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Immunohistochemical characterization of microglia in Nasu-Hakola disease brains
Satoh J, Tabunoki H, Ishida T, Yagishita S, Jinnai K, Futamura N, Kobayashi M, Toyoshima I et al.. Neuropathology : official journal of the Japanese Society of Neuropathology, 2010-12-01
Topic: Brain proteins, microglia and lab models
Nasu-Hakola disease (NHD) is a rare autosomal recessive disorder, characterized by progressive presenile dementia and formation of multifocal bone cysts, caused by genetic mutations of DNAX-activation protein 12 (DAP12) or triggering receptor expressed on myeloid cells 2 (TREM2). TREM2 and DAP12 constitute a receptor/adapter signaling complex expressed on osteoclasts, dendritic cells (DC), macrophages and microglia. Previous studies using knockout mice and mouse brain cell cultures suggest that a loss-of-function of DAP12/TREM2 in microglia plays a central role in the neuropathological manifestation of NHD.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Satoh, J., Tabunoki, H., Ishida, T., Yagishita, S., Jinnai, K., Futamura, N., et al. (2011). Immunohistochemical characterization of microglia in Nasu-Hakola disease brains. Neuropathology : official journal of the Japanese Society of Neuropathology. https://doi.org/10.1111/j.1440-1789.2010.01174.x
Vancouver
Satoh J, Tabunoki H, Ishida T, Yagishita S, Jinnai K, Futamura N, et al. Immunohistochemical characterization of microglia in Nasu-Hakola disease brains. Neuropathology : official journal of the Japanese Society of Neuropathology. 2011. doi:10.1111/j.1440-1789.2010.01174.x. PMID: 21118401.
BibTeX
@article{satoh2011-21118401,
author = {Satoh, J. and Tabunoki, H. and Ishida, T. and Yagishita, S. and Jinnai, K. and Futamura, N. and Kobayashi, M. and Toyoshima, I. and others},
title = {{Immunohistochemical characterization of microglia in Nasu-Hakola disease brains}},
journal = {Neuropathology : official journal of the Japanese Society of Neuropathology},
year = {2011},
doi = {10.1111/j.1440-1789.2010.01174.x},
pmid = {21118401},
url = {https://doi.org/10.1111/j.1440-1789.2010.01174.x}
}
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Key findings
- TREM2 and DAP12 constitute a receptor/adapter signaling complex expressed on osteoclasts, dendritic cells (DC), macrophages and microglia.
- Previous studies using knockout mice and mouse brain cell cultures suggest that a loss-of-function of DAP12/TREM2 in microglia plays a central role in the neuropathological manifestation of NHD.
- However, there exist no immunohistochemical studies that focus attention on microglia in NHD brains.
- To elucidate a role of microglia in the pathogenesis of NHD, we searched NHD-specific biomarkers and characterized their expression on microglia in NHD brains.
Why it matters
This immunohistochemical study examined microglia in brains from people with Nasu-Hakola disease, a rare disorder caused by DAP12 or TREM2 mutations. It describes disease pathology in a rare condition and does not establish a treatment, cure or prevention for Alzheimer's disease.
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Study details
- Evidence strengthLow
How this study scored 37/100
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 (Neuropathology : official journal of the Japanese Society of Neuropathology) |
| Journal's citation record | 1 / 4 | Neuropathology: journal h-index 83 (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 | 2011 — 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) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 4 / 7 | Cited 66 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 3.9 citations a year over 17 year(s) since 2011 |
| Impact for its field and year | 2 / 6 | Cited 2.0× 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 | 1 / 4 | Cited 6 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Kunimasa Arima: h-index 46 (OpenAlex, whole career) |
| Institution's track record | 0 / 3 | National Center of Neurology and Psychiatry: institution h-index 356 (OpenAlex) |
| Multicenter collaboration | 2 / 3 | OpenAlex lists 8 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 21118401) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 37 / 100 | — |
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