ArticleNeurobiology of pain (Cambridge, Mass.)
Sensory-specific peripheral nerve pathology in a rat model of Fabry disease.
Article in Neurobiology of pain (Cambridge, Mass.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Not Just Neurons: Pain Is Orchestrated in Partnership with Many Non-neuronal Cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Review
- Article
- The Importance of Early Treatment of Inherited Neuromuscular Conditions.Journal of neuromuscular diseases · 2024Review
- Molecular Pathogenesis of Central and Peripheral Nervous System Complications in Anderson-Fabry Disease.International journal of molecular sciences · 2023Review
- Novel Therapeutic Approaches in Inherited Neuropathies: A Systematic Review.Pharmaceutics · 2023Review
- Age-related neuroimmune signatures in dorsal root ganglia of a Fabry disease mouse model.Immunity & ageing : I & A · 2023Article
- HomeCageScan analysis reveals ongoing pain in Fabry rats.Neurobiology of pain (Cambridge, Mass.)Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Fabry disease (FD) causes life-long pain, the mechanisms of which are unclear. Patients with FD have chronic pain that mirrors symptoms of other painful peripheral neuropathies. However, it is unclear what underlying damage occurs in FD peripheral nerves that may contribute to chronic pain. Here, we characterized myelinated and unmyelinated fiber pathology in peripheral nerves of a rat model of FD. Decreased nerve fiber density and increased nerve fiber pathology were noted in unmyelinated and myelinated fibers from FD rats; both observations were dependent on sampled nerve fiber modality and anatomical location. FD myelinated axons exhibited lipid accumulations that were determined to be the FD-associated lipid globotriaosylceramide (Gb3), and to a lesser extent lysosomes. These findings suggest that axonal Gb3 accumulation may drive peripheral neuron dysfunction and subsequent pain in FD.
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Registered trials
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