Evidence map›Paper›PMID 17400334›Full record

ArticleNeurobiology of aging2008

Genetic loci modulating amyloid-beta levels in a mouse model of Alzheimer's disease.

Davis Ryman, Yuan Gao, Bruce T Lamb

Abstract read
In one paragraph

Article in Neurobiology of aging, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.5field-weighted citation impact, top 18% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

26 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Genetic diversity promotes resilience in a mouse model of Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Article
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  17. Transcriptome analysis of distinct mouse strains reveals kinesin light chain-1 splicing as an amyloid-β accumulation modifier.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  18. Complement in the brain.Molecular immunology · 2011
    Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Davis RymanLerner Research Institute, Cleveland Clinic Foundation, Department of Neurosciences, NC3-164, 9500 Euclid Avenue, Cleveland, OH 44195 USA.
Yuan Gao
Bruce T Lamb
Case Western Reserve University · USCleveland Clinic · US

Funding

TUMOR METABOLISM PROGRAMP30CA043703 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI MARK R CHANCE · 1987 to 2026
$142.3M
MEDICAL SCIENTIST TRAINING PROGRAMT32GM007250 · NIGMS · CASE WESTERN RESERVE UNIVERSITY · PI HUANG, ALEX YEE-CHEN · 1985 to 2023
$33.4M
TRAINING IN GENETICST32GM008613 · NIGMS · CASE WESTERN RESERVE UNIVERSITY · PI SALZ, HELEN KAREN · 1996 to 2010
$3.1M
Modifiers of Beta-Amyloid Metabolism and DepositionR01AG023012 · NIA · CLEVELAND CLINIC LERNER COM-CWRU · PI LAMB, BRUCE T · 2004 to 2013
$2.9M
NCI NIH HHS CA43703NCI NIH HHS P30 CA043703NIA NIH HHS AG023012NIA NIH HHS R01 AG023012NIGMS NIH HHS T32 GM007250NIGMS NIH HHS T32 GM008613NIGMS NIH HHS T32 GM07250
6 · The paper itself

Abstract

Genetic studies have demonstrated very high heritability for Alzheimer's disease (AD) risk in humans; however, these genetic contributions have proven extremely challenging to map in large studies of AD patients. Processing of the amyloid precursor protein (APP) to produce amyloid-beta (Abeta) peptide is increasingly believed to be of central importance in AD pathogenesis. Intriguingly, mice from the C57BL/6J and DBA2/J inbred strains carrying the R1.40 APP transgene produce identical levels of unprocessed APP, but demonstrate significant, heritable differences in Abeta levels. To identify specific loci responsible for the observed genetic control of Abeta metabolism in this model system, we have performed a whole-genome quantitative trait locus (QTL) mapping experiment on a total of 516 animals from a C57BL/6JxDBA/2J intercross using a dense set of SNP genetic markers. Our studies have identified three loci on mouse chromosomes 1, 2, and 7 showing significant or suggestive associations with brain Abeta levels, several of which contain regions syntenic to previous reports of linkage in human AD.

Indexed as

Disease Models, AnimalAlzheimer DiseaseAmyloid beta-PeptidesAnimalsBrainFemaleGene Expression RegulationMaleMiceMice, Inbred C57BLMice, Inbred DBAMice, TransgenicQuantitative Trait, HeritableQuantitative Trait LociAmyloid beta-Peptides

Identifiers

PMID17400334
PMCPMC3745768
OpenAlexW2036695223

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.