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39/100

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Disease mechanisms

Topic: Disease mechanisms in lab and animal studies

Plain-language summary

Synapse loss is a key feature of dementia, but it is unclear whether synaptic dysfunction precedes degenerative phases of the disease. Here, we show that even before any decrease in synapse density, there is abnormal turnover of cortical axonal boutons and dendritic spines in a mouse model of tauopathy-associated dementia. Strikingly, tauopathy drives a mismatch in synapse turnover; postsynaptic spines turn over more rapidly, whereas presynaptic boutons are stabilized. This imbalance between pre- and post-synaptic stability coincides with reduced synaptically driven neuronal activity in pre-degenerative stages of the disease.

Cite this study APA, Vancouver, BibTeX · download .bib or .ris

APA 7th

Jackson, J. S., Witton, J., Johnson, J. D., Ahmed, Z., Ward, M., Randall, A. D., et al. (2017). Altered Synapse Stability in the Early Stages of Tauopathy. Cell reports. https://doi.org/10.1016/j.celrep.2017.03.013

Vancouver

Jackson JS, Witton J, Johnson JD, Ahmed Z, Ward M, Randall AD, et al. Altered Synapse Stability in the Early Stages of Tauopathy. Cell reports. 2017. doi:10.1016/j.celrep.2017.03.013. PMID: 28355559.

BibTeX

@article{jackson2017-28355559,
  author  = {Jackson, Johanna S and Witton, Jonathan and Johnson, James D and Ahmed, Zeshan and Ward, Mark and Randall, Andrew D and Hutton, Michael L and Isaac, John T and others},
  title   = {{Altered Synapse Stability in the Early Stages of Tauopathy}},
  journal = {Cell reports},
  year    = {2017},
  doi     = {10.1016/j.celrep.2017.03.013},
  pmid    = {28355559},
  url     = {https://doi.org/10.1016/j.celrep.2017.03.013}
}

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How to read this study

Design: our record does not state a study design, so check the methods section of the original before weighing the result.
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Effect: the record gives no effect size, so the summary above cannot say how large any difference was.

What the evidence grade means here

This page is graded low. alzhub.org assigns the grade automatically from keywords in the abstract, not from reading the paper. Low means the abstract matched neither pattern. It is the default label, and it does not mean the work is poor; many sound lab and imaging papers land here. It can add at most 5 of the 100 points in the study score, and it is a label about design, not a verdict on whether the findings are true.

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Key findings

Synapse loss is a key feature of dementia, but it is unclear whether synaptic dysfunction precedes degenerative phases of the disease.
Here, we show that even before any decrease in synapse density, there is abnormal turnover of cortical axonal boutons and dendritic spines in a mouse model of tauopathy-associated dementia.
Strikingly, tauopathy drives a mismatch in synapse turnover; postsynaptic spines turn over more rapidly, whereas presynaptic boutons are stabilized.
This imbalance between pre- and post-synaptic stability coincides with reduced synaptically driven neuronal activity in pre-degenerative stages of the disease.

Study details

Evidence strengthLow

How this study scored 39/100

Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomized / 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, multicenter collaboration and free to read, so those were left out: it earned 22 of the 56 points we could judge it on, which is 39 out of 100.

Component	Points	Why
Journal tier	7 / 10	Tier 3 — peer-reviewed journal (Cell 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	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)
Randomized / blinded	0 / 2	No randomization 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
Multicenter collaboration	— / 3	Institutions not listed — left out of this score
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 28355559)
Free to read	— / 2	Access not recorded — left out of this score
Points	22 / 56	Scored on 10 of 20 parts. We have no data for the rest, so they are left out: 22 of the 56 points we could judge it on is 39 out of 100.
Total	39 / 100	—

What each of these 20 components measures, and what this score is not →

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