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51/100

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Brain tissue and pathology

Topic: Brain proteins, microglia and lab models

Plain-language summary

Alzheimer's disease (AD) is the most prevalent form of dementia in the elderly population. Accumulation, aggregation, and deposition of amyloid-β (Aβ) peptides generated through proteolytic cleavage of amyloid precursor protein (APP) are likely initiating events in the pathogenesis of AD. While Aβ production is accelerated in familial AD, increasing evidence indicates that impaired clearance of Aβ is responsible for late-onset AD.

What this study adds

Evidence grade: Low

This paper discusses evidence that impaired clearance of amyloid-β, rather than its production, is responsible for late-onset Alzheimer's disease, and examines the role of the endocytic receptor LRP1 in neuronal clearance. It is a review of clearance mechanisms and does not report any treatment, cure or prevention.

Taken from this record’s own fields, not from reading the paper. The grade is assigned from the abstract’s wording; what that means.

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

APA 7th

Kanekiyo, T., Cirrito, JR., Liu, C. C., Shinohara, M., Li, J., Schuler, D. R., et al. (2013). Neuronal clearance of amyloid-β by endocytic receptor LRP1. The Journal of neuroscience : the official journal of the Society for Neuroscience. https://doi.org/10.1523/jneurosci.3487-13.2013

Vancouver

Kanekiyo T, Cirrito JR, Liu CC, Shinohara M, Li J, Schuler DR, et al. Neuronal clearance of amyloid-β by endocytic receptor LRP1. The Journal of neuroscience : the official journal of the Society for Neuroscience. 2013. doi:10.1523/jneurosci.3487-13.2013. PMID: 24305823.

BibTeX

@article{kanekiyo2013-24305823,
  author  = {Kanekiyo, T. and Cirrito, JR. and Liu, C. C. and Shinohara, M. and Li, J. and Schuler, D. R. and Holtzman, D. M. and others},
  title   = {{Neuronal clearance of amyloid-β by endocytic receptor LRP1}},
  journal = {The Journal of neuroscience : the official journal of the Society for Neuroscience},
  year    = {2013},
  doi     = {10.1523/jneurosci.3487-13.2013},
  pmid    = {24305823},
  url     = {https://doi.org/10.1523/jneurosci.3487-13.2013}
}

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's author list ends in “et al.”, so not every author is named. Check the citation against the original before you use it.

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.
Size: the record gives no participant count. Look for one in the original before trusting a pattern.
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.

New to reading papers? Six questions to ask of any Alzheimer’s study · how we score.

Key findings

Accumulation, aggregation, and deposition of amyloid-β (Aβ) peptides generated through proteolytic cleavage of amyloid precursor protein (APP) are likely initiating events in the pathogenesis of AD.
While Aβ production is accelerated in familial AD, increasing evidence indicates that impaired clearance of Aβ is responsible for late-onset AD.
Because Aβ is mainly generated in neurons, these cells are predicted to have the highest risk of encountering Aβ among all cell types in the brain.
However, it is still unclear whether they are also involved in Aβ clearance.

Why it matters

Study details

Evidence strengthLow

How this study scored 51/100

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.

Component	Points	Why
Journal tier	7 / 10	Tier 3 — peer-reviewed journal (The Journal of neuroscience : the official journal of the Society for Neuroscience)
Journal's citation record	4 / 4	Journal of Neuroscience: journal h-index 651 (OpenAlex, 2026-10-29)
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	2013 — within 20 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	5 / 7	Cited 281 times (OpenAlex, 2026-10-10)
Citations per year	3 / 5	18.7 citations a year over 15 year(s) since 2013
Impact for its field and year	4 / 6	Cited 12.5× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here	3 / 6	Cited by 10 other studies in this library
Still being cited	3 / 4	Cited 70 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	4 / 4	Last-listed author Guojun Bu: h-index 120 (OpenAlex, whole career)
Institution's track record	2 / 3	Washington University in St. Louis: institution h-index 1,962 (OpenAlex)
Multicenter collaboration	2 / 3	OpenAlex lists 5 institution(s) in 2 countries
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 24305823)
Free to read	0 / 2	Behind a paywall — scores zero
Total	51 / 100	—

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

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