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41/100

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Risk genes beyond APOE

Topic: Amyloid, tau and blood-test diagnosis

Plain-language summary

The amyloid-beta (Aβ) peptide is the derivative of amyloid precursor protein (APP) generated through sequential proteolytic processing by β- and γ-secretases. Excessive accumulation of Aβ, the main constituent of amyloid plaques, has been implicated in the etiology of Alzheimer's disease (AD). It was found recently that the impairments of neurogenesis in brain were associated with the pathogenesis of AD.

What this study adds

Evidence grade: Low

This is a narrative review. This review discusses roles of amyloid precursor protein in neurogenesis and how impaired neurogenesis has been associated with Alzheimer's disease pathogenesis. It is a summary of laboratory findings and does not establish a 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

Zhou, Z. D., Chan, C. H., Ma, Q. H., Xu, X. H., Xiao, Z. C., & Tan, E. K. (2011). The roles of amyloid precursor protein (APP) in neurogenesis: Implications to pathogenesis and therapy of Alzheimer disease. Cell adhesion & migration. https://doi.org/10.4161/cam.5.4.16986

Vancouver

Zhou ZD, Chan CH, Ma QH, Xu XH, Xiao ZC, Tan EK. The roles of amyloid precursor protein (APP) in neurogenesis: Implications to pathogenesis and therapy of Alzheimer disease. Cell adhesion & migration. 2011. doi:10.4161/cam.5.4.16986. PMID: 21785276.

BibTeX

@article{zhou2011-21785276,
  author  = {Zhou, Z. D. and Chan, C. H. and Ma, Q. H. and Xu, X. H. and Xiao, Z. C. and Tan, E. K.},
  title   = {{The roles of amyloid precursor protein (APP) in neurogenesis: Implications to pathogenesis and therapy of Alzheimer disease}},
  journal = {Cell adhesion \& migration},
  year    = {2011},
  doi     = {10.4161/cam.5.4.16986},
  pmid    = {21785276},
  url     = {https://doi.org/10.4161/cam.5.4.16986}
}

Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.

How to read this study

Design: this is a narrative review. It summarises a field without a fixed search method, so it shows how authors read the evidence rather than measuring it. Use it to find the primary studies, not as a result in itself.
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.

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Key findings

Excessive accumulation of Aβ, the main constituent of amyloid plaques, has been implicated in the etiology of Alzheimer's disease (AD).
It was found recently that the impairments of neurogenesis in brain were associated with the pathogenesis of AD.
Furthermore recent findings implicated that APP could function to influence proliferation of neural progenitor cells (NPC) and might regulate transcriptional activity of various genes.
Studies demonstrated that influence of neurogenesis by APP is conferred differently via its two separate domains, soluble secreted APPs (sAPPs, mainly sAPPα) and APP intracellular domain (AICD).

Why it matters

This review discusses roles of amyloid precursor protein in neurogenesis and how impaired neurogenesis has been associated with Alzheimer's disease pathogenesis. It is a summary of laboratory findings and does not establish a treatment, cure, or prevention.

New to this subject? Start with our plain-English guide: Genetics →

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 randomized / blinded because the record does not state it.

Component	Points	Why
Journal tier	7 / 10	Tier 3 — peer-reviewed journal (Cell adhesion & migration)
Journal's citation record	1 / 4	Cell Adhesion & Migration: journal h-index 91 (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	2011 — 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 163 times (OpenAlex, 2026-10-10)
Citations per year	3 / 5	9.6 citations a year over 17 year(s) since 2011
Impact for its field and year	3 / 6	Cited 6.0× 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	2 / 4	Cited 43 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	2 / 4	Last-listed author Eng‐King Tan: h-index 33 (OpenAlex, whole career)
Institution's track record	1 / 3	National University of Singapore: institution h-index 1,166 (OpenAlex)
Multicenter collaboration	2 / 3	OpenAlex lists 8 institution(s) in 3 countries
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 21785276)
Free to read	0 / 2	Behind a paywall — scores zero
Total	41 / 100	—

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

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