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Colocalization of transactivation-responsive DNA-binding protein 43 and huntingtin in inclusions of Huntington disease
Schwab C, Arai T, Hasegawa M, Yu S, McGeer PL.. Journal of neuropathology and experimental neurology, 2008-12-01
Topic: Brain proteins, microglia and lab models
Transactivation-responsive DNA-binding protein 43 (TDP-43) is a component of pathological inclusions in amyotrophic lateral sclerosis and several forms of sporadic and familial frontotemporal lobar degeneration. Transactivation-responsive DNA-binding protein 43-immunostained inclusions have also been found in other neurodegenerative disorders including Alzheimer disease, dementia with Lewy bodies, and parkinsonism dementia complex of Guam. Here, we analyzed the occurrence of TDP-43 immunostaining in Huntington disease, which is characterized by inclusions containing mutated huntingtin.
Key findings
- Transactivation-responsive DNA-binding protein 43-immunostained inclusions have also been found in other neurodegenerative disorders including Alzheimer disease, dementia with Lewy bodies, and parkinsonism dementia complex of Guam.
- Here, we analyzed the occurrence of TDP-43 immunostaining in Huntington disease, which is characterized by inclusions containing mutated huntingtin.
- In all Huntington disease cases studied, TDP-43 was frequently colocalized with huntingtin in dystrophic neurites and various intracellular inclusions, but not in intranuclear inclusions; the latter were only stained with huntingtin and anti-ubiquitin antibodies.
- Two phosphorylation-dependent TDP-43 antibodies proved to be superior for detecting pathological inclusions because they did not stain nonphosphorylated TDP-43 in normal nuclei; staining of normal nuclei with phosphorylation-independent antibodies obscured the inclusions.
Why it matters
This laboratory analysis found TDP-43 protein together with huntingtin in brain inclusions of people with Huntington disease, a condition different from Alzheimer's. It offers no treatment, cure or prevention for Alzheimer's disease.
Study details
- Evidence strengthLow
How this study scored 45/100
Published in a peer-reviewed 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 | 7 / 10 | Tier 3 — peer-reviewed journal (Journal of neuropathology and experimental neurology) |
| Journal's citation record | 2 / 4 | Journal of Neuropathology & Experimental Neurology: journal h-index 239 (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 | 2008 — 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 271 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 13.6 citations a year over 20 year(s) since 2008 |
| Impact for its field and year | 3 / 6 | Cited 6.2× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 3 / 6 | Cited by 17 other studies in this library |
| Still being cited | 3 / 4 | Cited 50 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 4 / 4 | Last-listed author Patrick L. McGeer: h-index 119 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | University of British Columbia: institution h-index 1,424 (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 19018245) |
| 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 →
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Cite this study APA, Vancouver, BibTeX · download .bib or .ris
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APA 7th
Schwab, C., Arai, T., Hasegawa, M., Yu, S., & McGeer, P. L. (2008). Colocalization of transactivation-responsive DNA-binding protein 43 and huntingtin in inclusions of Huntington disease. Journal of neuropathology and experimental neurology. https://doi.org/10.1097/nen.0b013e31818e8951
Vancouver
Schwab C, Arai T, Hasegawa M, Yu S, McGeer PL. Colocalization of transactivation-responsive DNA-binding protein 43 and huntingtin in inclusions of Huntington disease. Journal of neuropathology and experimental neurology. 2008. doi:10.1097/nen.0b013e31818e8951. PMID: 19018245.
BibTeX
@article{schwab2008-19018245,
author = {Schwab, C. and Arai, T. and Hasegawa, M. and Yu, S. and McGeer, P. L.},
title = {{Colocalization of transactivation-responsive DNA-binding protein 43 and huntingtin in inclusions of Huntington disease}},
journal = {Journal of neuropathology and experimental neurology},
year = {2008},
doi = {10.1097/nen.0b013e31818e8951},
pmid = {19018245},
url = {https://doi.org/10.1097/nen.0b013e31818e8951}
}
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