ArticleThe American journal of pathology2006
Transmission of amyloidosis in offspring of mice with AApoAII amyloidosis.
Article in The American journal of pathology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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.
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.
Who cites it
19 citing papers in PubMed, 32 citations in OpenAlex.
- Food protein-derived amyloids do not accelerate amyloid β aggregation.Scientific reports · 2023Article
- Huntington's disease: lessons from prion disorders.Journal of neurology · 2021Article
- Suppression of Mouse AApoAII Amyloidosis Progression by Daily Supplementation with Oxidative Stress Inhibitors.Oxidative medicine and cellular longevity · 2019Article
- Amyloidosis-inducing activity of blood cells in mouse AApoAII amyloidosis.Experimental animals · 2018Article
- Article
- Extracellular deposition of mouse senile AApoAII amyloid fibrils induced different unfolded protein responses in the liver, kidney, and heart.Laboratory investigation; a journal of technical methods and pathology · 2015Article
- Hot spots in apolipoprotein A-II misfolding and amyloidosis in mice and men.FEBS letters · 2014Article
- When amyloids become prions.Prion · 2014Article
- Review
- Article
- Review
- Renal amyloidosis caused by apolipoprotein A-II without a genetic mutation in the coding sequence.Clinical and experimental nephrology · 2011Article
- Misfolded protein aggregates: mechanisms, structures and potential for disease transmission.Seminars in cell & developmental biology · 2011Review
- Mouse senile amyloid fibrils deposited in skeletal muscle exhibit amyloidosis-enhancing activity.PLoS pathogens · 2010Article
- Animal models of human amyloidoses: are transgenic mice worth the time and trouble?FEBS letters · 2009Review
- Prion diseases and their biochemical mechanisms.Biochemistry · 2009Review
- Fecal transmission of AA amyloidosis in the cheetah contributes to high incidence of disease.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- Cross-seeding and cross-competition in mouse apolipoprotein A-II amyloid fibrils and protein A amyloid fibrils.The American journal of pathology · 2007Article
- Amyloidogenic potential of foie gras.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pre-existing amyloid fibrils can induce further polymerization of endogenous precursor proteins in vivo. Thus, transmission of amyloid fibrils (AApoAII) may induce a conformational change in endogenous apolipoprotein A-II and accelerate amyloid deposition in mouse senile amyloidosis. To characterize transmissibility, we examined amyloidosis in the offspring of AApoAII-injected mother mice that possessed the amyloidogenic Apoa2(c) allele of the apolipoprotein A-II gene. At 4 months of age, amyloid deposits were detected in the intestines of offspring born from and nursed by amyloid fibril-injected mothers, with intensity of deposition increasing thereafter. No amyloid deposits were detected in the offspring of noninjected control mothers. Accelerated amyloidosis was also observed in offspring born from mothers without injection but nursed by amyloid fibril-injected mothers. However, this was not observed in offspring born from amyloid fibril-injected mothers but nursed by control mothers. This fostering excluded vertical transmission through the placenta, suggesting the presence of factors that accelerate amyloidosis during the nursing period. In addition, milk obtained from amyloid fibril-injected mothers induced AApoAII amyloidosis in young mice, and transmission electron microscopy detected noodle-like amyloid fibrils in milk of amyloid fibril-injected mothers. These results provide important insight into the etiology and pathogenesis of amyloid diseases.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.