ArticleFrontiers in aging neuroscience2014
Axonal degeneration in an Alzheimer mouse model is PS1 gene dose dependent and linked to intraneuronal Aβ accumulation.
Article in Frontiers in aging neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 28 citations in OpenAlex.
- Advanced Immunolabeling Method for Optical Volumetric Imaging Reveals Dystrophic Neurites of Dopaminergic Neurons in Alzheimer's Disease Mouse Brain.Molecular neurobiology · 2024Article
- Glial Gap Junction Pathology in the Spinal Cord of the 5xFAD Mouse Model of Early-Onset Alzheimer's Disease.International journal of molecular sciences · 2022Article
- Pathophysiology of neurodegenerative diseases: An interplay among axonal transport failure, oxidative stress, and inflammation?Seminars in immunology · 2022Review
- Cleavage of human tau at Asp421 inhibits hyperphosphorylated tau induced pathology in a Drosophila model.Scientific reports · 2020Article
- Review
- mRNP assembly, axonal transport, and local translation in neurodegenerative diseases.Brain research · 2018Review
- Dendrobium nobile Lindl alkaloid, a novel autophagy inducer, protects against axonal degeneration induced by AβCNS neuroscience & therapeutics · 2017Article
- Article
- Article
- Synaptophysin depletion and intraneuronal Aβ in organotypic hippocampal slice cultures from huAPP transgenic mice.Molecular neurodegeneration · 2016Article
- Nmnat1 protects neuronal function without altering phospho-tau pathology in a mouse model of tauopathy.Annals of clinical and translational neurology · 2016Article
- Neuroprotective effects of salidroside through PI3K/Akt pathway activation in Alzheimer's disease models.Drug design, development and therapy · 2016Article
- Analyzing dendritic spine pathology in Alzheimer's disease: problems and opportunities.Acta neuropathologica · 2015Review
- Differential roles of Aβ processing in hypoxia-induced axonal damage.Neurobiology of disease · 2015Article
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Abnormalities and impairments in axonal transport are suggested to strongly contribute to the pathological alterations underlying AD. The exact mechanisms leading to axonopathy are currently unclear, but it was recently suggested that APP expression itself triggers axonal degeneration. We used APP transgenic mice and crossed them on a hemi- or homozygous PS1 knock-in background (APP/PS1KI). Depending on the mutant PS1 dosage, we demonstrate a clear aggravation in both plaque-associated and plaque-distant axonal degeneration, despite of an unchanged APP expression level. Amyloid-β (Aβ) peptides were found to accumulate in axonal swellings as well as in axons and apical dendrites proximate to neurons accumulating intraneuronal Aβ in their cell bodies. This suggests that Aβ can be transported within neurites thereby contributing to axonal deficits. In addition, diffuse extracellular Aβ deposits were observed in the close vicinity of axonal spheroids accumulating intracellular Aβ, which might be indicative of a local Aβ release from sites of axonal damage.
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