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Disrupted ubiquitin proteasome system underlying tau accumulation in Alzheimer's disease
Fang-Lin Weng, Ling He. Neurobiology of aging, 2020-12-08
Topic: Disease mechanisms in lab and animal studies
Accumulation of phosphorylated tau (p-tau) has long been an underappreciated hallmark of Alzheimer's disease. Tau is one of the major components of microtubule networks in neurons, and its abnormal phosphorylation and aggregation are closely related to the impairment of axonal transport. Abnormalities in axonal transport can impede autophagy in neurons, interrupting the autophagic clearance of amyloid beta. The ubiquitin proteasome system (UPS) maintains intracellular proteostasis by degrading abnormal or redundant proteins. Ever-mounting evidence suggests that UPS deficits contribute to p-tau accumulation. And targeting UPS attenuates tau pathology. This review endeavors to exam the potential role of UPS in p-tau aggregation, and how pathogenic tau may inflict other abnormalities such as amyloid beta accumulation in Alzheimer's disease.
Key findings
- Ever-mounting evidence suggests that UPS deficits contribute to p-tau accumulation.
Study details
- Evidence strengthLow
How this study scored 41/100
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. 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, multi-centre collaboration and free to read, so those were left out: it earned 23 of the 56 points we could judge it on, which is 41 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Neurobiology of aging) |
| 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 | 2021 — 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 33422896) |
| Free to read | — / 2 | Access not recorded — left out of this score |
| Points | 23 / 56 | Scored on 10 of 20 parts. We have no data for the rest, so they are left out: 23 of the 56 points we could judge it on is 41 out of 100. |
| Total | 41 / 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
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.
APA 7th
Weng, F.-L., & He, L. (2021). Disrupted ubiquitin proteasome system underlying tau accumulation in Alzheimer's disease. Neurobiology of aging. https://doi.org/10.1016/j.neurobiolaging.2020.11.015
Vancouver
Weng F.-L, He L. Disrupted ubiquitin proteasome system underlying tau accumulation in Alzheimer's disease. Neurobiology of aging. 2021. doi:10.1016/j.neurobiolaging.2020.11.015. PMID: 33422896.
BibTeX
@article{weng2021-33422896,
author = {Weng, Fang-Lin and He, Ling},
title = {{Disrupted ubiquitin proteasome system underlying tau accumulation in Alzheimer's disease}},
journal = {Neurobiology of aging},
year = {2021},
doi = {10.1016/j.neurobiolaging.2020.11.015},
pmid = {33422896},
url = {https://doi.org/10.1016/j.neurobiolaging.2020.11.015}
}
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