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Tau Antibody Targeting Pathological Species Blocks Neuronal Uptake and Interneuron Propagation of Tau in Vitro
Nobuhara CK, DeVos SL, Commins C, Wegmann S, Moore BD, Roe AD, Costantino I, Frosch MP et al.. The American journal of pathology, 2017-04-11
Topic: Brain proteins, microglia and lab models
The clinical progression of Alzheimer disease (AD) is associated with the accumulation of tau neurofibrillary tangles, which may spread throughout the cortex by interneuronal tau transfer. If so, targeting extracellular tau species may slow the spreading of tau pathology and possibly cognitive decline. To identify suitable target epitopes, we tested the effects of a panel of tau antibodies on neuronal uptake and aggregation in vitro.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Nobuhara, C. K., DeVos, S. L., Commins, C., Wegmann, S., Moore, B. D., Roe, A. D., et al. (2017). Tau Antibody Targeting Pathological Species Blocks Neuronal Uptake and Interneuron Propagation of Tau in Vitro. The American journal of pathology. https://doi.org/10.1016/j.ajpath.2017.01.022
Vancouver
Nobuhara CK, DeVos SL, Commins C, Wegmann S, Moore BD, Roe AD, et al. Tau Antibody Targeting Pathological Species Blocks Neuronal Uptake and Interneuron Propagation of Tau in Vitro. The American journal of pathology. 2017. doi:10.1016/j.ajpath.2017.01.022. PMID: 28408124.
BibTeX
@article{nobuhara2017-28408124,
author = {Nobuhara, C. K. and DeVos, S. L. and Commins, C. and Wegmann, S. and Moore, B. D. and Roe, A. D. and Costantino, I. and Frosch, M. P. and others},
title = {{Tau Antibody Targeting Pathological Species Blocks Neuronal Uptake and Interneuron Propagation of Tau in Vitro}},
journal = {The American journal of pathology},
year = {2017},
doi = {10.1016/j.ajpath.2017.01.022},
pmid = {28408124},
url = {https://doi.org/10.1016/j.ajpath.2017.01.022}
}
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Key findings
- If so, targeting extracellular tau species may slow the spreading of tau pathology and possibly cognitive decline.
- To identify suitable target epitopes, we tested the effects of a panel of tau antibodies on neuronal uptake and aggregation in vitro.
- Immunodepletion was performed on brain extract from tau-transgenic mice and postmortem AD brain and added to a sensitive fluorescence resonance energy transfer-based tau uptake assay to assess blocking efficacy.
- The antibodies reduced tau uptake in an epitope-dependent manner: N-terminal (Tau13) and middomain (6C5 and HT7) antibodies successfully prevented uptake of tau species, whereas the distal C-terminal-specific antibody (Tau46) had little effect.
Why it matters
This in vitro study tested a panel of tau antibodies for their ability to block neuronal uptake and aggregation of tau, with the idea that targeting extracellular tau might slow the spread of tau pathology. It is early laboratory work and does not test any treatment, cure, or prevention in people.
New to this subject? Start with our plain-English guide: Blood tests & biomarkers →
Study details
- Evidence strengthLow
How this study scored 48/100
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 (The American journal of pathology) |
| Journal's citation record | 3 / 4 | American Journal Of Pathology: journal h-index 328 (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 | 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) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 5 / 7 | Cited 119 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 10.8 citations a year over 11 year(s) since 2017 |
| Impact for its field and year | 4 / 6 | Cited 9.0× 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 | 2 / 4 | Cited 23 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Shuko Takeda: h-index 35 (OpenAlex, whole career) |
| Institution's track record | 3 / 3 | Harvard University: institution h-index 3,235 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 5 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 28408124) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 48 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1016/j.ajpath.2017.01.022
- PubMed: 28408124
- Original source →
- Free full text: American Journal Of Pathology →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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