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Localization, induction, and cellular effects of tau phosphorylated at threonine 217
Rajbanshi B, Guruacharya A, Mandell JW, Bloom GS.. Alzheimer's & dementia : the journal of the Alzheimer's Association, 2023-01-12
Topic: Brain proteins, microglia and lab models
Introduction Tau phosphorylation at T217 is a promising Alzheimer's disease (AD) biomarker, but its functional consequences were unknown. Methods Human brain and cultured mouse neurons were analyzed by immunoblotting and immunofluorescence for total tau, tau pT217 , tau pT181 , tau pT231 , and tau pS396/pS404 . Direct stochastic optical reconstruction microscopy (dSTORM) super resolution microscopy was used to localize tau pT217 in cultured neurons. Enhanced green fluorescent protein (EGFP)-tau was expressed in fibroblasts as wild type and T217E pseudo-phosphorylated tau, and fluorescence recovery after photobleaching (FRAP) reported tau turnover rates on microtubules. Results In the brain, tau pT217 appears in neurons at Braak stages I and II, becomes more prevalent later, and co-localizes partially with other phospho-tau epitopes. In cultured neurons, tau pT217 is increased by extracellular tau oligomers (xcTauOs) and is associated with developing post-synaptic sites. FRAP recovery was fastest for EGFP-tau T217E . Conclusion Tau pT217 increases in the brain as AD progresses and is induced by xcTauOs. Post-synaptic tau pT217 suggests a role for T217 phosphorylation in synapse impairment. T217 phosphorylation reduces tau's affinity for microtubules. Highlights Validation of anti-tau phosphorylated at threonine-217 (tau pT217 ) specificity is essential due to epitope redundancy. tau pT217 increases as Alzheimer's disease progresses and is found throughout diseased neurons. tau pT217 is associated with developing post-synaptic sites in cultured neurons. Extracellular oligomers of tau, but not amyloid beta, increase intracellular tau pT217 . T217E pseudo-phosphorylation reduces tau's affinity for microtubules.
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APA 7th
Rajbanshi, B., Guruacharya, A., Mandell, J. W., & Bloom, G. S. (2023). Localization, induction, and cellular effects of tau phosphorylated at threonine 217. Alzheimer's & dementia : the journal of the Alzheimer's Association. https://doi.org/10.1002/alz.12892
Vancouver
Rajbanshi B, Guruacharya A, Mandell JW, Bloom GS. Localization, induction, and cellular effects of tau phosphorylated at threonine 217. Alzheimer's & dementia : the journal of the Alzheimer's Association. 2023. doi:10.1002/alz.12892. PMID: 36633254.
BibTeX
@article{rajbanshi2023-36633254,
author = {Rajbanshi, B. and Guruacharya, A. and Mandell, J. W. and Bloom, G. S.},
title = {{Localization, induction, and cellular effects of tau phosphorylated at threonine 217}},
journal = {Alzheimer's \& dementia : the journal of the Alzheimer's Association},
year = {2023},
doi = {10.1002/alz.12892},
pmid = {36633254},
url = {https://doi.org/10.1002/alz.12892}
}
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Key findings
- Results In the brain, tau pT217 appears in neurons at Braak stages I and II, becomes more prevalent later, and co-localizes partially with other phospho-tau epitopes.
- In cultured neurons, tau pT217 is increased by extracellular tau oligomers (xcTauOs) and is associated with developing post-synaptic sites.
- Highlights Validation of anti-tau phosphorylated at threonine-217 (tau pT217 ) specificity is essential due to epitope redundancy. tau pT217 increases as Alzheimer's disease progresses and is found throughout diseased neurons. tau pT217 is associated with developing post-synaptic sites in cultured neurons.
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Study details
- Evidence strengthLow
How this study scored 43/100
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. We have no data on journal's citation record, times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record and multi-centre collaboration, so those were left out: it earned 25 of the 58 points we could judge it on, which is 43 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 9 / 10 | Tier 2 — leading specialty journal (Alzheimer's & dementia : the journal of the Alzheimer's Association) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| 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 | 3 / 5 | 2023 — within 6 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 | — / 7 | No citation count (not found in OpenAlex) — left out of this score |
| Citations per year | — / 5 | No citation count or no year — left out of this score |
| Impact for its field and year | — / 6 | No field-weighted citation impact (OpenAlex has none yet) — left out of this score |
| Cited by studies here | — / 6 | Not yet checked against this library's citation graph — left out of this score |
| Still being cited | — / 4 | No yearly citation counts — left out of this score |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | — / 3 | No institution listed in OpenAlex — left out of this score |
| Multi-centre collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 36633254) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 25 / 58 | Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 25 of the 58 points we could judge it on is 43 out of 100. |
| Total | 43 / 100 | — |
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