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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 57 out of 100. Disease mechanisms

Topic: Brain proteins, microglia and lab models

Many potential treatments for Alzheimer's disease target amyloid-beta peptides (Abeta), which are widely presumed to cause the disease. The microtubule-associated protein tau is also involved in the disease, but it is unclear whether treatments aimed at tau could block Abeta-induced cognitive impairments. Here, we found that reducing endogenous tau levels prevented behavioral deficits in transgenic mice expressing human amyloid precursor protein, without altering their high Abeta levels. Tau reduction also protected both transgenic and nontransgenic mice against excitotoxicity. Thus, tau reduction can block Abeta- and excitotoxin-induced neuronal dysfunction and may represent an effective strategy for treating Alzheimer's disease and related conditions.

Why it matters

In mice engineered to make human amyloid precursor protein, reducing the mice's own tau prevented behavioral deficits without changing their high amyloid-beta levels. Tau reduction also protected mice against excitotoxicity, and the authors suggest it may represent an effective strategy for treating Alzheimer's disease.

How this study scored 57/100
How this study's score is builtJournal tier 10 of 10; Journal's citation record 4 of 4; Study design 0 of 12; Strength of evidence left out, no data; 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 7 of 7; Citations per year 5 of 5; Impact for its field and year 6 of 6; Cited by studies here 0 of 6; Still being cited 3 of 4; Senior author's track record 4 of 4; Institution's track record 2 of 3; Multi-centre collaboration 1 of 3; Indexed in PubMed 1 of 2; Free to read 0 of 2. 54 of the 95 points it could be judged on, which is 57 of 100. Total 57 of 100.54 of the 95 points we could judge = 57 of 100

Published in a top-tier journal. Scored zero for study design, sample size, effect reported and randomised / blinded because the record does not state it. We have no data on strength of evidence, so that was left out: it earned 54 of the 95 points we could judge it on, which is 57 out of 100.

ComponentPointsWhy
Journal tier 10 / 10 Tier 1 — top-tier general journal (Science)
Journal's citation record 4 / 4 Science: journal h-index 1,754 (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 — / 5 No evidence rating recorded — left out of this score
Peer-review validation 10 / 10 Peer-reviewed. Published as an article in a named peer-reviewed journal.
How recent 1 / 5 2007 — 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 “mouse”) — scores zero
Randomised / blinded 0 / 2 No randomisation or blinding stated — scores zero (not stated in the record — scored 0)
Times cited 7 / 7 Cited 1,901 times (OpenAlex, 2026-10-10)
Citations per year 5 / 5 90.5 citations a year over 21 year(s) since 2007
Impact for its field and year 6 / 6 Cited 56.2× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here 0 / 6 No other study in this library cites it
Still being cited 3 / 4 Cited 187 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record 4 / 4 Last-listed author Lennart Mucke: h-index 108 (OpenAlex, whole career)
Institution's track record 2 / 3 University of California, San Francisco: institution h-index 1,915 (OpenAlex)
Multi-centre collaboration 1 / 3 OpenAlex lists 2 institution(s) in 1 country
Indexed in PubMed 1 / 2 Not in PubMed, but has a DOI
Free to read 0 / 2 Behind a paywall — scores zero
Points 54 / 95 Scored on 19 of 20 parts. We have no data for the rest, so they are left out: 54 of the 95 points we could judge it on is 57 out of 100.
Total 57 / 100 —

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

Read the original

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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. The record names 9 authors; APA and Vancouver show the first six, BibTeX and the downloads carry all of them. Check the citation against the original before you use it.

APA 7th

Roberson, E. D., Scearce-Levie, K. A., Palop, J. J., Yan, F., Cheng, I. H.-J., Wu, T. Z., et al. (2007). Reducing Endogenous Tau Ameliorates Amyloid ß-Induced Deficits in an Alzheimer's Disease Mouse Model. Science. https://doi.org/10.1126/science.1141736

Vancouver

Roberson ED, Scearce-Levie KA, Palop JJ, Yan F, Cheng IH.-J, Wu TZ, et al. Reducing Endogenous Tau Ameliorates Amyloid ß-Induced Deficits in an Alzheimer's Disease Mouse Model. Science. 2007. doi:10.1126/science.1141736.

BibTeX

@article{roberson2007-2d6a1a5f,
  author  = {Roberson, Erik D. and Scearce-Levie, Kimberly A. and Palop, Jorge J. and Yan, Fengrong and Cheng, Irene Han-Juo and Wu, Tiffany Z. and Gerstein, Hilary and Yu, Gui-Qiu and Mucke, Lennart},
  title   = {{Reducing Endogenous Tau Ameliorates Amyloid ß-Induced Deficits in an Alzheimer's Disease Mouse Model}},
  journal = {Science},
  year    = {2007},
  doi     = {10.1126/science.1141736},
  url     = {https://doi.org/10.1126/science.1141736}
}

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