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High complement levels in astrocyte-derived exosomes of Alzheimer disease
Goetzl EJ, Schwartz JB, Abner EL, Jicha GA, Kapogiannis D.. Annals of neurology, 2018-03-10
Topic: Brain proteins, microglia and lab models
Objective Astrocytes fulfill neuronal trophic roles normally, but are transformed in Alzheimer disease (AD) into A1-type reactive astrocytes that may destroy neurons through unknown mechanisms. Methods To investigate astrocyte inflammatory mechanisms, astrocyte-derived exosomes (ADEs) were isolated immunochemically from plasma samples of AD patients and matched controls for enzyme-linked immunosorbent assay quantification of complement proteins. Results ADE levels of C1q, C4b, C3d, factor B, factor D, Bb, C3b, and C5b-C9 terminal complement complex, but not mannose-binding lectin, normalized by the CD81 exosome marker were significantly higher for AD patients (n = 28) than age- and gender-matched controls (all p Interpretation ADE complement effector proteins in AD are produced by dysregulated systems, attain higher levels than in controls, and may potentially damage neurons in the late
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Goetzl, E. J., Schwartz, J. B., Abner, E. L., Jicha, G. A., & Kapogiannis, D. (2018). High complement levels in astrocyte-derived exosomes of Alzheimer disease. Annals of neurology. https://doi.org/10.1002/ana.25172
Vancouver
Goetzl EJ, Schwartz JB, Abner EL, Jicha GA, Kapogiannis D. High complement levels in astrocyte-derived exosomes of Alzheimer disease. Annals of neurology. 2018. doi:10.1002/ana.25172. PMID: 29406582.
BibTeX
@article{goetzl2018-29406582,
author = {Goetzl, E. J. and Schwartz, J. B. and Abner, E. L. and Jicha, G. A. and Kapogiannis, D.},
title = {{High complement levels in astrocyte-derived exosomes of Alzheimer disease}},
journal = {Annals of neurology},
year = {2018},
doi = {10.1002/ana.25172},
pmid = {29406582},
url = {https://doi.org/10.1002/ana.25172}
}
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Key findings
- Methods To investigate astrocyte inflammatory mechanisms, astrocyte-derived exosomes (ADEs) were isolated immunochemically from plasma samples of AD patients and matched controls for enzyme-linked immunosorbent assay quantification of complement proteins.
- Results ADE levels of C1q, C4b, C3d, factor B, factor D, Bb, C3b, and C5b-C9 terminal complement complex, but not mannose-binding lectin, normalized by the CD81 exosome marker were significantly higher for AD patients (n = 28) than age- and gender-matched controls (all p < 0.0001).
Why it matters
In plasma samples from 28 Alzheimer's disease patients and matched controls, astrocyte-derived exosomes showed higher levels of several complement proteins. This is a small study of a possible inflammatory mechanism and does not show that targeting complement would treat, cure, or prevent Alzheimer's disease.
Study details
- Participants28
- Evidence strengthLow
How this study scored 58/100
Published in a leading specialty journal. Scored zero for study design, effect reported and randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 9 / 10 | Tier 2 — leading specialty journal (Annals of neurology) |
| Journal's citation record | 3 / 4 | Annals of Neurology: journal h-index 437 (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 | 2 / 5 | 2018 — within 10 year(s) of the newest study here |
| Sample size | 1 / 4 | 28 participants |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 3 / 3 | Studied in people (participant count stated) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 6 / 7 | Cited 371 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 37.1 citations a year over 10 year(s) since 2018 |
| Impact for its field and year | 5 / 6 | Cited 21.9× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 7 other studies in this library |
| Still being cited | 3 / 4 | Cited 126 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Dimitrios Kapogiannis: h-index 70 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | University of California, San Francisco: institution h-index 1,915 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 4 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 29406582) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 58 / 100 | — |
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