IL18 and amyotrophic lateral sclerosis: Among secondary biological outcome measures we observed changes on B and T cell subpopulations, monocytes, and on IL-18, which could be suggestive of a rapamycin-mediated effect on neuroinflammation in ALS, where misfolded protein aggregates may activate a cascade of events that drives chronic inflammation and secretion of proinflammatory cytokines, among which IL-18, that finally leads to tissue damage and cell death24.