ArticleThe American journal of pathology2002
Lens defects and age-related fiber cell degeneration in a mouse model of increased AbetaPP gene dosage in Down syndrome.
Article in The American journal of pathology, 2002. 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
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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.
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Who cites it
19 citing papers in PubMed, 33 citations in OpenAlex.
- Alzheimer's Disease Seen through the Eye: Ocular Alterations and Neurodegeneration.International journal of molecular sciences · 2022Review
- Alzheimer's Retinopathy: Seeing Disease in the Eyes.Frontiers in neuroscience · 2020Review
- Peripheral Biomarkers for Early Detection of Alzheimer's and Parkinson's Diseases.Molecular neurobiology · 2019Review
- Inhibition of AMD-Like Pathology With a Neurotrophic Compound in Aged Rats and 3xTg-AD Mice.Frontiers in aging neuroscience · 2019Article
- Ocular indicators of Alzheimer's: exploring disease in the retina.Acta neuropathologica · 2016Review
- The Eye As a Biomarker for Alzheimer's Disease.Frontiers in neuroscience · 2016Review
- A test of lens opacity as an indicator of preclinical Alzheimer Disease.Experimental eye research · 2015Article
- FE65 and FE65L1 amyloid precursor protein-binding protein compound null mice display adult-onset cataract and muscle weakness.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015Article
- At the interface of sensory and motor dysfunctions and Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2015Review
- Promise and challenge: the lens model as a biomarker for early diagnosis of Alzheimer's disease.Disease markers · 2014Review
- PTBP-dependent PSD-95 and CamKIIα alternative splicing in the lens.Molecular vision · 2014Article
- Article
- Differential accumulation of secreted AbetaPP metabolites in ocular fluids.Journal of Alzheimer's disease : JAD · 2010Article
- Amyloid-peptide vaccinations reduce {beta}-amyloid plaques but exacerbate vascular deposition and inflammation in the retina of Alzheimer's transgenic mice.The American journal of pathology · 2009Article
- Beta-amyloid deposition and functional impairment in the retina of the APPswe/PS1DeltaE9 transgenic mouse model of Alzheimer's disease.Investigative ophthalmology & visual science · 2009Article
- Cataracts in transgenic mice caused by a human papillomavirus type 18 E7 oncogene driven by KRT1-14.Experimental and molecular pathology · 2008Article
- Article
- miRNA and Dicer in the mammalian lens: expression of brain-specific miRNAs in the lens.Histochemistry and cell biology · 2006Article
- Clinicopathological study of bilateral developmental cataracts diagnosed in utero.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2006Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Early-onset cataract and Alzheimer's disease occur with high frequency in Down syndrome (trisomy 21), the most common chromosome duplication in human live births. Previously, we used in vivo and lens organ culture models to demonstrate Alzheimer pathophysiology in oxidative stress-related lens degeneration. Currently, well-characterized Alzheimer transgenic mouse models are used to extend these findings. Here, we report on mice carrying a complete copy of a wild-type human AbetaPP (hAbetaPP) gene from the Down syndrome critical region on chromosome 21. hAbetaPP mice produce fiber cell membrane defects similar to those described in human cataracts and increased age-related lens degeneration. hAbetaPP expression and mRNA alternative splicing in human and mouse lens and cornea favor longer, potentially more amyloidogenic forms. Endogenous mouse AbetaPP expression is increased in transgenic lenses, consistent with the cycle of oxidative stress proposed in the mechanism of Alzheimer pathophysiology. Alternative splicing previously designated as neuron-specific occurs in human lens and cornea, and is maintained by hAbetaPP expressed in mouse tissues. These present data implicate AbetaPP in fiber cell formation and in early-onset cataracts in Down syndrome. Finally, our findings provide further support for our hypothesis that Alzheimer pathophysiology contributes to the cataract formation that is increasing in the aging population.
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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.