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FUS pathology in basophilic inclusion body disease
Munoz DG, Neumann M, Kusaka H, Yokota O, Ishihara K, Terada S, Kuroda S, Mackenzie IR.. Acta neuropathologica, 2009-10-15
Topic: Brain proteins, microglia and lab models
Basophilic Inclusion Body Disease (BIBD) is a tau-negative form of frontotemporal lobar degeneration (FTLD), characterized by neuronal cytoplasmic inclusions (NCI) that are visible on hematoxylin and eosin stain (HE), contain RNA, and are inconsistently ubiquitin-immunoreactive (ir). The normal nuclear expression of TDP-43 is not altered. Here we investigate whether the distribution of the structurally and functionally related protein fused in sarcoma (FUS) is altered in BIBD.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Munoz, D. G., Neumann, M., Kusaka, H., Yokota, O., Ishihara, K., Terada, S., et al. (2009). FUS pathology in basophilic inclusion body disease. Acta neuropathologica. https://doi.org/10.1007/s00401-009-0598-9
Vancouver
Munoz DG, Neumann M, Kusaka H, Yokota O, Ishihara K, Terada S, et al. FUS pathology in basophilic inclusion body disease. Acta neuropathologica. 2009. doi:10.1007/s00401-009-0598-9. PMID: 19830439.
BibTeX
@article{munoz2009-19830439,
author = {Munoz, D. G. and Neumann, M. and Kusaka, H. and Yokota, O. and Ishihara, K. and Terada, S. and Kuroda, S. and Mackenzie, I. R.},
title = {{FUS pathology in basophilic inclusion body disease}},
journal = {Acta neuropathologica},
year = {2009},
doi = {10.1007/s00401-009-0598-9},
pmid = {19830439},
url = {https://doi.org/10.1007/s00401-009-0598-9}
}
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
- The normal nuclear expression of TDP-43 is not altered.
- Here we investigate whether the distribution of the structurally and functionally related protein fused in sarcoma (FUS) is altered in BIBD.
- Mutations in the FUS gene have recently been identified as a cause of familial amyotrophic lateral sclerosis (ALS).
- In addition to these familial ALS cases, FUS protein has recently been demonstrated in NCI in a subset of FTLD with ubiquitinated inclusions (atypical FTLD-U) and in neuronal intermediate filament inclusion disease (NIFID).
Why it matters
This study investigated whether the distribution of the FUS protein is altered in basophilic inclusion body disease, a tau-negative form of frontotemporal lobar degeneration. It concerns a different disease and does not address treating, curing or preventing Alzheimer's disease.
Study details
- Evidence strengthLow
How this study scored 51/100
Published in a leading specialty journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 9 / 10 | Tier 2 — leading specialty journal (Acta neuropathologica) |
| Journal's citation record | 3 / 4 | Acta Neuropathologica: journal h-index 287 (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 | 2009 — 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 253 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 13.3 citations a year over 19 year(s) since 2009 |
| Impact for its field and year | 4 / 6 | Cited 18.4× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 3 / 6 | Cited by 16 other studies in this library |
| Still being cited | 2 / 4 | Cited 19 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 4 / 4 | Last-listed author Ian R. Mackenzie: h-index 103 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | University of Toronto: institution h-index 1,923 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 7 institution(s) in 3 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 19830439) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 51 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1007/s00401-009-0598-9
- PubMed: 19830439
- Original source →
- Free full text: cIRcle (University of British Columbia) →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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