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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 49 out of 100. Risk genes beyond APOE

Topic: Brain proteins, microglia and lab models

To analyze the relationship between the deposition of amyloid beta peptides (Abeta) and neuronal loss in transgenic models of Alzheimer's disease (AD), we examined the frontal neocortex (Fc) and CA1 portion of hippocampus (CA1) in PSAPP mice doubly expressing AD-associated mutant presenilin 1 (PS1) and Swedish-type mutant beta amyloid precursor protein (APPsw) by morphometry of Abeta burden and neuronal counts. Deposition of Abeta was detected as early as 3 months of age in the Fc and CA1 of PSAPP mice and progressed to cover 28.3% of the superior frontal cortex and 18.4% of CA1 at 12 months: approximately 20- (Fc) and approximately 40- (CA1) fold greater deposition than in APPsw mice. There was no significant difference in neuronal counts in either CA1 or the frontal cortex between nontransgenic (non-tg), PS1 transgenic, APPsw, and PSAPP mice at 3 to 12 months of age.

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

APA 7th

Takeuchi, A., Irizarry, M. C., Duff, K., Saido, T. C., Hsiao Ashe, K., Hasegawa, M., et al. (2000). Age-related amyloid beta deposition in transgenic mice overexpressing both Alzheimer mutant presenilin 1 and amyloid beta precursor protein Swedish mutant is not associated with global neuronal loss. The American journal of pathology. https://doi.org/10.1016/s0002-9440(10)64544-0

Vancouver

Takeuchi A, Irizarry MC, Duff K, Saido TC, Hsiao Ashe K, Hasegawa M, et al. Age-related amyloid beta deposition in transgenic mice overexpressing both Alzheimer mutant presenilin 1 and amyloid beta precursor protein Swedish mutant is not associated with global neuronal loss. The American journal of pathology. 2000. doi:10.1016/s0002-9440(10)64544-0. PMID: 10880403.

BibTeX

@article{takeuchi2000-10880403,
  author  = {Takeuchi, A. and Irizarry, M. C. and Duff, K. and Saido, T. C. and Hsiao Ashe, K. and Hasegawa, M. and Mann, D. M. and Hyman, B. T. and others},
  title   = {{Age-related amyloid beta deposition in transgenic mice overexpressing both Alzheimer mutant presenilin 1 and amyloid beta precursor protein Swedish mutant is not associated with global neuronal loss}},
  journal = {The American journal of pathology},
  year    = {2000},
  doi     = {10.1016/s0002-9440(10)64544-0},
  pmid    = {10880403},
  url     = {https://doi.org/10.1016/s0002-9440(10)64544-0}
}

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.

Key findings

Why it matters

This study found that transgenic mice with both mutant presenilin 1 and mutant APP developed amyloid-beta deposits early but showed no significant difference in neuronal counts compared with other mice. It is animal research and does not test any treatment, cure, or prevention in people.

Study details

How this study scored 49/100
How this study's score is builtJournal tier 7 of 10; Journal's citation record 3 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 2 of 3; Studied in people 0 of 3; Randomised / blinded 0 of 2; Times cited 5 of 7; Citations per year 3 of 5; Impact for its field and year 4 of 6; Cited by studies here 2 of 6; Still being cited 1 of 4; Senior author's track record 4 of 4; Institution's track record 2 of 3; Multi-centre collaboration 2 of 3; Indexed in PubMed 2 of 2; Free to read 0 of 2. Total 49 of 100.49 of 100 points earned51 not earned

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

ComponentPointsWhy
Journal tier 7 / 10 Tier 3 — peer-reviewed journal (The American journal of pathology)
Journal's citation record 3 / 4 American Journal Of Pathology: journal h-index 328 (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 2000 — older than 20 years, still counted
Sample size 0 / 4 Participant count not stated — scores zero (not stated in the record — scored 0)
Effect reported 2 / 3 Effect reported as a number, without an interval or test
Studied in people 0 / 3 Laboratory or animal study (title names “transgenic”) — scores zero
Randomised / blinded 0 / 2 No randomisation or blinding stated — scores zero (not stated in the record — scored 0)
Times cited 5 / 7 Cited 230 times (OpenAlex, 2026-10-10)
Citations per year 3 / 5 8.2 citations a year over 28 year(s) since 2000
Impact for its field and year 4 / 6 Cited 9.7× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here 2 / 6 Cited by 8 other studies in this library
Still being cited 1 / 4 Cited 11 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record 4 / 4 Last-listed author Takeshi Iwatsubo: h-index 115 (OpenAlex, whole career)
Institution's track record 2 / 3 Massachusetts General Hospital: institution h-index 2,057 (OpenAlex)
Multi-centre collaboration 2 / 3 OpenAlex lists 7 institution(s) in 3 countries
Indexed in PubMed 2 / 2 Indexed in PubMed (PMID 10880403)
Free to read 0 / 2 Behind a paywall — scores zero
Total 49 / 100 —

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Read the original

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