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Aggregate-prone proteins are cleared from the cytosol by autophagy: therapeutic implications
Williams A, Jahreiss L, Sarkar S, Saiki S, Menzies FM, Ravikumar B, Rubinsztein DC.. Current topics in developmental biology, 2006-01-01
Topic: Brain proteins, microglia and lab models
Intracellular protein misfolding/aggregation are features of many late-onset neurodegenerative diseases, called proteinopathies. These include Alzheimer's disease, Parkinson's disease, tauopathies, and polyglutamine expansion diseases [e.g., Huntington's disease; and various spinocerebellar ataxias (SCAs), like SCA3]. There are no effective strategies to slow or prevent the neurodegeneration resulting from these diseases in humans.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Williams, A., Jahreiss, L., Sarkar, S., Saiki, S., Menzies, F. M., Ravikumar, B., et al. (2006). Aggregate-prone proteins are cleared from the cytosol by autophagy: therapeutic implications. Current topics in developmental biology. https://doi.org/10.1016/s0070-2153(06)76003-3
Vancouver
Williams A, Jahreiss L, Sarkar S, Saiki S, Menzies FM, Ravikumar B, et al. Aggregate-prone proteins are cleared from the cytosol by autophagy: therapeutic implications. Current topics in developmental biology. 2006. doi:10.1016/s0070-2153(06)76003-3. PMID: 17118264.
BibTeX
@article{williams2006-17118264,
author = {Williams, A. and Jahreiss, L. and Sarkar, S. and Saiki, S. and Menzies, F. M. and Ravikumar, B. and Rubinsztein, D. C.},
title = {{Aggregate-prone proteins are cleared from the cytosol by autophagy: therapeutic implications}},
journal = {Current topics in developmental biology},
year = {2006},
doi = {10.1016/s0070-2153(06)76003-3},
pmid = {17118264},
url = {https://doi.org/10.1016/s0070-2153(06)76003-3}
}
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. The record names 7 authors; APA and Vancouver show the first six, BibTeX and the downloads carry all of them. Check the citation against the original before you use it.
Key findings
- These include Alzheimer's disease, Parkinson's disease, tauopathies, and polyglutamine expansion diseases [e.g., Huntington's disease; and various spinocerebellar ataxias (SCAs), like SCA3].
- There are no effective strategies to slow or prevent the neurodegeneration resulting from these diseases in humans.
- The mutations causing many proteinopathies (e.g., polyglutamine diseases and tauopathies) confer novel toxic functions on the specific protein, and disease severity frequently correlates with the expression levels of the protein.
- Thus, the factors regulating the synthesis and clearance of these aggregate-prone proteins are putative therapeutic targets.
Why it matters
This review discusses how autophagy clears aggregate-prone proteins and its therapeutic implications for proteinopathies including Alzheimer's disease. It is a discussion of a possible approach and does not report a treatment or cure.
Study details
- Evidence strengthLow
How this study scored 44/100
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, so that was left out: it earned 42 of the 96 points we could judge it on, which is 44 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Current topics in developmental biology) |
| 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 | 1 / 5 | 2006 — older than 20 years, still counted |
| 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 287 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 13.0 citations a year over 22 year(s) since 2006 |
| Impact for its field and year | 6 / 6 | Cited 78.6× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 1 / 6 | Cited by 2 other studies in this library |
| Still being cited | 1 / 4 | Cited 9 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 4 / 4 | Last-listed author David Chaim Rubinsztein: h-index 144 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | Addenbrooke's Hospital: institution h-index 1,025 (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 17118264) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 42 / 96 | Scored on 19 of 20 parts. We have no data for the rest, so they are left out: 42 of the 96 points we could judge it on is 44 out of 100. |
| Total | 44 / 100 | — |
What each of these 20 components measures, and what this score is not →
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