Abstract
Introduction CDV‐DL (Canine distemper virus‐induced demyelinating leukoencephalitis) represents a spontaneously occurring animal model for demyelinating disorders. Axonopathy represents a key pathomechanism in this disease; however, its underlying pathogenesis has not been addressed in detail so far. This study aimed at the characterization of axonal cytoskeletal, transport, and potential regenerative changes with a parallel focus upon Schwann cell remyelination.MethodsImmunohistochemistry of canine cerebellar tissue as well as a comparative analysis of genes from an independent microarray study were performed.ResultsIncreased axonal immunoreactivity for nonphosphorylated neurofilament was followed by loss of cytoskeletal and motor proteins. Interestingly, a subset of genes encoding for neurofilament subunits and motor proteins was up‐regulated in the chronic stage compared to dogs with subacute CDV‐DL. However, immunohistochemically, hints for axonal regeneration were restricted to up‐regulated axonal positivity of hypoxia‐inducible factor 1 alpha, while growth‐associated protein 43, erythropoietin and its receptor were not or even down‐regulated. Periaxin‐positive structures, indicative of Schwann cell remyelination, were only detected within few advanced lesions.ConclusionsThe present findings demonstrate a complex sequence of axonal cytoskeletal breakdown mechanisms. Moreover, though sparse, this is the first report of Schwann cell remyelination in CDV‐DL. Facilitation of these very limited endogenous regenerative responses represents an important topic for future research.
Highlights
CDV-DL (Canine distemper virus-induced demyelinating leukoencephalitis) represents a spontaneously occurring animal model for demyelinating disorders
Axonopathy represents a key pathomechanism in this disease; its underlying pathogenesis has not been addressed in detail so far
Though sparse, this is the first report of Schwann cell remyelination in CDV-DL
Summary
CDV-DL (Canine distemper virus-induced demyelinating leukoencephalitis) represents a spontaneously occurring animal model for demyelinating disorders. Conclusions: The present findings demonstrate a complex sequence of axonal cytoskeletal breakdown mechanisms. Though sparse, this is the first report of Schwann cell remyelination in CDV-DL. Demyelination during CDV-DL appears to represent a biphasic process with a primary virus-induced oligodendroglial dystrophy followed by a secondary wave of immune-mediated myelin destruction (Vandevelde et al 1982; Ulrich et al 2014). Substantiating this hypothesis, a recent microarray study of CDV-DL in canine brain tissue a 2016 The Authors.
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