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Neocortical and hippocampal TREM2 protein levels during the progression of Alzheimer's disease
Perez SE, Nadeem M, He B, Miguel JC, Malek-Ahmadi MH, Chen K, Mufson EJ.. Neurobiology of aging, 2017-03-09
Topic: Brain proteins, microglia and lab models
Heterozygous triggering receptor expressed on myeloid cells (TREM2) mutations are an Alzheimer's disease (AD) risk factor. Nonmutated TREM2 dysregulation occurs in AD brain. Whether TREM2 is altered in prodromal AD remains unknown. Western blotting was used to determine levels of TREM2 (∼25 kDa) and Iba1 in the frontal cortex and TREM2 in the hippocampus from people who died with an ante-mortem clinical diagnosis of non- and mild-cognitive impairment, mild/moderate AD, and severe AD (sAD). Immunohistochemistry defined the relationship between amyloid and Iba1 profiles. Polymerase chain reaction analysis revealed that all subjects did not carry the most common R47H TREM2 variant. TREM2 was significantly upregulated in sAD frontal cortex but stable in hippocampus. Frontal TREM2 mRNA and protein level patterns were similar but not significantly different. Iba1 immunopositive microglia counts increased significantly in frontal cortex containing plaques in sAD. TREM2 and Iba1 levels were not associated with plaques, tangles, neuropathological criteria, or cognitive performance. Frontal cortex TREM2 upregulation is a late event and may not play a major role early in the pathogenesis of the disease.
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APA 7th
Perez, S. E., Nadeem, M., He, B., Miguel, J. C., Malek-Ahmadi, M. H., Chen, K., et al. (2017). Neocortical and hippocampal TREM2 protein levels during the progression of Alzheimer's disease. Neurobiology of aging. https://doi.org/10.1016/j.neurobiolaging.2017.02.012
Vancouver
Perez SE, Nadeem M, He B, Miguel JC, Malek-Ahmadi MH, Chen K, et al. Neocortical and hippocampal TREM2 protein levels during the progression of Alzheimer's disease. Neurobiology of aging. 2017. doi:10.1016/j.neurobiolaging.2017.02.012. PMID: 28365005.
BibTeX
@article{perez2017-28365005,
author = {Perez, S. E. and Nadeem, M. and He, B. and Miguel, J. C. and Malek-Ahmadi, M. H. and Chen, K. and Mufson, E. J.},
title = {{Neocortical and hippocampal TREM2 protein levels during the progression of Alzheimer's disease}},
journal = {Neurobiology of aging},
year = {2017},
doi = {10.1016/j.neurobiolaging.2017.02.012},
pmid = {28365005},
url = {https://doi.org/10.1016/j.neurobiolaging.2017.02.012}
}
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. The record names 7 authors; APA and Vancouver show the first six, BibTeX and the downloads carry all of them. Check the citation against the original before you use it.
Key findings
- Polymerase chain reaction analysis revealed that all subjects did not carry the most common R47H TREM2 variant.
- TREM2 was significantly upregulated in sAD frontal cortex but stable in hippocampus.
- Frontal TREM2 mRNA and protein level patterns were similar but not significantly different.
- Iba1 immunopositive microglia counts increased significantly in frontal cortex containing plaques in sAD.
- TREM2 and Iba1 levels were not associated with plaques, tangles, neuropathological criteria, or cognitive performance.
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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 randomized / 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 multicenter collaboration, so those were left out: it earned 22 of the 58 points we could judge it on, which is 38 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Neurobiology of aging) |
| 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 | 2 / 5 | 2017 — within 10 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) |
| Randomized / blinded | 0 / 2 | No randomization 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 |
| Multicenter collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 28365005) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 22 / 58 | Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 22 of the 58 points we could judge it on is 38 out of 100. |
| Total | 38 / 100 | — |
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