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Glycoprotein NMB: a novel Alzheimer's disease associated marker expressed in a subset of activated microglia
Hüttenrauch M, Ogorek I, Klafki H, Otto M, Stadelmann C, Weggen S, Wiltfang J, Wirths O.. Acta neuropathologica communications, 2018-10-19
Topic: Amyloid, tau and blood-test diagnosis
Alzheimer's disease (AD) is an irreversible, devastating neurodegenerative brain disorder characterized by the loss of neurons and subsequent cognitive decline. Despite considerable progress in the understanding of the pathophysiology of AD, the precise molecular mechanisms that cause the disease remain elusive. By now, there is ample evidence that activated microglia have a critical role in the initiation and progression of AD.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Hüttenrauch, M., Ogorek, I., Klafki, H., Otto, M., Stadelmann, C., Weggen, S., et al. (2018). Glycoprotein NMB: a novel Alzheimer's disease associated marker expressed in a subset of activated microglia. Acta neuropathologica communications. https://doi.org/10.1186/s40478-018-0612-3
Vancouver
Hüttenrauch M, Ogorek I, Klafki H, Otto M, Stadelmann C, Weggen S, et al. Glycoprotein NMB: a novel Alzheimer's disease associated marker expressed in a subset of activated microglia. Acta neuropathologica communications. 2018. doi:10.1186/s40478-018-0612-3. PMID: 30340518.
BibTeX
@article{huttenrauch2018-30340518,
author = {Hüttenrauch, M. and Ogorek, I. and Klafki, H. and Otto, M. and Stadelmann, C. and Weggen, S. and Wiltfang, J. and Wirths, O.},
title = {{Glycoprotein NMB: a novel Alzheimer's disease associated marker expressed in a subset of activated microglia}},
journal = {Acta neuropathologica communications},
year = {2018},
doi = {10.1186/s40478-018-0612-3},
pmid = {30340518},
url = {https://doi.org/10.1186/s40478-018-0612-3}
}
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 8 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
- Despite considerable progress in the understanding of the pathophysiology of AD, the precise molecular mechanisms that cause the disease remain elusive.
- By now, there is ample evidence that activated microglia have a critical role in the initiation and progression of AD.
- The present study describes the identification of Glycoprotein nonmetastatic melanoma protein B (GPNMB) as a novel AD-related factor in both transgenic mice and sporadic AD patients by expression profiling, immunohistochemistry and ELISA measurements.
- We show that GPNMB levels increase in an age-dependent manner in transgenic AD models showing profound cerebral neuron loss and demonstrate that GPNMB co-localizes with a distinct population of IBA1-positive microglia cells that cluster around amyloid plaques.
Why it matters
This study identified GPNMB as an Alzheimer's-related factor found in a subset of activated microglia in transgenic mice and in people with sporadic Alzheimer's. It describes a possible marker and does not report a treatment, cure or prevention.
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Study details
- Evidence strengthLow
How this study scored 47/100
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.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Acta neuropathologica communications) |
| Journal's citation record | 1 / 4 | Acta Neuropathologica Communications: journal h-index 129 (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 | 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 | 5 / 7 | Cited 167 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 16.7 citations a year over 10 year(s) since 2018 |
| Impact for its field and year | 3 / 6 | Cited 5.1× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 3 other studies in this library |
| Still being cited | 3 / 4 | Cited 72 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Oliver Wirths: h-index 54 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | University of Göttingen: institution h-index 934 (OpenAlex) |
| Multicenter collaboration | 2 / 3 | OpenAlex lists 5 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 30340518) |
| Free to read | 2 / 2 | Free to read |
| Total | 47 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1186/s40478-018-0612-3
- PubMed: 30340518
- Original source →
- Free full text: Acta Neuropathologica Communications →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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