Deletion of the inflammatory S100-A9/MRP14 protein does not influence survival in hSOD1G93A ALS mice

Neuroinflammation is a hallmark of Amyotrophic Lateral Sclerosis (ALS) in hSOD1G93A mouse models where microglial cells contribute to the progressive motor neuron degenerative process. S100-A8 and S100-A9 (also known as MRP8 MRP14, respectively) are cytoplasmic proteins expressed by inflammatory myeloid cells, including microglia macrophages. Mainly acting heterodimer, S100-A8/A9, when secreted, can activate Toll-like Receptor 4 on immune leading deleterious proinflammatory cytokine production. Deletion S100a9 Alzheimer's disease showed positive outcome, reducing pathology. We now assessed its role ALS. Unexpectedly, our results show that deleting ALS mice had no impact survival, but rather accelerated symptoms with activation suggesting blocking would not be valuable strategy for