A role for Apolipoprotein A-I in the pathogenesis of multiple sclerosis

- We identified the differential expression of Apo A-I protein in human plasma.
- MS patients on average had less Apo A-I compared to healthy controls.
- The lowest expression of Apo A-I was found in progressive MS patients.
- Mouse deficient in murine Apo A-I had worse EAE disease, an animal model for MS.

Apolipoprotein A1 (Apo A-I), the most abundant component of high-density lipoprotein (HDL), is an anti-inflammatory molecule, yet its potential role in the pathogenesis of multiple sclerosis (MS) has not been fully investigated. In this study, Western blot analyses of human plasma showed differential Apo A-I expression in healthy controls compared to MS patients. Further, primary progressive MS patients had less plasma Apo A-I than other forms of MS. Using experimental allergic encephalomyelitis (EAE) as a model for MS, Apo A-I deficient mice exhibited worse clinical disease and more neurodegeneration concurrent with increased levels of pro-inflammatory cytokines compared to wild-type animals. These data suggest that Apo A-I plays a role in the pathogenesis of EAE, a model for MS, creating the possibility for agents that increase Apo A-I levels as potential therapies for MS.