Several groups have utilized animal models of Alzheimer’s disease to demonstrate that altering the microglial activation state can be beneficial (Table 2). As previously mentioned for multiple sclerosis, GA is a promising molecule that can alter the inflammatory environment by recruiting Th2 T cells to the CNS and induce production of IL-4. Since it has shown positive benefits in patients with multiple sclerosis, there is the potential that GA could be a useful Alzheimer’s disease treatment. Data from Michal Schwartz’s group demonstrated that GA treatment leads to increased Aβ clearance and elevated levels of neurotropic cytokines such as IGF-1 [99]. The phenotype of microglia after treatment was similar to those treated with IL-4, suggesting that the GA effect could be IL-4 (and subsequently M2) dependent [135]. PPARγ activation is another approach that can robustly induce the polarization of M2 microglia and may be a promising therapy for Alzheimer’s disease. Several groups have observed that prolonged treatment with PPARγ agonists can reduce Alzheimer’s disease pathology, demonstrating its potential therapeutic efficacy [102,136,137]. In addition to reducing plaques, the PPARγ agonist pioglitazone increased
