4 increases AD risk by both mechanisms: allowing amyloid deposition and failing to repair neurites.
- In either case, introducing apoE3 or apoE2 into the brain, for example by gene therapy or cell grafts, might delay AD progression.
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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 (Microscopy research and technique) |
| 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 | 2000 — 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 | 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 10936880) |
| 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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