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Homocysteine exacerbates β-amyloid pathology, tau pathology, and cognitive deficit in a mouse model of Alzheimer disease with plaques and tangles
Li JG, Chu J, Barrero C, Merali S, Praticò D.. Annals of neurology, 2014-05-28
Topic: Brain proteins, microglia and lab models
Objective High level of homocysteine (Hcy) is a recognized risk factor for developing Alzheimer disease (AD). However, the mechanisms involved are unknown. Previously, it was shown that high Hcy increases brain β-amyloid (Aβ) levels in amyloid precursor protein transgenic mice, but no data are available on the effect that it may have on the other main pathologic features of AD such as tau.
Key findings
- However, the mechanisms involved are unknown.
- Previously, it was shown that high Hcy increases brain β-amyloid (Aβ) levels in amyloid precursor protein transgenic mice, but no data are available on the effect that it may have on the other main pathologic features of AD such as tau.
- Methods 3xTg mice with diet-induced high Hcy were compared with mice having normal Hcy.
- Neuronal cells were incubated with and without Hcy.
Why it matters
In 3xTg mice, diet-induced high homocysteine worsened amyloid pathology, tau pathology and cognitive deficit. This is animal work on a risk factor and does not show that lowering homocysteine treats or prevents Alzheimer's disease in people.
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Study details
- Evidence strengthLow
How this study scored 45/100
Published in a leading specialty journal. Scored zero for study design, sample size, 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 | 1 / 5 | 2014 — 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 | 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 | 5 / 7 | Cited 129 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 9.2 citations a year over 14 year(s) since 2014 |
| Impact for its field and year | 3 / 6 | Cited 7.6× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 5 other studies in this library |
| Still being cited | 2 / 4 | Cited 30 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Domenico Praticò: h-index 92 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | Temple University: institution h-index 742 (OpenAlex) |
| Multi-centre collaboration | 0 / 3 | OpenAlex lists 1 institution(s) in 1 country — scores zero (affiliation lists can be incomplete) |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 24644038) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 45 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.
APA 7th
Li, J. G., Chu, J., Barrero, C., Merali, S., & Praticò, D. (2014). Homocysteine exacerbates β-amyloid pathology, tau pathology, and cognitive deficit in a mouse model of Alzheimer disease with plaques and tangles. Annals of neurology. https://doi.org/10.1002/ana.24145
Vancouver
Li JG, Chu J, Barrero C, Merali S, Praticò D. Homocysteine exacerbates β-amyloid pathology, tau pathology, and cognitive deficit in a mouse model of Alzheimer disease with plaques and tangles. Annals of neurology. 2014. doi:10.1002/ana.24145. PMID: 24644038.
BibTeX
@article{li2014-24644038,
author = {Li, J. G. and Chu, J. and Barrero, C. and Merali, S. and Praticò, D.},
title = {{Homocysteine exacerbates β-amyloid pathology, tau pathology, and cognitive deficit in a mouse model of Alzheimer disease with plaques and tangles}},
journal = {Annals of neurology},
year = {2014},
doi = {10.1002/ana.24145},
pmid = {24644038},
url = {https://doi.org/10.1002/ana.24145}
}
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