Presenting Author: Lillia Baird
, Doctoral Candidate at Univ. of Michigan
Abstract:
There is overwhelming evidence that the immune system plays a significant role in amyotrophic lateral sclerosis (ALS), a devastating neurodegenerative disease characterized by motor neuron degeneration. Expected survival is 2-4 years from disease onset and treatment options are limited. There is significant clinical and pathogenic heterogeneity and an incomplete understanding of the underlying pathogenesis, including mechanisms of immune contribution. Neutrophils are consistently implicated in ALS, with increased count in the blood and infiltration into the spinal cord. Increased neutrophil count and activation are associated with shortened survival and neutrophil levels are the single best predictor of future ALS progression. Despite this, little is known about which neutrophil subpopulations are dysregulated or the underlying mechanisms contributing to disease progression. Primary neutrophils were assessed via flow and ex vivo stimulation. NET remnants (MPO:DNA, elastase, extracellular DNA) were quantitated in plasma. Distinct populations were observed in controls and ALS subjects, and ex vivo analysis of primary neutrophils and analysis of NET remnants demonstrates changes in effector functions that may contribute to BBB disruption and neuronal damage in ALS. These differences in neutrophil populations and function provide compelling evidence that neutrophils play a role in ALS progression, as well as provide novel targets for therapeutics.
Amyotrophic lateral sclerosis is associated with changes in peripheral neutrophil heterogeneity and function
Category
Poster and Podium (Block Symposium)
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Date: May 4 Presentation Time: 03:15 PM to 04:30 PM Room: Exhibit Hall F1