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This page is alzhub.org's plain-English summary of a published study, not the paper itself. It is generated from the record we hold for this study, sourced and linked below — check the original for the full text and methods.

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Getting a diagnosis

Topic: Amyloid, tau and blood-test diagnosis

Alzheimer's disease (AD), the most common cause of dementia among the elderly, may either represent the far end of a continuum that begins with age-related memory decline or a distinct pathobiological process. Although mice that faithfully model all aspects of AD do not yet exist, current mouse models have provided valuable insights into specific aspects of AD pathogenesis. We will argue that transgenic mice expressing amyloid precursor protein should be considered models of accelerated brain aging or asymptomatic AD, and the results of interventional studies in these mice should be considered in the context of primary prevention. Studies in mice have pointed to the roles of soluble beta-amyloid (Abeta) oligomers and soluble tau in disease pathogenesis and support a model in which soluble Abeta oligomers trigger synaptic dysfunction, but formation of abnormal tau species leads to neuron death and cognitive decline severe enough to warrant a dementia diagnosis.

Key findings

Why it matters

This review argues that transgenic mice expressing amyloid precursor protein should be seen as models of accelerated brain aging or asymptomatic Alzheimer's disease, so intervention studies in them relate to primary prevention. It also points to roles for soluble beta-amyloid oligomers and soluble tau in disease processes, but these are animal-model findings.

Study details

How this study scored 50/100
How this study's score is builtJournal tier 7 of 10; Journal's citation record 4 of 4; Study design 0 of 12; Strength of evidence 1 of 5; Peer-review validation 10 of 10; How recent 1 of 5; Sample size 0 of 4; Effect reported 0 of 3; Studied in people 0 of 3; Randomised / blinded 0 of 2; Times cited 6 of 7; Citations per year 4 of 5; Impact for its field and year 5 of 6; Cited by studies here 3 of 6; Still being cited 2 of 4; Senior author's track record 2 of 4; Institution's track record 2 of 3; Multi-centre collaboration 1 of 3; Indexed in PubMed 2 of 2; Free to read 0 of 2. Total 50 of 100.50 of 100 points earned50 not earned

Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported and randomised / blinded because the record does not state it.

ComponentPointsWhy
Journal tier 7 / 10 Tier 3 — peer-reviewed journal (Neuron)
Journal's citation record 4 / 4 Neuron: journal h-index 689 (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 2010 — 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 Laboratory or animal study (title names “mice”) — scores zero
Randomised / blinded 0 / 2 No randomisation or blinding stated — scores zero (not stated in the record — scored 0)
Times cited 6 / 7 Cited 416 times (OpenAlex, 2026-10-10)
Citations per year 4 / 5 23.1 citations a year over 18 year(s) since 2010
Impact for its field and year 5 / 6 Cited 33.0× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here 3 / 6 Cited by 12 other studies in this library
Still being cited 2 / 4 Cited 26 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record 2 / 4 Last-listed author Kathleen R. Zahs: h-index 29 (OpenAlex, whole career)
Institution's track record 2 / 3 University of Minnesota: institution h-index 1,568 (OpenAlex)
Multi-centre collaboration 1 / 3 OpenAlex lists 2 institution(s) in 1 country
Indexed in PubMed 2 / 2 Indexed in PubMed (PMID 20547123)
Free to read 0 / 2 Behind a paywall — scores zero
Total 50 / 100 —

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

Read the original

Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).

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

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.

APA 7th

Ashe, K. H., & Zahs, K. R. (2010). Probing the biology of Alzheimer's disease in mice. Neuron. https://doi.org/10.1016/j.neuron.2010.04.031

Vancouver

Ashe KH, Zahs KR. Probing the biology of Alzheimer's disease in mice. Neuron. 2010. doi:10.1016/j.neuron.2010.04.031. PMID: 20547123.

BibTeX

@article{ashe2010-20547123,
  author  = {Ashe, K. H. and Zahs, K. R.},
  title   = {{Probing the biology of Alzheimer's disease in mice}},
  journal = {Neuron},
  year    = {2010},
  doi     = {10.1016/j.neuron.2010.04.031},
  pmid    = {20547123},
  url     = {https://doi.org/10.1016/j.neuron.2010.04.031}
}

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