ArticleJournal of aging research2011
Fiber Tracts Anomalies in APPxPS1 Transgenic Mice Modeling Alzheimer's Disease.
Article in Journal of aging research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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.
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.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Amyloid-β-induced pyroptosis drives retinal neurodegeneration in a TgAPPswePS1 mouse model.International journal of ophthalmology · 2025Article
- White matter injury, cholesterol dysmetabolism, and APP/Abeta dysmetabolism interact to produce Alzheimer's disease (AD) neuropathology: A hypothesis and review.Frontiers in aging neuroscience · 2023Article
- Brain microstructural alterations in the left precuneus mediate the association between KIBRA polymorphism and working memory in healthy adults: a diffusion kurtosis imaging study.Brain imaging and behavior · 2022Article
- Widespread Reduced Density of Noradrenergic Locus Coeruleus Axons in the App Knock-In Mouse Model of Amyloid-β Amyloidosis.Journal of Alzheimer's disease : JAD · 2021Article
- No differences in brain microstructure between young KIBRA-C carriers and non-carriers.Oncotarget · 2018Article
- Axonal degeneration in an Alzheimer mouse model is PS1 gene dose dependent and linked to intraneuronal Aβ accumulation.Frontiers in aging neuroscience · 2014Article
- Axonal degeneration in Alzheimer's disease: when signaling abnormalities meet the axonal transport system.Experimental neurology · 2013Review
- Identification of the protein target of myelin-binding ligands by immunohistochemistry and biochemical analyses.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Amyloid beta (Aβ) peptides are known to accumulate in the brain of patients with Alzheimer's disease (AD). However, the link between brain amyloidosis and clinical symptoms has not been elucidated and could be mediated by secondary neuropathological alterations such as fiber tracts anomalies. In the present study, we have investigated the impact of Aβ overproduction in APPxPS1 transgenic mice on the integrity of forebrain axonal bundles (corpus callosum and anterior commissure). We found evidence of fiber tract volume reductions in APPxPS1 mice that were associated with an accelerated age-related loss of axonal neurofilaments and a myelin breakdown. The severity of these defects was neither correlated with the density of amyloid plaques nor associated with cell neurodegeneration. Our data suggest that commissural fiber tract alterations are present in Aβ-overproducing transgenic mice and that intracellular Aβ accumulation preceding extracellular deposits may act as a trigger of such morphological anomalies.
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.