Described are methods of treating or preventing an inflammatory disease or condition caused by excessive expression, secretion, or concentration of alpha synuclein. The methods comprise administering compositions that reduce the effective concentration of alpha-synuclein present in the surrounding tissues. In addition, the invention encompasses methods of inhibiting alpha-synuclein interaction with CD11b, comprising administering an agent that binds to alpha-synuclein to prevent binding productively to the integrin CD11b, or administering an active agent that interacts with CD11b on an immune cell to prevent alpha-synuclein from directing chemotaxis of that cell. In addition, the invention discloses a method of identifying an individual with a condition amenable to treatment targeting alpha-synuclein CD11b interaction.
