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Favorably against the odds - autophagy control despite advanced amyloid- ß toxicity
Claudia M Ntsapi, Andre du Toit, Ben Loos. Autophagy reports, 2022-05-30
Topic: Disease mechanisms in lab and animal studies
Alzheimer disease (AD) is a devastating condition associated with loss of proteostasis control and autophagy failure, leading to progressive neuronal cell death. However, the relationship between the activity in macroautophagy (MA) and chaperone-mediated autophagy (CMA) in the context of cargo clearance remains poorly dissected. We have found that cell death is observed as early as 24 h into amyloid-induced toxicity, despite enhanced and fully functional autophagy activity even at late stages of injury progression, whereas inhibition of autophagosome degradation indeed shifts apoptosis onset to an earlier point in time. A prolonged intermittent fasting (IF) regimen during severe paraquat-induced neuronal injury enhances both MA- and CMA-associated protein clearance in the brain differentially and region-specifically. These results have a number of practical implications that point towards a major focus to decrease proteinaceous cargo burden, while enhancing autophagy flux early and late in the pathogenesis, so as to rapidly offset the disequilibrium between cargo and machinery flux. In this punctum, we summarize these findings.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Ntsapi, C. M., du Toit, A., & Loos, B. (2022). Favorably against the odds - autophagy control despite advanced amyloid- ß toxicity. Autophagy reports. https://doi.org/10.1080/27694127.2022.2082631
Vancouver
Ntsapi CM, du Toit A, Loos B. Favorably against the odds - autophagy control despite advanced amyloid- ß toxicity. Autophagy reports. 2022. doi:10.1080/27694127.2022.2082631. PMID: 40396009.
BibTeX
@article{ntsapi2022-40396009,
author = {Ntsapi, Claudia M and du Toit, Andre and Loos, Ben},
title = {{Favorably against the odds - autophagy control despite advanced amyloid- ß toxicity}},
journal = {Autophagy reports},
year = {2022},
doi = {10.1080/27694127.2022.2082631},
pmid = {40396009},
url = {https://doi.org/10.1080/27694127.2022.2082631}
}
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Key findings
- Alzheimer disease (AD) is a devastating condition associated with loss of proteostasis control and autophagy failure, leading to progressive neuronal cell death.
- These results have a number of practical implications that point towards a major focus to decrease proteinaceous cargo burden, while enhancing autophagy flux early and late in the pathogenesis, so as to rapidly offset the disequilibrium between cargo and machinery flux.
- In this punctum, we summarize these findings.
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 (Autophagy reports) |
| 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 | 2022 — 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 40396009) |
| 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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