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45/100

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Drug development

Topic: Brain proteins, microglia and lab models

Plain-language summary

Introduction Synapse loss is the structural correlate of the cognitive decline indicative of dementia. In the brains of Alzheimer's disease sufferers, amyloid β (Aβ) peptides aggregate to form senile plaques but as soluble peptides are toxic to synapses. We previously demonstrated that Aβ induces Dickkopf-1 (Dkk1), which in turn activates the Wnt-planar cell polarity (Wnt-PCP) pathway to drive tau pathology and neuronal death. Methods We compared the effects of Aβ and of Dkk1 on synapse morphology and memory impairment while inhibiting or silencing key elements of the Wnt-PCP pathway. Results We demonstrate that Aβ synaptotoxicity is also Dkk1 and Wnt-PCP dependent, mediated by the arm of Wnt-PCP regulating actin cytoskeletal dynamics via Daam1, RhoA and ROCK, and can be blocked by the drug fasudil. Discussion Our data add to the importance of aberrant Wnt signaling in Alzheimer's disease neuropathology and indicate that fasudil could be repurposed as a treatment for the disease.

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APA 7th

Sellers, K. J., Elliott, C., Jackson, J., Ghosh, A., Ribe, E., Rojo, A. I., et al. (2018). Amyloid β synaptotoxicity is Wnt-PCP dependent and blocked by fasudil. Alzheimer's & dementia : the journal of the Alzheimer's Association. https://doi.org/10.1016/j.jalz.2017.09.008

Vancouver

Sellers KJ, Elliott C, Jackson J, Ghosh A, Ribe E, Rojo AI, et al. Amyloid β synaptotoxicity is Wnt-PCP dependent and blocked by fasudil. Alzheimer's & dementia : the journal of the Alzheimer's Association. 2018. doi:10.1016/j.jalz.2017.09.008. PMID: 29055813.

BibTeX

@article{sellers2018-29055813,
  author  = {Sellers, K. J. and Elliott, C. and Jackson, J. and Ghosh, A. and Ribe, E. and Rojo, A. I. and Jarosz-Griffiths, H. H. and Watson, I. A. and others},
  title   = {{Amyloid β synaptotoxicity is Wnt-PCP dependent and blocked by fasudil}},
  journal = {Alzheimer's \& dementia : the journal of the Alzheimer's Association},
  year    = {2018},
  doi     = {10.1016/j.jalz.2017.09.008},
  pmid    = {29055813},
  url     = {https://doi.org/10.1016/j.jalz.2017.09.008}
}

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How to read this study

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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

We previously demonstrated that Aβ induces Dickkopf-1 (Dkk1), which in turn activates the Wnt-planar cell polarity (Wnt-PCP) pathway to drive tau pathology and neuronal death.
Results We demonstrate that Aβ synaptotoxicity is also Dkk1 and Wnt-PCP dependent, mediated by the arm of Wnt-PCP regulating actin cytoskeletal dynamics via Daam1, RhoA and ROCK, and can be blocked by the drug fasudil.
Discussion Our data add to the importance of aberrant Wnt signaling in Alzheimer's disease neuropathology and indicate that fasudil could be repurposed as a treatment for the disease.

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Study details

Evidence strengthLow

How this study scored 45/100

Published in a leading specialty 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 and multicenter collaboration, so those were left out: it earned 26 of the 58 points we could judge it on, which is 45 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	2 / 5	2018 — 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 29055813)
Free to read	2 / 2	Free to read
Points	26 / 58	Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 26 of the 58 points we could judge it on is 45 out of 100.
Total	45 / 100	—

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

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