2016 ACVIM Forum Research Abstract Program

11TxB 2 was reliably detected in urine, but not in serum or CSF. Storage at 4°C up to 7 days did not significantly affect urine TxB 2 levels, and concurrent corticosteroid or non-steroidal anti-inflammatory medication did not apparently affect levels within the study group as a whole. Overlap of 11TxB 2 urine levels was seen between clinically normal and neurological animal groups. Although some of the highest 11TxB 2 values were seen in animals with intracranial neoplasia, overlap with other neurological disease groups was present. Assay of 11TxB 2 is feasible; however, additional analysis of a large study population will be necessary to determine whether a threshold urine 11TxB 2 level may be useful as a diagnostic biomarker. Canine degenerative myelopathy (DM) is an adult-onset neurodegenerative disorder. Clinical progression is homogeneous within and across breeds, thus four distinct disease stages have been identified (Kanazono et al., 2013; Coates and Wininger, 2010) . DM shares similarities with some forms of amyotrophic lateral sclerosis (ALS), including underlying mutations in superoxide dismutase-1 (SOD1). SOD1-mutant microglia play a central role in ALS progression in rodent models. Microglia behavior is complex, as expression patterns of classic M1 and M2 molecules are variable throughout disease and between species studied. The mechanism(s) underlying microglial phenotype determination within ALS is not known. Fractalkine, a neuronally produced chemokine, has been shown to suppress SOD1 mutant microglial-mediated neurotoxicity in vitro. Thus, fractalkine is a possible contributor to microglial phenotype determination in ALS. Increased spinal cord microglia have been documented in end-stage DM-affected dogs, however, their response and phenotype throughout disease progression is unknown. The goals of this study were to (1) quantify and phenotype microglial cells in close proximity to lumbar spinal cord motor neurons of DM-affected dogs at each disease stage and compare these findings to age-matched, neurologically normal dogs and (2) correlate microglial phenotype with fractalkine protein levels in lumbar spinal cord throughout disease progression.