Therapeutics: Intercellular adhesion molecule-1 (ICAM-1; CD54); interferon (IFN) γ
Mouse and patient sample studies suggest Copaxone glatiramer acetate or depletion of T regulatory (Treg) cells could help treat AD. Choroid plexus levels of ICAM-1 were lower in postmortem brain tissue samples from AD patients than from age-matched controls, and choroid plexus levels of ICAM-1 and numbers of IFNγ-positive immune cells were lower and numbers of Tregs were higher in a mouse model of AD than in normal mice. In the mouse model, Copaxone or diphtheria toxin-induced systemic depletion of Tregs increased levels of ICAM-1 and the number of IFNγ-positive immune cells in the choroid plexus, increased cognitive function and decreased neuroinflammation in the brain compared with vehicle or no Treg depletion, respectively. Next steps include testing undisclosed cancer immunotherapies in AD mice...