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Microbiome-generated amyloid and potential impact on amyloidogenesis in Alzheimer's disease (AD)
Zhao Y, Lukiw WJ.. Journal of nature and science, 2015-07-01
Topic: Amyloid, tau and blood-test diagnosis
According to the ' amyloid cascade hypothesis of Alzheimer's disease ' first proposed about 16 years ago, the accumulation of Aβ peptides in the human central nervous system (CNS) is the primary influence driving Alzheimer's disease (AD) pathogenesis, and Aβ peptide accretion is the result of an imbalance between Aβ peptide production and clearance. In the last 18 months multiple laboratories have reported two particularly important observations: (i) that because the microbes of the human microbiome naturally secrete large amounts of amyloid, lipopolysaccharides (LPS) and other related pro-inflammatory pathogenic signals, these may contribute to both the systemic and CNS amyloid burden in aging humans; and (ii) that the clearance of Aβ peptides appears to be intrinsically impaired by deficits in the microglial plasma-membrane enriched triggering receptor expressed in microglial/myeloid-2
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Zhao, Y., & Lukiw, W. J. (2015). Microbiome-generated amyloid and potential impact on amyloidogenesis in Alzheimer's disease (AD). Journal of nature and science.
Vancouver
Zhao Y, Lukiw WJ. Microbiome-generated amyloid and potential impact on amyloidogenesis in Alzheimer's disease (AD). Journal of nature and science. 2015. PMID: 26097896.
BibTeX
@article{zhao2015-26097896,
author = {Zhao, Y. and Lukiw, W. J.},
title = {{Microbiome-generated amyloid and potential impact on amyloidogenesis in Alzheimer's disease (AD)}},
journal = {Journal of nature and science},
year = {2015},
pmid = {26097896}
}
Built from the record alzhub holds for this paper, not looked up. This record has no DOI, so the citation leaves it out. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.
Key findings
- In the last 18 months multiple laboratories have reported two particularly important observations: (i) that because the microbes of the human microbiome naturally secrete large amounts of amyloid, lipopolysaccharides (LPS) and other related pro-inflammatory pathogenic signals, these may contribute to both the systemic and CNS amyloid burden in aging humans; and (ii) that the clearance of Aβ peptides appears to be intrinsically impaired by deficits in the microglial plasma-membrane enriched triggering receptor expressed in microglial/myeloid-2 cells (TREM2).
- This brief general commentary-perspective paper: (i) will highlight some of these very recent findings on microbiome-secreted amyloids and LPS and the potential contribution of these microbial-derived pro-inflammatory and neurotoxic exudates to age-related inflammatory and AD-type neurodegeneration in the host; and (ii) will discuss the contribution of a defective microglial-based TREM2 transmembrane sensor-receptor system to amyloidogenesis in AD that is in contrast to the normal, homeostatic clearance of Aβ peptides from the human CNS.
Why it matters
This commentary discusses the idea that amyloid and inflammatory signals from microbiome microbes might add to amyloid burden, and that clearance of amyloid may be impaired by deficits in TREM2. It is a perspective paper and reports no treatment, cure, or prevention.
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Study details
- Evidence strengthLow
How this study scored 42/100
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, so that was left out: it earned 40 of the 96 points we could judge it on, which is 42 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Journal of nature and science) |
| 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 | 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) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 5 / 7 | Cited 152 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 11.7 citations a year over 13 year(s) since 2015 |
| Impact for its field and year | 4 / 6 | Cited 10.4× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 0 / 6 | No other study in this library cites it |
| Still being cited | 2 / 4 | Cited 19 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Walter J. Lukiw: h-index 75 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | Louisiana State University: institution h-index 856 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 2 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 26097896) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 40 / 96 | Scored on 19 of 20 parts. We have no data for the rest, so they are left out: 40 of the 96 points we could judge it on is 42 out of 100. |
| Total | 42 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
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