Fig. 5

Putative mechanisms linking glycosphingolipids and neuroinflammation in Parkinson’s disease. Glycosphingolipid participation to neuroinflammation in neurodegenerative diseases could involve multiple mechanisms: autophagy impairments and inflammasome activation with the secretion of pro-inflammatory cytokine IL-1beta and IL-18; increased functional Ca²⁺ stores and increased agonist-induced Ca²⁺ release; increased blood–brain barrier permeability with increased expression of adhesion molecules ICAM-1 and VCAM-1 and caveolin-1 oligomerization; increased production of CCL2 and infiltration of CCR2+ peripheral immune cells; evocation of autoimmune responses and production of anti-glycosphingolipid autoantibodies.