2016 ACVIM Forum Research Abstract Program

These data suggest that M2, but not M1, microglia are progressively recruited to motor neurons during disease progression. Increased lumbar spinal cord fractalkine correlates with progressive M2 microglia in DM-affected dogs. Canine degenerative myelopathy (DM) is an adult-onset neurodegenerative disorder with four defined disease stages. DM initially manifests as spastic upper motor neuron paraparesis and general proprioceptive ataxia (stage 1). Progressive neurodegeneration results in non-ambulatory paraparesis/paraplegia (stage 2) and thoracic limb paresis (stage 3). End-stage disease culminates in flaccid tetraplegia, widespread muscle atrophy and signs of brainstem dysfunction (stage 4). The clinical spectrum of DM is homogeneous within and across breeds. Phosphorylated neurofilament heavy (pNF-H), a major structural protein of myelinated motor axons, has shown promise as a prognostic biomarker in other diseases of the nervous system such as amyotrophic lateral sclerosis (ALS). The goals of this study were to 1) quantify the concentration of pNF-H in the CSF of DM-affected dogs throughout disease progression and compare these finding to age-matched, neurologically normal dogs with and without SOD1 mutations and 2) compare CSF concentrations of pNF-H between DM-affected and dogs with other chronic spinal cord disease that mimic DM.