ArticleActa neuropathologica communications2017
High plasticity of axonal pathology in Alzheimer's disease mouse models.
Article in Acta neuropathologica communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 63 citations in OpenAlex.
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- Pre-plaque glutamatergic hyperexcitability, mitochondrial dysfunction, and dendritic remodeling in the hippocampus of one-month-old 5xFAD mice.Frontiers in aging neuroscience · 2026Article
- Axonal spheroids are regulated by Schwann cells after peripheral nerve injury.bioRxiv : the preprint server for biology · 2024Article
- Xenografted human iPSC-derived neurons with the familial Alzheimer's disease APPActa neuropathologica · 2024Article
- White matter alterations and their associations with biomarkers and behavior in subjective cognitive decline individuals: a fixel-based analysis.Behavioral and brain functions : BBF · 2024Article
- Neuritic Plaques - Gateways to Understanding Alzheimer's Disease.Molecular neurobiology · 2024Review
- Transformation of non-neuritic into neuritic plaques during AD progression drives cortical spread of tau pathology via regenerative failure.Acta neuropathologica communications · 2023Article
- Article
- Diosgenin restores memory function via SPARC-driven axonal growth from the hippocampus to the PFC in Alzheimer's disease model mice.Molecular psychiatry · 2023Article
- Metals in Alzheimer's Disease.Biomedicines · 2023Review
- Accelerating the in vitro emulation of Alzheimer's disease-associated phenotypes using a novel 3D blood-brain barrier neurosphere co-culture model.Frontiers in bioengineering and biotechnology · 2023Article
- From cradle to grave: neurogenesis, neuroregeneration and neurodegeneration in Alzheimer's and Parkinson's diseases.Neural regeneration research · 2022Review
- Animal models of Alzheimer's disease: Applications, evaluation, and perspectives.Zoological research · 2022Review
- JIP3 links lysosome transport to regulation of multiple components of the axonal cytoskeleton.Communications biology · 2022Article
- Excessive/Aberrant and Maladaptive Synaptic Plasticity: A Hypothesis for the Pathogenesis of Alzheimer's Disease.Frontiers in aging neuroscience · 2022Article
- BRUCE silencing leads to axonal dystrophy by repressing autophagosome-lysosome fusion in Alzheimer's disease.Translational psychiatry · 2021Article
- Nutraceutical and Probiotic Approaches to Examine Molecular Interactions of the Amyloid Precursor Protein APP inInternational journal of molecular sciences · 2021Review
- Neuronal loss and microgliosis are restricted to the core of Aβ deposits in mouse models of Alzheimer's disease.Aging cell · 2021Article
- The variability of MR axon radii estimates in the human white matter.Human brain mapping · 2021Article
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Axonal dystrophies (AxDs) are swollen and tortuous neuronal processes that are associated with extracellular depositions of amyloid β (Aβ) and have been observed to contribute to synaptic alterations occurring in Alzheimer's disease. Understanding the temporal course of this axonal pathology is of high relevance to comprehend the progression of the disease over time. We performed a long-term in vivo study (up to 210 days of two-photon imaging) with two transgenic mouse models (dE9xGFP-M and APP-PS1xGFP-M). Interestingly, AxDs were formed only in a quarter of GFP-expressing axons near Aβ-plaques, which indicates a selective vulnerability. AxDs, especially those reaching larger sizes, had long lifetimes and appeared as highly plastic structures with large variations in size and shape and axonal sprouting over time. In the case of the APP-PS1 mouse only, the formation of new long axonal segments in dystrophic axons (re-growth phenomenon) was observed. Moreover, new AxDs could appear at the same point of the axon where a previous AxD had been located before disappearance (re-formation phenomenon). In addition, we observed that most AxDs were formed and developed during the imaging period, and numerous AxDs had already disappeared by the end of this time. This work is the first in vivo study analyzing quantitatively the high plasticity of the axonal pathology around Aβ plaques. We hypothesized that a therapeutically early prevention of Aβ plaque formation or their growth might halt disease progression and promote functional axon regeneration and the recovery of neural circuits.
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